Category Archives: Immunology

Immunology

When Flight 752 was shot down, Canadian schools lost some of their best and brightest – Yahoo News Canada

The tragic loss of Ukrainian International Airlines Flight 752, shot down near Tehran killing all 176 on board, has had a terrible impact on friends and family, and also on Canada's academic community.

At least 19 universities in six provinces lost researchers, professors and students in the disaster. Their expertise ranged across diverse fields, from engineering to medicine, and business to biology.

CBC News spoke to colleagues of three of those individuals about what they were like, and the incredible contributions they were making through their work.

Forough Khadem

Forough Khadem's research had immense promise.

The 36-year-old moved from Tehran to Winnipeg in 2010 to pursue a PhD in immunology at the University of Manitoba, after a chance encounter with a Canadian researcher visiting Iran.

Jude Uzonna, a professor of immunology and medical microbiology, met Khadem 10 years ago at a conference in Tehran. He says he was so impressed by her energy and intelligence, he offered her the chance to study in Winnipeg.

Khadem's background was in plant biotechnology, but working in a completely different field didn't seem to faze her. She jumped at the opportunity.

"She excelled," said Uzonna, who became her PhD adviser. "She was a very bright student."

Khadem's PhD focused on visceral leishmaniasis a deadly parasitic disease that affects people in nearly 100 countries. She discovered where and how the parasite hides in the body, including inside liver cells.

This research could be life saving, according to Uzonna.

"The type of disease she worked on is lethal. It's fatal if not treated," said Uzonna. "She was able to find this pathway, and that if you block this pathway and target these particular cells, you can cure it."

Khadem's findings were featured on the cover of the American Association for the Study of Liver Diseases' Hepatology journal in 2016.

"How many people get their work on the cover of the journal?" said Uzonna. "I've trained seven or eight PhD students only her work has made it onto the cover of a journal."

After graduating, Khadem worked at MITACS, a Canada-wide non-profit that makes connections between industry and researchers. But her link to the University of Manitoba stayed strong, and on Jan. 17 a vigil for Khadem was held on campus.

Story continues

"She loved the university and she loved science," said Saeid Ghavami, her friend and colleague. "She was so connected to her professional life that she always felt that university was her second home."

Uzonna says Forough's work lays the foundation for another person to continue with it. "When that person moves forward, she's always going to get the credit."

"That's the beauty of science," he said. "She lives on that way."

Mohammad Asadi Lari

Mohammad Asadi Lari was in his second year of an eight-year MD/PhD program at the University of Toronto when he was killed on Jan. 8.

Fewer than 10 students are accepted into the program each year.

"You can imagine, in a program where we're training the next generation of physician scientists that are going to make new discoveries and change health care, there are lots of amazing students," said Dr. Nicola Jones, the program's director.

"Within that group, Mohammad was exceptional. He really stood out."

At 23, Asadi Lari had already accomplished so much.

He started a STEM fellowship five years ago when he was an undergraduate student at the University of British Columbia. The program, which provides youth with tools and skills to help them excel in STEM fields, now has 20 university branches and 15 high school chapters in eight provinces.

He gave a TedX Talk in 2019, urging young people to find what they're passionate about and take action on it.

"He had a way of connecting people and making other people feel great," said Dr. Vipan Nikore, an assistant professor at the University of Toronto.

At a Toronto vigil for victims of the crash, deputy Prime Minister Chrystia Freeland remembered meeting Mohammad just a few months earlier.

"He cornered me," recalled Freeland, "and said 'Minister, the government has to do more about this! And I need to meet with you and talk to you about it.'"

Asadi Lari was to decide on his PhD research focus the week after he died. For his friends, teachers and mentors, the loss of his enormous potential in their community is immeasurable.

"People like Mohammad don't come around that often. And to me, there's no question he was going to change the world," said Dr. Nikore.

Zahra Naghibi

Zahra Naghibi, a thermodynamicist, was just about to launch two new projects. She was in her third year of a PhD at the University of Windsor when she died.

Naghibi's work in the university's turbulence and energy lab focused on energy consumption in greenhouses. She had just completed the delicate and painstaking task of creating a model of a micro-climate.

"Zahra's model could tell you minute to minute what the energy consumption would be in a greenhouse at any time," said her PhD supervisor, Rupp Carriveau.

"She could also show what was going to happen in the future, which enables you to do things like design a better or more innovative energy supply system."

Carriveau said it was Naghibi's work that facilitated the acquisition of the two large projects for the university. With Naghibi gone, the turbulence and energy lab faces the challenge of carrying on and developing them without her.

"We'll never be the same. The lab won't be the same," said Carriveau. "The research won't be the same."

Naghibi lived in Windsor, Ont., with her husband, Mohammad Abaspour Ghadi, who also died in the crash.

Carriveau said Naghibi was being courted for various positions in the agriculture and energy industries, and would have had her pick of opportunities when she graduated a year from now.

"As a country we lost so much, when you consider what one life can do," said Carriveau.

"I think we lost a lot as a nation. I can't imagine the collective impact."

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When Flight 752 was shot down, Canadian schools lost some of their best and brightest - Yahoo News Canada

Immunology

Hundreds of frontline NHS staff in Salisbury don’t have flu jab – Spire FM

The Society for Acute Medicine says it's concerning that many NHS staff across England who deal with patients have not been vaccinated.

According to Public Health England:

On Friday (31 Jan 2020) Lorna Wilkinson, Director of Nursing at Salisbury NHS Foundation Trust told Spire FM News:

"Staff flu vaccination forms a key part of our overall plans to protect staff and patients in hospital and through our staff flu campaign we put in place a number of measures to encourage and make it as easy possible for staff to get the flu vaccination."

"80% of our frontline staff have now received the flu vaccination. This is an improvement on our uptake rate compared to this time last year and we have not only met but are now likely to exceed the 80% target, which is a great achievement."

"We are continuing to offer all our staff the flu vaccination and would encourage anyone who hasn't yet to contact their Peer Vaccinator/Occupational Health to arrange a convenient time."

The NHS's own guidelines say the flu vaccine reduces the risk of catching flu, as well as spreading it to others. The best time to have the vaccine is before the start of the flu season, usually December to March.

Doctors, nurses, clinical staff and support workers involved in direct patient care are encouraged to have the jab. Trusts have financial incentives for staff uptake, receiving full payment if at least 80% have it, and a decreasing amount down to 60% coverage, below which they get nothing.

The target is measured between September and February, and the payment varies depending on the size of the trust's contract. The proportion of staff who had the vaccine by the end of December differed widely across the 235 trusts that submitted figures.

Dr Nick Scriven, President of the Society for Acute Medicine, said:

"The NHS has enough to worry about without further issues with staff being unwell when it may have been prevented. We know there is a financial incentive for NHS trusts to get their staff vaccinated but I would hope the health need and protection it offers would be more than enough to persuade people."

Across England, the 68.5% uptake rate at the end of December was better than at the same point a year earlier, when it stood at 65.8%.

Dr Doug Brown, chief executive of the British Society for Immunology, said

"The flu vaccine is the best protection we have against a virus that can lead to serious illness in vulnerable groups. It is extremely important to continue to increase seasonal flu vaccine uptake among frontline healthcare workers to reduce the risk of spreading the virus and causing serious illness in at-risk groups."

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Hundreds of frontline NHS staff in Salisbury don't have flu jab - Spire FM

Immunology

Operations Officer job with KINGS COLLEGE LONDON | 195056 – Times Higher Education (THE)

We are seeking an enthusiastic Operations Officer to join the professional services team supporting the School of Immunology & Microbial Sciences. We are one of seven Schools in the Faculty of Life Sciences & Medicine at Kings College London. The School is based across three Campuses, and the successful candidate will be expected to work across these locations, as and when required.

This post will work closely with the two School Senior Operations Officers as well as with staff and students across the School, Faculty and University, to ensure that the Schools Operations are fully supported, including research grant management, staffing and financial processes, oversight of local estates and facilities, supporting the day-to-day administration of the School.

The post is responsible for a variety of tasks and the successful candidate must be:

versatile, adaptable, with the capacity to deal with competing requests and priorities, for action;

highly motivated;

approachable and confident in liaising with colleagues in the University and with external partners, including the NHS, to ensure a smooth exchange of information and collaboration to meet deadlines.

This post will be offered on an indefinite contract.

This is a full-time post - 100% full time equivalent.

The selection process will include a panel interview, an assessment, a test.

For an informal discussion about the role, please contact:

Denise Jamieson denise.jamieson@kcl.ac.uk

To apply, please register with the Kings College London application portal and complete your application online.

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Operations Officer job with KINGS COLLEGE LONDON | 195056 - Times Higher Education (THE)

Immunology

Technical comment on Synovial fibroblast-neutrophil interactions promote pathogenic adaptive immunity in rheumatoid arthritis – Science

Abstract

Reassessment of citrullinome cargo in neutrophil extracellular traps confirms the presence of citrullinated peptides.

In an article previously published in Science Immunology (1), we reported a previously unidentified mechanism of induction of pathogenic adaptive immunity against citrullinated antigens in rheumatoid arthritis (RA). This mechanism was mediated by an interaction between neutrophil extracellular traps (NETs) and synovial fibroblasts (FLS) that promote the presentation of citrullinated peptides identified in NETs by the FLS to the adaptive immune system. The identification of citrullinated peptides in NETs was performed by a variety of methods described in this and previous manuscripts and included the use of citrulline-specific probes, antibodies, and mass spectrometry (MS) (1, 2).

Following this publication, we were contacted by an investigator with concerns about our MS analysis. Given the magnitude of the mass shift expected between a citrulline and an arginine residue (+0.984 Da), misannotation of citrulline-containing peptides can occur because of fragmentation of misassigned monoisotopic mass peaks. In addition, the +0.984-Da mass increase upon citrullination is identical to the mass increase observed upon protein deamination of asparagine and glutamine residues within a peptide, thereby confounding the correct assignment of citrullinated species. Last, most of the previously identified peptides contained a C-terminal citrulline. Whereas several endogenous proteases, including cathepsin B, cleave after citrulline, trypsin, the protease used in sample preparation, does not (3). These discrepancies prompted us to reevaluate the initial proteomic data more stringently. Upon reevaluation, the spectra were either not consistent with citrullination or not definitive enough to be consistent with a citrullinated residue. Therefore, we generated new samples for analysis. Herein, we report the identification of 58 sites of citrullination on 32 proteins that are present in NETs using a highly stringent data analysis workflow.

In the analysis, healthy neutrophils were purified as described (1), resuspended in RPMI, seeded in 12-well plates, and incubated with 2.5 M calcium ionophore (A23187, Sigma-Aldrich) or 100 g of rheumatoid factor for 4 hours at 37C. Supernatants were carefully removed, and NETs were harvested with micrococcal nuclease (MNase) (10 U/ml) in RPMI for 15 min at 37C. Supernatant-containing NETs were isolated via centrifugation and stored at 80C until analysis. Note that the proteomic analysis was performed on NETs and not from cells treated with ionophore or rheumatoid factor; hence, it is not possible to generate control proteomes.

NETs (50 g) were precipitated with 20% trichloroacetic acid. The pellets were washed with acetone and then resuspended in urea (8 M). Ammonium bicarbonate (100 mM) was then added to the solution. Samples were reduced with dithiothreitol (15 mM) and alkylated with iodoacetamide (12.5 mM). Next, samples were diluted to 1.8 M urea with phosphate buffer (pH 7.4). Samples were then digested overnight at 37C with Trypsin Gold (2 g, Promega) and 1 mM CaCl2. Tryptic peptides were separated on a ZORBAX extended C18 column (Agilent) over a 1-hour, biphasic gradient from 0% buffer A (10 mM ammonium bicarbonate plus 5% acetonitrile) to 100% buffer B (10 mM ammonium bicarbonate and 90% acetonitrile). The resulting 96 fractions were pooled to yield 6 fractions for liquid chromatographytandem MS (MS/MS) analysis.

Fractions were dried and resuspended in 25 l of 5% acetonitrile/0.1% trifluoroacetic acid. Peptides were eluted from a gravity-pulled analytical column packed with 3-m (100 ) Magic C18AQ particles using a biphasic linear gradient from 5 to 60% of B (acetonitrile and 0.1% formic acid) in mobile phase A (water and 0.1% formic acid) over 120 min. Ions were introduced by positive electrospray ionization at 1.4 kV into a Thermo Scientific Q Exactive hybrid mass spectrometer. Raw data files were peak processed by MaxQuant 1.6.3.4, and identifications were searched by Andromeda against the Human SwissProt database. First-search mass tolerance was 20 parts per million (ppm) for precursors and 20 ppm for fragment ions, and main search tolerance after precursor mass recalibration was 4.5 ppm for precursors and 20 ppm for fragments. All positive citrullination sites were verified manually.

To unambiguously detect and verify the presence of citrullinated arginines, we followed a recently proposed workflow (4). First, we filtered the data to remove C-terminal citrullines. Next, we compared the observed MS isotopic envelopes to predicted envelopes for arginine- and citrulline-containing (+0.984 Da) peptides. If the MS spectra demonstrated a mass shift correlating with citrulline, then we searched for a neutral loss of isocyanic acid (CNOH, 43.0058 Da) in the MS/MS fragmentation spectra. Neutral loss of isocyanic acid, which is unique to citrulline-containing ion fragments, is frequently observed during high-energy collision dissociation (4). It is important to note that, although deamination of glutamine and asparagine results in a similar mass shift, it does not yield the neutral loss. Using this algorithm, we identified 58 sites of citrullination on 32 proteins (Table 1; spectra data available upon request).

r, citrulline; c, alkylated cysteine; m, oxidized methionine; n or q, deamination; m/z, mass/charge ratio; IO, ionophore; RF, rheumatoid factor.

Notably, three of the proteins we found as being citrullinated, actin, heat shock protein 90 (HSP90), and plastin-2 (PLSL), were also identified as being citrullinated in RA patient samples (5). In addition, over half of the proteins found in the NETs were also previously found in the proteome of RA synovial fluid and neutrophils treated with ionophores (6). Together, our new data uncovered 15 previously unreported citrullinated proteins present in NETs.

The identified proteins include vimentin and myeloperoxidase (MPO), the latter also identified in the original report (1). Notably, citrullinated vimentin, /-tubulin, -actin, and NCF1 are known RA antigens (1, 4, 7, 8). In addition, we identified S100-A8, plastin, coronin, moesin, and erzin, which are all linked to RA (9). Several inflammation-associated proteins were also observed (S100A8, MPO, LKHA, and HMGB1). Furthermore, our list of citrullinated proteins includes numerous cytoskeletal and cell motility proteins such as PLSL, myosin, vimentin, tubulin, and actin. S100A8 is interesting because several targets of the iNOS-S100A8 transnitrosylase complex (i.e., EZR1, MOES, and VIME) are also present as citrullinated proteins in these NETs. Last, linking our analysis to NETosis is our identification of several citrullinated chromatin binding proteins (HMGB1, HP1B3, and HNRPU) and NCF1, which is a component of the nicotinamide adenine dinucleotide phosphate oxidase complex.

In summary, these findings continue to support the conclusions of our previous publications (1, 2), mainly, that NETs are a source of citrullinated autoantigens. We have identified 58 sites of citrullination in 32 proteins from purified NET samples induced via rheumatoid factor or calcium ionophore. Because citrullination is a modification in such low abundance, generating a comprehensive database of citrulline-containing peptides found in any complex proteome is challenging (10). In addition, the need to verify each identified peptide via manual inspection of MS and MS/MS spectra has hampered the growing field exploring this specific modification. Methods to enrich for citrulline-containing peptides and/or computationally automate the process of picking out true citrulline peptides by neutral loss MS/MS analysis would further facilitate the process of decoding the citrullinome.

Funding: This work was supported by the Intramural Research Program at the National Institute of Arthritis and Musculoskeletal and Skin Disease/NIH (ZIAAR041199). This work was also supported in part by NIH grants R35GM118112 (P.R.T.), F32GM128231 (A.J.S.), 1R01GM117004 (E.W.), and 1R01GM118431-01A1 (E.W.).

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Technical comment on Synovial fibroblast-neutrophil interactions promote pathogenic adaptive immunity in rheumatoid arthritis - Science

Immunology

Improving CAR-T therapy for cancer by regulating 2 proteins – FierceBiotech

Chimeric antigen receptor T-cell (CAR-T) therapies that are made from a patients own T cells haveproven effective in blood cancers, and they are showingpromise for treating solid tumors, too. But scientists are still looking for ways to fine-tune this form of immunotherapy.

Now, scientists at the University of North Carolina (UNC) at Chapel Hill havefound new methods for either dialing up CAR-T cells cancer-killing effects when needed or dampening their activity to avoid severe side effects. The technique involvestwo proteins that are responsible for stimulating the cells. The team published the results in Cancer Cell.

In immunology, its always about balance; you don't want to have too much T-cell activation, and you don't want T-cell activation to be too low, the studys co-first author Peishun Shou, Ph.D., said in a statement. We wanted to keep the T-cell activation and tumor killing at a suitable or sustainable level.

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Shou worked in a team led by UNC Lineberger Comprehensive Cancer Centers Gianpietro Dotti, M.D. In 2018, Dottis team developed CARs that can target a protein called CSPG4, and they showed the treatment worked in mice with glioblastoma.

For the current study, the researchers zeroed in on two different types of CARs, whichare differentiated by the signals that activate them. CAR-T cells tumor-regression ability is first triggered by a signal called CD3-zeta, which is commonly used as the main CAR component to recognize markers on tumors. But the cellsalso require co-stimulatory moleculeseither CD28 or 4-1BB proteinin addition to CD3-zeta to further boosttheir activation.

The UNC team found that they could improvethe activityof T cellsthat areco-stimulated by 4-1BBby increasing the expression of a tyrosine kinase called LCK.

What we found is that the LCK molecule can bind to the CAR, enhancing the CAR-T cell activation and signaling transduction, which therefore will help CAR-T cells get a better tumor-killing effect, Shou said.

RELATED:Redesigned CAR-T eliminates dangerous cytokine release syndrome in lymphoma trial

Use of CAR-T therapy has been linked to a dangerous side effect called cytokine release syndrome, so scientists have also been working on methods to rein in CAR-T activitywhen necessary.

Shou and colleagues found such a safety switch in CAR-T cells that are co-stimulated by CD28. They showed that an enzyme called SHP1 attenuates T-cell activity. They discovered that adding a drug named AP21967which is an analog to Pfizers immunosuppressive drug Sirolimus (rapamycin)can pull SHP1 to the CAR to reduce cytokine release. Whats more, the transient recruitment of SHP1 didnt kill the CAR-T cells or impair their antitumor effects, the researchers demonstrated in a mouse model.

Many other efforts have been made to reduce CAR-Ts toxic side effects. For example, a research team led by the University of Southern California Norris Comprehensive Cancer Center developed a CAR variant called CD19-BBz(86) that didnt trigger any serious side effect in 25 lymphoma patients.

As for4-1BB, it's a target that has already attracted some interest among drug developers. Pfizer is developing utomilumab (PF-05082566), a 4-1BB agonist, to leverage the receptors T-cell stimulation effect. The drug is being paired with Pfizer and Merck KGaAs anti-PD-L1 immunotherapy Bavencio in a phase 2 study in solid tumors.

The UNC scientists want to use their findings on CD28 and 4-1BB to improve CAR-T treatments against blood cancers and to potentially make them viable for solid tumors.

Researchers in the CAR-T immunotherapy field now want to solve the solid tumor problem, Shou said. Solid tumors have an immunosuppressive microenvironment, so you need stronger CAR-T activation.

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Improving CAR-T therapy for cancer by regulating 2 proteins - FierceBiotech

Immunology

Coronavirus outbreak in US may depend on this: ‘We just don’t know yet’ says infectious disease doc – Home – WSFX

A top infectious disease doctor warned that the likelihood of preventing a U.S. outbreak of the coronavirus dependson whether the virusis transmitted by peoplewho are not exhibiting symptoms.And that information, he warned, is something that world health experts do not know yet.

You could be carrying it and not know so you wouldnt have the symptoms. Doesnt that make it extremely dangerous? Wall Street Journal columnist Mary Anastasia OGradyasked a panel of doctors on Fox NationsDeep Dive.

The Chinese Ministry of Health has said that they believe this is possible, that people can be spreading it before they show symptoms, said Dr. Stephen Morse, who is a professor of epidemiologyat the Columbia University Medical Center.

But thats why were doing a lot of screening at the airports based largely on geography, he continued. But once it spreads further, its going to be hard to be that targeted.

I agree that we have heard that from the Chinese, but we havent seen the evidence thats behind that, saidDr. Mark Mulligan, whois a senior professor in the NYU Langone Department of Medicine anddirector of both NYU Langone Vaccine Center and theDivision of Infectious Diseases and Immunology.

We do know you can have asymptomatic infection, he went on. There are reports of people that were shown to be infected but we dont know that those people can transmit.

The World Health Organization on Thursday declared the newcoronavirus outbreaka global emergency, as38 new deaths and 1,737 new infected cases have been reported in the last 24 hours.

In general, the transmission occurs when an ill person is coughing a lot. When youre sicker, you have more virus around. It may be that older people get more illness and transmit more. Younger people, less illness, maybe transmit less. But we dont know everything yet., Dr. Mulliganwarned.

Roughly 99 percent of all cases of the virus have appeared in China but it has spread to at least 18 countries.

The American officials are all saying, Dont panic, dont panic. But you can be carrying the disease without showing the symptoms, you have all this air travel going on, its already gotten out of China. How reasonable is it to think that were not going to have a serious outbreak here? asked OGrady.

I dont think we should panic, saidDr. Janette Nesheiwat,the medical director at CityMD,an urgent care practice in New York City. But we should remain on alert and be vigilant because it can take up to two weeks for symptoms to appear.

We know that the usual sort of shoe leather, public healthsteps of isolationof cases, contact tracing, quarantining of them works, notedMulligan. So I think if those things also work for this novel coronavirus, that we do have the opportunity to contain it.

However, Mulligan cautioned if it is shown that individuals can carry and transmit the virus without exhibiting symptoms that would be a troubling discovery.

We think that we have a real opportunity [to contain coronavirus], assuming there arent any curves like this thing about asymptomatic individuals transmitting. If that were true, that would change things, he concluded.

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Fox News Vandana Rambaran contributed to this report.

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Coronavirus outbreak in US may depend on this: 'We just don't know yet' says infectious disease doc - Home - WSFX

Immunology

This week: Coronavirus, vaping and drugs of abuse – WRVO Public Media

China is dealing with the outbreak of a respiratory illness caused by a new coronavirus. Thousands of people have been infected; some have died. And more cases are being diagnosed in people all over the world, including a relatively small number in the United States.

Providing perspective on this outbreak is Stephen Thomas, MD, a professor of medicine and microbiology and immunology at Upstate and its chief of infectious disease.

Also on "HealthLink on Air" this week, toxicologist Christine Stork from the Upstate New York Poison Center talks about vaping dangers and the most common drugs of abuse. Tune in this Sunday, February 2 at 6 a.m. and 9 p.m. for "HealthLink on Air."

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This week: Coronavirus, vaping and drugs of abuse - WRVO Public Media

Immunology

THSTI to hold basic course on Immunology – BSI bureau

Faridabad-based Translational Health Science and Technology Institute will be conducting the third edition of its basic course in Immunology from March 16 to 18.

Dr. Shiv Pillai, Professor, Harvard Medical School, Boston along with Dr. Dipankar Nandi from the Department of Biochemistry, Indian Institute of Science, Bengaluru will be covering the various topics of this domain.

The target audience for this course are Masters and PhD students, research associates and post-doctoral fellows, early career investigators. However, the course is open to other investigators also who would like to update on the knowledge of Immunology.

The last years course was attended by more than 250 participants comprising faculty members, research fellows and PhD students from institutes across the country. Researchers at Banaras Hindu University, AIIMS Delhi, PGIMER Chandigarh, SRM Sonipat, Tezpur University and others could attend by joining a live streaming session.

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THSTI to hold basic course on Immunology - BSI bureau

Immunology

Immunologist Wendy Havran Dies – The Scientist

Immunologist Wendy Havran, who had been researching the role of gamma-delta T cells in wound healing at the Scripps Research Institute since 1991, died from complications following a heart attack on January 20, according to a Scripps statement. She was 64.

The entire Scripps Research community is stunned and saddened by this tragic loss, Scripps colleague Jamie Williamson says in the statement. Wendy not only made significant contributions to the field of immunology and wound healing, but she inspired countless Scripps Research graduate students and postdocs through her enthusiastic mentorship spanning nearly three decades.

Havran was born on September 1, 1955, in Houston, Texas. Her father was an engineer while her mother was an elementary teacher.

She began her undergraduate degree at Duke University in 1973 with the initial desire to practice medicine. She began to stray from that path during her sophomore year when she started research under hematologist Gerald Logue. While working as a lab technician after graduation in 1977, she met thenDuke professor John Cambier, who introduced her to immunology. She instantly knew how she wanted to spend her career. It just clicked, and there was no going back, she told The Scientist in a 2019 profile. I wanted to understand how the immune system worked.

She pursued her doctorate at the University of Chicago, working in a T cell immunology lab. She became well-versed in creating monoclonal antibodies, as the lab was the first to be able to isolate and clone T cells capable of surviving and multiplying in culture.

Defending her thesis after four years in the program, Havran moved on to the lab of James Allison at the University of California, Berkeley, to work on gamma-delta T cells, a subgroup of unconventional T cells with gamma and delta T cell receptor chains, which were still relatively novel at the time. One notable accomplishment during this period was a paper published in 1990, showing for the first time that while gamma-delta T cells are scarce in areas such as the spleen and lymph nodes, they abound in epithelial tissue that makes up skin and intestines.

Dermatologists were convinced that there were no T cells in the skin, so this finding was very unexpected, Havran told The Scientist. These cells were unique because T cells typically each express a unique T-cell receptor that recognizes a unique antigen, but these cells all expressed the same T-cell receptor, so they were basically clones.

When it was time for Havran to establish her own lab, she continued her gamma-delta T cell research at Scripps. Early on, she found evidence that these cells contribute to wound healing. Later studies would find that they also help with tissue repair in the intestines. The last paper she published appeared in Nature Immunology and explained how gamma-delta T cells and immunoglobulins work in concert to suppress tumors by healing damaged epithelial tissue.

In addition to being dedicated to the work in her lab, Havran was passionate about mentoring up-and-coming scientists, and she was awarded the Scripps Research Outstanding Mentor Award in 2018. During her acceptance speech, she claimed that mentoring is one of the best parts of her job.

Havran is survived by her father, two sisters, three nieces, and two nephews.

Lisa Winter is the social media editor forThe Scientist. Email her at lwinter@the-scientist.com or follow her on Twitter @Lisa831.

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Immunologist Wendy Havran Dies - The Scientist

Immunology

Study reveals why more than a week of keto may not be beneficial – News-Press Now

If the start of the new year led you to go on the ketogenic diet in an effort to lose weight, a new study suggests you may have been on it a little too long.

Researchers at Yale University have conducted a mice study to review the effects of the keto diet. They discovered that beyond a week, the benefits begin to cease.

The study was recently published in Nature Metabolism and results indicate that over a limited time period, consuming a high-fat, low-carb diet can possibly offer health benefits to humans, Yale News reported. They include lowering the risk of diabetes and inflammation. The diets positive effects are related to immune cells called gamma delta T-cells, immune cells that protect the tissue and lower the risk of diabetes and inflammation. However, the same cells are also tied to negative effects of keto.

Vishwa Deep Dixit, Ph.D., lead author of the study who is a a professor of comparative medicine and immunology at the Yale School of Medicine, said keto tricks the body into burning fat. The body acts as if its in starvation mode when the low consumption of carbohydrates causes glucose levels to drop. Despite the body not actually being in starvation mode, it begins burning fat instead of carbohydrates. That leads to the release of ketone bodies, which are an alternative source of fuel. As ketone bodies burn in the body, gamma delta T-cells expand throughout.

Dixit said this process improves metabolism and reduces diabetes risk and inflammation. He said mice showed decreased blood sugar levels and inflammation after a week on keto.

However, when the body acts as if its in starvation mode, researchers found fat gets stored in the body at the same time that fat breakdown occurs. As mice continue the high-fat diet, Dixit said they start to store more fat than they can burn and obesity and diabetes begins to develop.

They lose the protective gamma delta T-cells in the fat, Dixit said.

Our findings highlight the interplay between metabolism and the immune system, and how it coordinates maintenance of healthy tissue function, said comparative medicine postdoctoral fellow Emily Goldberg, who discovered that the keto diet expands gamma-delta T cells in mice.

Despite the findings of the mice trial, however, Dixit said long-term human clinical trials are needed.

Before such a diet can be prescribed, a large clinical trial in controlled conditions is necessary to understand the mechanism behind metabolic and immunological benefits or any potential harm to individuals who are overweight and pre-diabetic, Dixit said.

The results come after Dr. Donald Hensrud of the Mayo Clinic voiced opposition to the diet. Hensrund, author of The Mayo Clinic Diet Book, said the keto is not the magic formula people believe it is.

People want to believe, he said. They want an easy way out. They want the magic panacea.

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Study reveals why more than a week of keto may not be beneficial - News-Press Now