Category Archives: Immunology

Immunology Fair-Market Value Compensation Rates for US Health Care Providers: FMV/Fee Schedules for Thought … – Business Wire (press release)

DUBLIN--(BUSINESS WIRE)--Research and Markets has announced the addition of the "Fair-Market Value Compensation Rates for U.S. Health Care Providers: FMV/Fee Schedules for Thought Leaders/KOLs - Immunology" report to their offering.

Fair-Market Value Compensation Rates for U.S. HCPs - Immunology presents hourly and half-day flat compensation rates for four (4) Thought Leader levels based on degree of influence. The analysis includes rates for six (6) specific activities as well as for other non-specified activities. The findings presented in this report result from the input from executives at 16 life science organizations.

This study presents fair-market value (FMV) compensation rates by percentiles, with averages, for six (6) activities as well as for non-specific activities, for four (4) levels of Thought Leader influences (rare, international, national and local).

Payments made to physicians and thought leaders have been under scrutiny for a few years and companies have been working to adjust their rates to level with industry standards. Adjustments to market rates should be done periodically and are best done through 3rd party research, providing a fair and balanced assessment of rates.

The research findings deliver markets rates used in the conduct of exchanges with Thought Leaders from 16 life science organizations. These payment benchmarks help legal, compliance and medical affair executives refine and support the development of fee schedules that are aligned with market conditions.

Key Topics Covered:

1. Research Methodology

2. Definitions

- Therapeutic Area

- Thought Leader Levels

- Salary Data versus Market Rates

- Hourly Rates

- Flat Rates

3. Flat Rates

- Advisory Board Lead

- Advisory Board Non-lead

- Consulting Scientific / Clinical Content

- Consulting Commercial Content

- Speaking Scientific / Clinical Content

- Speaking Commercial Content

- Other Activities

4. Hourly Rates

- Advisory Board Lead

- Advisory Board Non-lead

- Consulting Scientific / Clinical Content

- Consulting Commercial Content

- Speaking Scientific / Clinical Content

- Speaking Commercial Content

- Other Activities

For more information about this report visit http://www.researchandmarkets.com/research/9429rg/fairmarket_value

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Immunology Fair-Market Value Compensation Rates for US Health Care Providers: FMV/Fee Schedules for Thought ... - Business Wire (press release)

Study reveals new role for cancer drug in tumor immunology – News-Medical.net

February 13, 2017 at 2:23 AM

A drug first designed to prevent cancer cells from multiplying has a second effect: it switches immune cells that turn down the body's attack on tumors back into the kind that amplify it. This is the finding of a study led by researchers from NYU Langone Medical Center and published recently in Cancer Immunology Research.

According to experiments in mice, macrophages - immune cells that home in on tumors - take in the drug nab-paclitaxel (brand name Abraxane). Once inside these cells, say the study authors, the drug changes them so that they signal for an aggressive anti-tumor immune response.

"Our study reveals a previously unappreciated role for Abraxane in tumor immunology," says corresponding author Dafna Bar-Sagi, PhD, Vice Dean for Science and Chief Scientific Officer at NYU Langone.

"In doing so, it suggests ways to improve the drug and argues for its inclusion in new kinds of combination treatments," says Bar-Sagi, also a professor in the Department of Biochemistry and Molecular Pharmacology at NYU Langone, and associated with its Perlmutter Cancer Center.

Abraxane over Paclitaxel

Abraxane is comprised of the decades-old cancer drug, paclitaxel, combined with nanoparticles of the protein albumin (nab). Paclitaxel alone is not effective against pancreatic cancer, but Abraxane (nab-paclitaxel) is part of a leading treatment for the disease. Why the albumin-bound form works better has been a major question in the field.

Paclitaxel prevents structures called microtubules inside cancer cells from breaking up, a required step if they are to multiply as part of abnormal growth. Many in the field assume that nab-paclitaxel too primarily targets microtubules in cancer cells, with albumin perhaps helping the drug to get inside cells, and with fewer toxic side-effects.

The new findings suggest that, on top of any effect on cancer cells, Abraxane's effectiveness may proceed from its impact on macrophages, which roam the bloodstream and build up in many tumors.

The study results revolve around the immune system, in which cells like macrophages trigger a massive attack on bacteria or other invading microbes. This system can also recognize and attack cancer cells. Factors secreted by tumor cells, however, dampen the immune response in part by switching macrophages from their immune-stimulating stance, termed M1, into an M2 mode that suppresses their immune function.

In experiments in macrophage cell lines, the study authors found that nab-paclitaxel is more effective than paclitaxel partly because albumin enables macrophages to take up the drug through a natural process called macropinocytosis.

Once inside macrophages, according to experiments in mice with pancreatic tumors, nab-paclitaxel causes the macrophages to switch from immune-suppressing M2 cells back into M1 cells that amplify the body's effort to kill cancer cells. Past studies had found that paclitaxel has a similar structure to substances given off by bacteria that trigger macrophage activation. The study authors show that the same pathway is evoked by nab-paclitaxel in pancreatic tumor-associated macrophages.

"Our findings argue that it may be possible to develop more treatments that selectively target macrophages by coupling albumin to immune-activating agents," said lead study author Jane Cullis, PhD, a postdoctoral fellow in Bar-Sagi's lab. "We may also be able to adjust albumin's structure such that drugs attached to it stay in macrophages longer, or combine Abraxane with T-cell treatments for greater therapeutic effect. In principle, such treatments should be useful against the many tumor types infiltrated by macrophages."

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Study reveals new role for cancer drug in tumor immunology - News-Medical.net

Best Treatment For Warts? Candida Antigen Immunology Injection Works Better And Faster Than Freezing – Medical Daily

Warts are a common butannoying health problem affliciting countless peopleworldwide. Cryotherapy traditionally has been regarded as the most effect wart removal treatment, but new research from the Mashhad University of Medical Sciences in Iransuggests that aninjection of candida antigen, a type of immunotherapy,may be able to get rid of warts faster and keep them away.

The study, now published online in International Journal of Dermatology,found that 76.7 percent of patients with either a verruca vulgaris wart (found anywhere on the body) or a plantar wart (found on the bottom of feet) were cured with immunotherapy, compared to only 56.7 percent of wart patients treated with cryotherapy. In addition, patients who recieved immunotherapy were cured with fewer sessions than those whose warts were frozen off.

Read: 'Tree Man' Finally Gets Surgery To Remove Warts Caused By Rare Genetic Disease Epidermodysplasia Verruciformis

"Intralesional immunotherapy is an effective treatment of warts," the authors wrote, according to a post on Medical Xpress. "This method has a better therapeutic response, needs fewer sessions, and is capable of treating distant warts."

Plantar warts, or warts found on the bottoms of feet, are common, especially among children. Photo Courtesy of Pixabay

For the study, 60 patients with either a body or footwart were divided into two groups. The first group recieved an immunotherapy treatment consistingof an injection of candida antigen into their warts every three weeks until complete improvement or a maximum of three sessions. The second group recieved cryotherapy consisting of liquid nitrogen for a maximum of 10 weeks of until the wart had completely cleared.

Warts occur when your skin comes in contact with one of the many viruses classifed as human papillomavirus. In most cases, warts are harmless causing little more than slight discomfort and embarrassment. According to WebMD, they are very contagious, and can spread not only from person to person but also from one part of the body to another.

While some warts can go away on their own, for the most part they need to be treated. Cryotherapy is the standard treatment for warts and involves freezing a wart using a very cold substance, usually liquid nitrogen. The treatment is often painful and may need several tries before the wart is completely removed. This treatment also comes with the risk of possible scarring.

Candida antigen injections are a relatively new treatment option for wart removal, and this is not the first time its success in wart thereapy has been documented. However, as reported by Dermotology News, this treatment also comes with its own set of possible side effects and may cause discomfort, redness, and swelling.

Source: Khozeimeh F, Jabbari F, Mahboubi Oskouei Y, et al. Intralesional immunotherapy compared to cryotherapy in the treatment of warts. International Journal of Dermatology. 2017

See Also:

Warts More Likely Contracted From Home, Not Public Hotspots

After HPV Vaccinations Rates of Genital Warts Decline Significantly in Women, but Not Men

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Best Treatment For Warts? Candida Antigen Immunology Injection Works Better And Faster Than Freezing - Medical Daily

Immunology takes new approach to beating cancer – The Advocate

Two years after she was diagnosed with stage 4 lung cancer, Wanda Poche has a hard time believing she ever had the disease.

"I always felt like from the date I was diagnosed that I didn't have cancer," she said.

The 65-year-old woman is cancer-free after receiving a newly developed treatment that uses the body's immune system to fight the disease.

Immunotherapy, doctors say, is an innovative advancement that could change the way certain cancers are viewed.

"Everybody's excited about it," said Dr. Vince Cataldo, an oncologist at Mary Bird Perkins Our Lady of the Cancer Center in Baton Rouge. "We're definitely on the forefront."

Chemotherapy attacks a cancer cell's DNA to stop the cell from dividing, thereby stopping the cancer's growth. Traditional chemotherapy "tears the immune system apart," Cataldo said.

"It suppresses the immune system, and people's biggest side effects from chemotherapy are the risk of infection because there is no immune system," he said.

Immunotherapy tries to "make the immune system smarter," he said.

Normally, the body's immune system remains inactive until it needs to fight a threat. But our bodies put the brakes on the immune system to slow it down. An unchecked immune response can eventually kill you.

The new immunotherapy cancer drugs remove those brakes, Cataldo said.

"It has truly changed the way we fight multiple diseases," Cataldo said.

Some prominent drugs, like the one Poche received, target certain cancer cells to make them prone to damage from the immune system.

Cataldo explained that the cancer cells have a receptor similar to an antenna. The immunotherapy drugs block that antenna and allow the immune system to attack the cells.

Poche's battle started in October of 2014 with what she thought was a nagging sinus infection. Her doctor took a chest X-ray and found lung cancer. Because she had quit smoking decades before, Poche was surprised.

"I never expected that," she said. "All through this, I never had shortness of breath. I could always climb stairs. I've always been pretty healthy."

But her cancer had spread to her adrenal gland and lymph nodes. The ear, nose and throat doctor had saved her life, she said.

After months of different chemotherapy treatments, Poche was making no progress against the tumors. Cataldo decided she would be a candidate for a trial of a drug marketed as OPDIVO.

Poche had no side effects from the drug, which Cataldo said is common.

"It doesn't beat up the immune system," he said. "We don't normally see hair loss. We don't typically see vomiting."

After 15 months of IV infusions, there were no signs of Poche's tumors in an August scan. Last month she had a full-body scan, and the cancer had not returned.

"It was still showing clear," she said. "God is great."

Poche will take the treatments every two weeks for the foreseeable future to stop the cancer from returning. But that's a small price to pay, she said.

While immunotherapy works well for lung cancer, it doesn't treat all cancers. This class of drug has been approved to treat kidney cancer, melanoma and Hodgkin lymphoma in addition to lung cancer, diseases that "have nothing in common," Cataldo said.

But the therapy doesn't work for everyone. Patients who have autoimmune disorders like rheumatoid arthritis or lupus may experience harsh side effects.

Doctors are hopeful that more cancers can be treated with this type of drug.

"Cancer centers are looking for new indications, and they're doing cutting-edge clinical trials to see what the next one is going to be," Cataldo said.

Follow Kyle Peveto on Twitter, @kylepeveto.

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Immunology takes new approach to beating cancer - The Advocate

Department of Immunology: UT Southwestern, Dallas, TX

The Department of Immunology at UTSouthwestern Medical Center was founded in 1998 with six faculty members and a relatively small research facility. Today, weve grown to include:

Our Department is part of the Division of Basic Science of UTSouthwesterns Graduate School of Biomedical Sciences.

At its core, our mission is two-fold: advance knowledge and understanding of disorders of the immune system, and train future generations of scientists. These dual functions make the Department of Immunology a key contributor in UTSouthwesterns promise of delivering the future of medicine, today.

Our primary research interests involve the characterization of animal models of human diseases and the delineation of molecular mechanisms mediating normal and abnormal immune functions. Learn more about some of the research currently underway in the Department of Immunology.

The Departments research programs are funded by a combination of endowments and external grant support.

Visit the labs of our faculty members to see their research.

The Department of Immunology trains graduate students and postdoctoral fellows and has new positions and opportunities available each year. Find out more about our broad-based program of graduate training in Immunology.

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Department of Immunology: UT Southwestern, Dallas, TX

Immunology Program | Memorial Sloan Kettering Cancer Center

The immune system represents a complex, interacting set of cells and molecules controlled by specific genes and their products. Immunology provides the basis for a whole range of problems relevant to other disciplines, including cell biology, structural biology, genetics, and medicine. Thus, the field of immunology crosses through and integrates multiple disciplines of biology and medicine.

The scope of immunology at the Sloan Kettering Instituteincorporates a range of areas and expertise (both basic and translational science). A strength of the Immunology Program is the ability to translate laboratory findings into effective clinical applications.

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Research in the Immunology Program focuses on several areas:

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Immunology Program | Memorial Sloan Kettering Cancer Center

Psychoneuroimmunology – Wikipedia

Psychoneuroimmunology (PNI), also referred to as psychoendoneuroimmunology (PENI) or psychoneuroendocrinoimmunology (PNEI), is the study of the interaction between psychological processes and the nervous and immune systems of the human body.[1] PNI takes an interdisciplinary approach, incorporating psychology, neuroscience, immunology, physiology, genetics, pharmacology, molecular biology, psychiatry, behavioral medicine, infectious diseases, endocrinology, and rheumatology.

The main interests of PNI are the interactions between the nervous and immune systems and the relationships between mental processes and health. PNI studies, among other things, the physiological functioning of the neuroimmune system in health and disease; disorders of the neuroimmune system (autoimmune diseases; hypersensitivities; immune deficiency); and the physical, chemical and physiological characteristics of the components of the neuroimmune system in vitro, in situ, and in vivo.

Interest in the relationship between psychiatric syndromes or symptoms and immune function has been a consistent theme since the beginning of modern medicine.

Claude Bernard, a French physiologist of the Musum national d'Histoire naturelle, formulated the concept of the milieu interieur in the mid-1800s. In 1865, Bernard described the perturbation of this internal state: "... there are protective functions of organic elements holding living materials in reserve and maintaining without interruption humidity, heat and other conditions indispensable to vital activity. Sickness and death are only a dislocation or perturbation of that mechanism" (Bernard, 1865). Walter Cannon, a professor of physiology at Harvard University coined the commonly used term, homeostasis, in his book The Wisdom of the Body, 1932, from the Greek word homoios, meaning similar, and stasis, meaning position. In his work with animals, Cannon observed that any change of emotional state in the beast, such as anxiety, distress, or rage, was accompanied by total cessation of movements of the stomach (Bodily Changes in Pain, Hunger, Fear and Rage, 1915). These studies looked into the relationship between the effects of emotions and perceptions on the autonomic nervous system, namely the sympathetic and parasympathetic responses that initiated the recognition of the freeze, fight or flight response. His findings were published from time to time in professional journals, then summed up in book form in The Mechanical Factors of Digestion, published in 1911.

Hans Selye, a student of Johns Hopkins University and McGill University, and a researcher at Universit de Montral, experimented with animals by putting them under different physical and mental adverse conditions and noted that under these difficult conditions the body consistently adapted to heal and recover. Several years of experimentation that formed the empiric foundation of Selye's concept of the General Adaptation Syndrome. This syndrome consists of an enlargement of the adrenal gland, atrophy of the thymus, spleen, and other lymphoid tissue, and gastric ulcerations.

Selye describes three stages of adaptation, including an initial brief alarm reaction, followed by a prolonged period of resistance, and a terminal stage of exhaustion and death. This foundational work led to a rich line of research on the biological functioning of glucocorticoids.[2]

Mid-20th century studies of psychiatric patients reported immune alterations in psychotic individuals, including lower numbers of lymphocytes[3][4] and poorer antibody response to pertussis vaccination, compared with nonpsychiatric control subjects.[5] In 1964, George F. Solomon, from the University of California in Los Angeles, and his research team coined the term "psychoimmunology" and published a landmark paper: "Emotions, immunity, and disease: a speculative theoretical integration."[6]

In 1975, Robert Ader and Nicholas Cohen, at the University of Rochester, advanced PNI with their demonstration of classic conditioning of immune function, and they subsequently coined the term "psychoneuroimmunology".[7][8] Ader was investigating how long conditioned responses (in the sense of Pavlov's conditioning of dogs to drool when they heard a bell ring) might last in laboratory rats. To condition the rats, he used a combination[clarification needed] of saccharin-laced water (the conditioned stimulus) and the drug Cytoxan, which unconditionally induces nausea and taste aversion and suppression of immune function. Ader was surprised to discover that after conditioning, just feeding the rats saccharin-laced water was associated with the death of some animals and he proposed that they had been immunosuppressed after receiving the conditioned stimulus. Ader (a psychologist) and Cohen (an immunologist) directly tested this hypothesis by deliberately immunizing conditioned and unconditioned animals, exposing these and other control groups to the conditioned taste stimulus, and then measuring the amount of antibody produced. The highly reproducible results revealed that conditioned rats exposed to the conditioned stimulus were indeed immuno suppressed. In other words, a signal via the nervous system (taste) was affecting immune function. This was one of the first scientific experiments that demonstrated that the nervous system can affect the immune system.

In 1981, David L. Felten, then working at the Indiana University School of Medicine, discovered a network of nerves leading to blood vessels as well as cells of the immune system. The researcher, along with his team, also found nerves in the thymus and spleen terminating near clusters of lymphocytes, macrophages, and mast cells, all of which help control immune function. This discovery provided one of the first indications of how neuro-immune interaction occurs.

Ader, Cohen, and Felten went on to edit the groundbreaking book Psychoneuroimmunology in 1981, which laid out the underlying premise that the brain and immune system represent a single, integrated system of defense.

In 1985, research by neuropharmacologist Candace Pert, of the National Institutes of Health at Georgetown University, revealed that neuropeptide-specific receptors are present on the cell walls of both the brain and the immune system.[9][10] The discovery that neuropeptides and neurotransmitters act directly upon the immune system shows their close association with emotions and suggests mechanisms through which emotions, from the limbic system, and immunology are deeply interdependent. Showing that the immune and endocrine systems are modulated not only by the brain but also by the central nervous system itself affected the understanding of emotions, as well as disease.

Contemporary advances in psychiatry, immunology, neurology, and other integrated disciplines of medicine has fostered enormous growth for PNI. The mechanisms underlying behaviorally induced alterations of immune function, and immune alterations inducing behavioral changes, are likely to have clinical and therapeutic implications that will not be fully appreciated until more is known about the extent of these interrelationships in normal and pathophysiological states.

PNI research is looking for the exact mechanisms by which specific brainimmunity effects are achieved. Evidence for nervous systemimmune system interactions exists at several biological levels.

The immune system and the brain talk to each other through signaling pathways. The brain and the immune system are the two major adaptive systems of the body. Two major pathways are involved in this cross-talk: the Hypothalamic-pituitary-adrenal axis (HPA axis) and the sympathetic nervous system (SNS). The activation of SNS during an immune response might be aimed to localize the inflammatory response.

The body's primary stress management system is the HPA axis. The HPA axis responds to physical and mental challenge to maintain homeostasis in part by controlling the body's cortisol level. Dysregulation of the HPA axis is implicated in numerous stress-related diseases, with evidence from meta-analyses indicating that different types/duration of stressors and unique personal variables can shape the HPA response.[11] HPA axis activity and cytokines are intrinsically intertwined: inflammatory cytokines stimulate adrenocorticotropic hormone (ACTH) and cortisol secretion, while, in turn, glucocorticoids suppress the synthesis of proinflammatory cytokines.

Molecules called pro-inflammatory cytokines, which include interleukin-1 (IL-1), Interleukin-2 (IL-2), interleukin-6 (IL-6), Interleukin-12 (IL-12), Interferon-gamma (IFN-Gamma) and tumor necrosis factor alpha (TNF-alpha) can affect brain growth as well as neuronal function. Circulating immune cells such as macrophages, as well as glial cells (microglia and astrocytes) secrete these molecules. Cytokine regulation of hypothalamic function is an active area of research for the treatment of anxiety-related disorders.[12]

Cytokines mediate and control immune and inflammatory responses. Complex interactions exist between cytokines, inflammation and the adaptive responses in maintaining homeostasis. Like the stress response, the inflammatory reaction is crucial for survival. Systemic inflammatory reaction results in stimulation of four major programs:[13]

These are mediated by the HPA axis and the SNS. Common human diseases such as allergy, autoimmunity, chronic infections and sepsis are characterized by a dysregulation of the pro-inflammatory versus anti-inflammatory and T helper (Th1) versus (Th2) cytokine balance.

Recent studies show pro-inflammatory cytokine processes take place during depression, mania and bipolar disease, in addition to autoimmune hypersensitivity and chronic infections.

Chronic secretion of stress hormones, glucocorticoids (GCs) and catecholamines (CAs), as a result of disease, may reduce the effect of neurotransmitters, including serotonin[medical citation needed], norepinephrine and dopamine, or other receptors in the brain, thereby leading to the dysregulation of neurohormones. Under stimulation, norepinephrine is released from the sympathetic nerve terminals in organs, and the target immune cells express adrenoreceptors. Through stimulation of these receptors, locally released norepinephrine, or circulating catecholamines such as epinephrine, affect lymphocyte traffic, circulation, and proliferation, and modulate cytokine production and the functional activity of different lymphoid cells.

Glucocorticoids also inhibit the further secretion of corticotropin-releasing hormone from the hypothalamus and ACTH from the pituitary (negative feedback). Under certain conditions stress hormones may facilitate inflammation through induction of signaling pathways and through activation of the Corticotropin-releasing hormone.

These abnormalities and the failure of the adaptive systems to resolve inflammation affect the well-being of the individual, including behavioral parameters, quality of life and sleep, as well as indices of metabolic and cardiovascular health, developing into a "systemic anti-inflammatory feedback" and/or "hyperactivity" of the local pro-inflammatory factors which may contribute to the pathogenesis of disease.

This systemic or neuro-inflammation and neuroimmune activation have been shown to play a role in the etiology of a variety of neurodegenerative disorders such as Parkinson's and Alzheimer's disease, multiple sclerosis, pain, and AIDS-associated dementia. However, cytokines and chemokines also modulate central nervous system (CNS) function in the absence of overt immunological, physiological, or psychological challenges.[14]

There is now sufficient data to conclude that immune modulation by psychosocial stressors and/or interventions can lead to actual health changes. Although changes related to infectious disease and wound healing have provided the strongest evidence to date, the clinical importance of immunological dysregulation is highlighted by increased risks across diverse conditions and diseases. For example, stressors can produce profound health consequences. In one epidemiological study, all-cause mortality increased in the month following a severe stressor the death of a spouse.[15] Theorists propose that stressful events trigger cognitive and affective responses which, in turn, induce sympathetic nervous system and endocrine changes, and these ultimately impair immune function.[16][17] Potential health consequences are broad, but include rates of infection[18][19] HIV progression[20][21] cancer incidence and progression,[15][22][23] and high rates of infant mortality.[24][25]

Stress is thought to affect immune function through emotional and/or behavioral manifestations such as anxiety, fear, tension, anger and sadness and physiological changes such as heart rate, blood pressure, and sweating. Researchers have suggested that these changes are beneficial if they are of limited duration,[16] but when stress is chronic, the system is unable to maintain equilibrium or homeostasis.

In one of the earlier PNI studies, which was published in 1960, subjects were led to believe that they had accidentally caused serious injury to a companion through misuse of explosives.[26] Since then decades of research resulted in two large meta-analyses, which showed consistent immune dysregulation in healthy people who are experiencing stress.

In the first meta-analysis by Herbert and Cohen in 1993,[27] they examined 38 studies of stressful events and immune function in healthy adults. They included studies of acute laboratory stressors (e.g. a speech task), short-term naturalistic stressors (e.g. medical examinations), and long-term naturalistic stressors (e.g. divorce, bereavement, caregiving, unemployment). They found consistent stress-related increases in numbers of total white blood cells, as well as decreases in the numbers of helper T cells, suppressor T cells, and cytotoxic T cells, B cells, and Natural killer cells (NK). They also reported stress-related decreases in NK and T cell function, and T cell proliferative responses to phytohaemagglutinin [PHA] and concanavalin A [Con A]. These effects were consistent for short-term and long-term naturalistic stressors, but not laboratory stressors.

In the second meta-analysis by Zorrilla et al. in 2001,[28] they replicated Herbert and Cohen's meta-analysis. Using the same study selection procedures, they analyzed 75 studies of stressors and human immunity. Naturalistic stressors were associated with increases in number of circulating neutrophils, decreases in number and percentages of total T cells and helper T cells, and decreases in percentages of Natural killer cell (NK) cells and cytotoxic T cell lymphocytes. They also replicated Herbert and Cohen's finding of stress-related decreases in NKCC and T cell mitogen proliferation to Phytohaemagglutinin (PHA) and Concanavalin A (Con A).

More recently, there has been increasing interest in the links between interpersonal stressors and immune function. For example, marital conflict, loneliness, caring for a person with a chronic medical condition, and other forms on interpersonal stress dysregulate immune function.[29]

Release of corticotropin-releasing hormone (CRH) from the hypothalamus is influenced by stress.

Furthermore, stressors that enhance the release of CRH suppress the function of the immune system; conversely, stressors that depress CRH release potentiate immunity.

Glutamate agonists, cytokine inhibitors, vanilloid-receptor agonists, catecholamine modulators, ion-channel blockers, anticonvulsants, GABA agonists (including opioids and cannabinoids), COX inhibitors, acetylcholine modulators, melatonin analogs (such as Ramelton), adenosine receptor antagonists and several miscellaneous drugs (including biologics like Passiflora edulis) are being studied for their psychoneuroimmunological effects.

For example, SSRIs, SNRIs and tricyclic antidepressants acting on serotonin, norepinephrine and dopamine receptors have been shown to be immunomodulatory and anti-inflammatory against pro-inflammatory cytokine processes, specifically on the regulation of IFN-gamma and IL-10, as well as TNF-alpha and IL-6 through a psychoneuroimmunological process.[32][33][34] Antidepressants have also been shown to suppress TH1 upregulation.[32][33][34][35][36]

Tricyclic and dual serotonergic-noradrenergic reuptake inhibition by SNRIs (or SSRI-NRI combinations), have also shown analgesic properties additionally.[37][38] According to recent evidences antidepressants also seem to exert beneficial effects in experimental autoimmune neuritis in rats by decreasing Interferon-beta (IFN-beta) release or augmenting NK activity in depressed patients.[12]

These studies warrant investigation for antidepressants for use in both psychiatric and non-psychiatric illness and that a psychoneuroimmunological approach may be required for optimal pharmacotherapy in many diseases.[39] Future antidepressants may be made to specifically target the immune system by either blocking the actions of pro-inflammatory cytokines or increasing the production of anti-inflammatory cytokines.[40]

Extrapolating from the observations that positive emotional experiences boost the immune system, Roberts speculates that intensely positive emotional experiences sometimes brought about during mystical experiences occasioned by psychedelic medicinesmay boost the immune system powerfully. Research on salivary IgA supports this hypothesis, but experimental testing has not been done.[41]

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Psychoneuroimmunology - Wikipedia

Department of Microbiology and Immunology | University of …

The Department of Microbiology and Immunology provides a stimulating environment for faculty scientists and trainees who will play a leadership role in academic, government and industrial research and in international health organizations.

Advances in molecular and cell biology and genetics have opened new approaches to the basic and applied aspects of infectious diseases and host defenses. We are applying these approaches to basic aspects of receptor signaling, regulation of gene expression in both prokaryotic and eukaryotic cells and interactions between these cells, genetic manipulation of cellular functions, microbial genomics and evolution, and development of new vaccination strategies. The techniques of functional genomics, gene delivery, stem cells and transgenic/gene disruption animal models are being developed to address specific questions.

TheGraduate Program in Molecular Microbiology and Immunologyprovides interactive, multi-departmental graduate education and research training. Our graduates receive comprehensive education in molecular and cell biology, microbiology and immunology and in-depth training in their chosen area of research.

Our Ph.D. and M.D./Ph.D. students train in the laboratories of participating faculty in theInstitute for Genome Sciences,Center for Vaccine Development,Institute of Human Virology,Department of Microbial Pathogenesisin the Dental School, theUniversity of Maryland Marlene & Stewart Greenebaum Cancer Center, theProgram in the Biology of Model Systems; and the Departments ofMedicine,SurgeryandPediatrics.

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Cancer immunology – Wikipedia

Cancer immunology is a branch of immunology that studies interactions between the immune system and cancer cells (also called tumors or malignancies). It is a field of research that aims to discover cancer immunotherapies to treat and retard progression of the disease. The immune response, including the recognition of cancer-specific antigens, forms the basis of targeted therapy (such as vaccines and antibody therapies) and tumor marker-based diagnostic tests.[1][2] For instance tumour infiltrating lymphocytes are significant in human colorectal cancer.[3] The host was given a better chance at survival if the cancer tissue showed infiltration of inflammatory cells, in particular those prompting lymphocytic reactions. The results yielded suggest some extent of anti-tumour immunity is present in colorectal cancers in humans.

Cancer immunosurveillance and immunoediting is based on (i) protection against development of spontaneous and chemically induced tumors in animal systems and (ii) identification of targets for immune recognition of human cancer.[4]

Cancer immunosurveillance is a theory formulated in 1957 by Burnet and Thomas, who proposed that lymphocytes act as sentinels in recognizing and eliminating continuously arising, nascent transformed cells.[4][5] Cancer immunosurveillance appears to be an important host protection process that decreases cancer rates through inhibition of carcinogenesis and maintaining of regular cellular homeostasis.[6] It has also been suggested that immunosurveillance primarily functions as a component of a more general process of cancer immunoediting.[4]

Immunoediting is a process by which a person is protected from cancer growth and the development of tumour immunogenicity by their immune system. It has three main phases: elimination, equilibrium and escape.[7] The elimination phase consists of the following four phases:

The first phase of elimination involves the initiation of an antitumor immune response. Cells of the innate immune system recognize the presence of a growing tumor which has undergone stromal remodeling, causing local tissue damage. This is followed by the induction of inflammatory signals which is essential for recruiting cells of the innate immune system (e.g. natural killer cells, natural killer T cells, macrophages and dendritic cells) to the tumor site. During this phase, the infiltrating lymphocytes such as the natural killer cells and natural killer T cells are stimulated to produce IFN-gamma.

In the second phase of elimination, newly synthesized IFN-gamma induces tumor death (to a limited amount) as well as promoting the production of chemokines CXCL10, CXCL9 and CXCL11. These chemokines play an important role in promoting tumor death by blocking the formation of new blood vessels. Tumor cell debris produced as a result of tumor death is then ingested by dendritic cells, followed by the migration of these dendritic cells to the draining lymph nodes. The recruitment of more immune cells also occurs and is mediated by the chemokines produced during the inflammatory process.

In the third phase, natural killer cells and macrophages transactivate one another via the reciprocal production of IFN-gamma and IL-12. This again promotes more tumor killing by these cells via apoptosis and the production of reactive oxygen and nitrogen intermediates. In the draining lymph nodes, tumor-specific dendritic cells trigger the differentiation of Th1 cells which in turn facilitates the development of cytotoxic CD8+ T cells also known as killer T-cells.

In the final phase of elimination, tumor-specific CD4+ and CD8+ T cells home to the tumor site and the cytotoxic T lymphocytes then destroy the antigen-bearing tumor cells which remain at the site.

Tumor cell variants which have survived the elimination phase enter the equilibrium phase. In this phase, lymphocytes and IFN-gamma exert a selection pressure on tumor cells which are genetically unstable and rapidly mutating. Tumor cell variants which have acquired resistance to elimination then enter the escape phase. In this phase, tumor cells continue to grow and expand in an uncontrolled manner and may eventually lead to malignancies. In the study of cancer immunoediting, knockout mice have been used for experimentation since human testing is not possible.[4]Tumor infiltration by lymphocytes is seen as a reflection of a tumor-related immune response.[8]

Obeid et al.[9] investigated how inducing immunogenic cancer cell death ought to become a priority of cancer chemotherapy. He reasoned, the immune system would be able to play a factor via a bystander effect in eradicating chemotherapy-resistant cancer cells.[10][11][12] However, extensive research is still needed on how the immune response is triggered against dying tumour cells.[13]

Professionals in the field have hypothesized that apoptotic cell death is poorly immunogenic whereas necrotic cell death is truly immunogenic.[14][15][16] This is perhaps because cancer cells being eradicated via a necrotic cell death pathway induce an immune response by triggering dendritic cells to mature, due to inflammatory response stimulation.[17][18] On the other hand, apoptosis is connected to slight alterations within the plasma membrane causing the dying cells to be attractive to phagocytic cells.[19] However, numerous animal studies have shown the superiority of vaccination with apoptotic cells, compared to necrotic cells, in eliciting anti-tumor immune responses.[20][21][22][23][24]

Thus Obeid et al.[9] propose that the way in which cancer cells die during chemotherapy is vital. Anthracyclins produce a beneficial immunogenic environment. The researchers report that when killing cancer cells with this agent uptake and presentation by antigen presenting dendritic cells is encouraged, thus allowing a T-cell response which can shrink tumours. Therefore activating tumour-killing T-cells is crucial for immunotherapy success.[25]

However, advanced cancer patients with immunosuppression have left researchers in a dilemma as to how to activate their T-cells. The way the host dendritic cells react and uptake tumour antigens to present to CD4+ and CD8+ T-cells is the key to success of the treatment.[26]

Various strains of human papillomavirus (HPV) have been found to play an important role in the development of cervical cancer. The HPV oncogenes E6 and E7 that these viruses possess have been shown to immortalise some human cells and thus promote cancer development.[27] Although these strains of HPV have not been found in all cervical cancers, they have been found to be the cause in roughly 70% of cases. The study of these viruses and their role in the development of various cancers is still continuing, however a vaccine has been developed that can prevent infection of certain HPV strains, and thus prevent those HPV strains from causing cervical cancer, and possibly other cancers as well.

A virus that has been shown to cause breast cancer in mice is mouse mammary tumor virus.[28][29] It is from discoveries such as this and the role of HPV in cervical cancer development that research is currently being undertaken to discover whether or not human mammary tumour virus is a cause of breast cancer in humans.[30][clarification needed]

Original post:
Cancer immunology - Wikipedia