FCE News: University of Alabama at Birmingham
Advancing Immunology in the Southeast: SIS 2026 and New UAB Immunophenotyping Services
Mark your calendar for the 13th Annual Southeastern Immunology Symposium, taking place June 2–5, 2026, in Asheville, North Carolina. This highly anticipated meeting will bring together immunologists from across the Southeast and beyond for several days of cutting-edge science. Attendees can look forward to exciting keynote lectures from Diane Mathis (Harvard University), Edward Pearce (Johns Hopkins University), and Dario Vignali (University of Pittsburgh), along with outstanding invited speakers representing leading institutions across the region. The symposium will also spotlight the next generation of scientists through selected trainee talks and poster awards, making SIS 2026 an energizing forum for discovery, networking, and innovation in immunology. Registration and program details are coming soon—stay tuned! Additionally, UAB would like to announce that we are expanding our core services to include Immunophenotyping – which is a powerful tool for monitoring the molecular, metabolic, phenotypic, and functional characteristics of circulating blood cells. Changes in these cellular attributes can be linked to specific disease manifestations, progression, and treatment response, especially when tracked over time. As such, immunophenotyping enables the identification of easily monitored biomarkers and cellular signatures that may serve as valuable diagnostic and prognostic indicators. This approach is particularly useful for monitoring patients undergoing immunotherapy, including treatments such as checkpoint inhibitors and targeted immune modulators, which are increasingly used in chronic disease management.
Learn more here: https://sis-inc.org/
FCE News: Vanderbilt
Director of Vanderbilt FOCIS Center of Excellence Named 2025 Scholar GPS Top Scholar
Annet Kirabo, DVM, MSc, PhD, Associate Professor of Medicine in the Division of Genetics and Clinical Pharmacology at Vanderbilt University Medical Center, has been named a 2025 Top Scholar by ScholarGPS, a global academic analytics platform that evaluates scholarly productivity, impact, and quality of research (https://scholargps.com). This distinction places Dr. Kirabo among the top 0.05% of scholars worldwide in her specialty of hypertension, recognizing her exceptional research influence over the past five years. She was honored for her pioneering work elucidating immune mechanisms that drive hypertension and cardiovascular disease, as well as her contributions to understanding inflammatory pathways underlying cardiometabolic disorders insights that are informing novel therapeutic strategies. Dr. Kirabo also serves as Director of the Vanderbilt Federation of Clinical Immunology Societies (FOCIS) Center of Excellence (FCE), which fosters multidisciplinary collaboration in translational immunology research and education (https://www.vumc.org/center-for-immunobiology/focis-center-excellence). She holds secondary appointments as Associate Professor of Molecular Physiology and Biophysics at Vanderbilt University. In addition to this recognition, Dr. Kirabo was named a Vanderbilt Chancellor Faculty Fellow in 2024 and is a Fellow of the American Heart Association. She joins 78 Vanderbilt faculty recognized as ScholarGPS Top Scholars for recent achievements, and more than 300 active Vanderbilt faculty honored for lifetime scholarly impact.
Learn more here: https://news.vumc.org/2025/12/23/annet-kirabo-named-top-scholar-in-hypertension/
FCE NEWS: FCE TOLERANCE, Toulouse, France
A new scientific publication: Tissue-resident memory CD4+ T cells sustain chronic CNS autoimmunity
Pignata A, Frieser D, Gonzalez-Fierro C, Hsiao CC, Engelenburg HJ, Alis M, Fijalkow I, Cazaentre V, Nozeran L, Miranda-Capet R, Dufourd E, Vermeulen T, Aïda A, Le Coz C, Van Gisbergen K, Blanchard N, Hamann J, Smolders J, Liblau RS*, Masson F*. Tissue-resident memory CD4+ T cells sustain chronic CNS autoimmunity. Science Transl. Med. 2025 Jul 23;17(808):eadp8109. * Co-last authors and co-corresponding auteurs.
Multiple sclerosis (MS) is a chronic inflammatory and neurodegenerative disorder of the central nervous system (CNS) characterized by demyelinating lesions and axonal damage driven, at least in part, by T lymphocytes specific for CNS autoantigens. Currently, MS treatments primarily prevent the migration of lymphocytes into the CNS or deplete defined immune cell subsets in the periphery. These treatments are effective in extending periods of remission in relapsing-remitting MS (RRMS) but have limited efficacy in treating the progressive forms of MS (PMS). This discrepancy suggests that, in PMS, local mechanisms within the CNS could sustain a state of smoldering inflammation and tissue injury, yet the mechanisms responsible for maintaining this chronic phase remain largely unclear.
In this study, we investigated the contribution of tissue-resident memory CD4+ T cells (CD4+ Trm) to the persistence of CNS autoimmunity. Using a model of MOG35-55 induced experimental autoimmune encephalomyelitis (EAE), in which the disease is triggered by autoreactive CD4+ T cells primed against myelin-derived antigens, we showed that a significant fraction of CD4+ T cells infiltrating the CNS during the chronic phase acquires a canonical Trm phenotype, defined by the expression of residency and retention markers and by down-regulation of egress receptors. These CD4+ Trm cells preferentially localize within inflammatory and demyelinating lesions in the brain and the spinal cord.
Single-cell transcriptomic analyses of CNS-infiltrating CD4+ T cells revealed marked transcriptional heterogeneity and inflammatory potential within the Trm compartment, with these cells adopting various specialization programs, suggesting that different Trm subpopulations may contribute distinctively to the pathological process. Functionally, we dissected the respectives contribution of circulating versus resident CD4+ T cells in sustaining the chronic EAE, by combining genetic and pharmacological depletion strategies. Depletion of either circulating or CNS-resident CD4+ T cells alone did not ameliorate the clinical scores during the chronic phase, whereas concomitant targeting of both compartments significantly alleviated neurological signs and reduced markers of ongoing CNS inflammation. Our results suggest that CD4+ Trm cells are not merely bystanders but actively sustain a chronic inflammatory state in the CNS, in concert with their circulating counterpart, and that their persistence may promote damage and/or hinder endogenous repair processes, thereby supporting the notion that future therapeutic strategies for PMS should also consider to target these CNS-resident T cell compartment.
A vaccine targeting human IgE induces sustained protection from anaphylaxis
A vaccine targeting human IgE induces sustained protection from anaphylaxis Immunoglobulin E (IgE) plays a central role in food allergy and its most severe and life-threatening manifestation, anaphylaxis. A monoclonal anti-IgE antibody, omalizumab, has been approved in 2024 for the treatment of food allergy. However, this mAb needs to be reinjected every two to four weeks to maintain clinical efficacy. In a recent article published in Science Translational Medicine (https://www.science.org/doi/10.1126/scitranslmed.ads0982), researchers from the Toulouse Institute for Infectious and Inflammatory Diseases (Infinity), the Pasteur Institute in Paris, and the French Biotech Neovacs reported development of a novel vaccine approach inducing sustained endogenous production of neutralizing anti-IgE antibodies. This vaccine was generated by coupling an IgE fragment containing the binding site to its high affinity receptor FcRI with the carrier protein diphtheria cross-reactive material 197 (CRM197; an enzymatically inactive and nontoxic form of diphtheria toxin already used in a number of approved conjugate vaccines). To assess the immunogenicity and efficacy of this conjugate vaccine, the team generated novel mice humanized for IgE and FcεRI. They demonstrated that the vaccine induces neutralizing anti-IgE antibodies for up to 12 months postvaccination. Furthermore, they showed that IgE vaccination induces sustained protection against severe systemic anaphylaxis in humanized mice. Thus, this conjugate vaccine represents a promising approach for the treatment of food allergy and several other IgE-mediated diseases.
FCE News: Benaroya Research Institute
Regulatory T Cell-Boosting Therapy Impacts Flu Responses—For Better or Worse—Depending on Timing
A study published in December in the Journal of Immunology from scientists at Benaroya Research Institute (BRI) explores how the timing of a regulatory T cell (Treg)-selective interleukin-2 (IL-2) mutein therapy could shape immune responses to viral infections — sometimes with opposing effects. The study was led by Daniel Campbell, PhD, and his graduate student Joe Albe, PhD, in collaboration with additional researchers at BRI and Seattle Children’s Research Institute.
While engineered IL-2 muteins aim to restore immune balance in disease, they also carry the risk of broadly suppressing immunity, reducing vaccine efficacy, or even fueling excessive immune activation that leads to tissue damage. To better understand these risks, BRI researchers used a mouse model of influenza infection to test how the specific IL-2 mutein, Fc.Mut24, impacts the immune response. When administered before infection, it significantly expanded Tregs and suppressed flu-specific CD8⁺ T cells. This shift reduced flu-specific CD8⁺ T cell abundance and changed their location and characteristics in the lungs, without increasing viral burden or worsening illness.
However, when given during an active infection, Fc.Mut24 expanded flu-specific CD8⁺ T cells, boosted flu-specific responses, and worsened disease symptoms, despite not affecting virus levels. These results suggest that IL-2 muteins can directly stimulate activated T cells during infection, potentially exacerbating tissue damage caused by an overactive immune response.
Importantly, the study also found that regardless of when the mutein was administered, mice developed strong long-term protection against future flu infections. Memory CD8⁺ T cells persisted for over five months, and vaccinated mice survived a lethal challenge with a different flu strain, indicating durable immunity was preserved.
These findings are especially relevant for patients with autoimmune diseases who may be treated with Treg-boosting therapies like IL-2 muteins. Respiratory infections such as influenza, respiratory syncytial virus (RSV), and SARS-CoV-2 pose serious risks to immunocompromised individuals, and the study underscores the need to carefully consider treatment timing to avoid unintended consequences.
View the full publication here: https://academic.oup.com/jimmunol/advance-article/doi/10.1093/jimmun/vkaf297/8376759.
Member Society NEWS: The Japanese Society of Clinical Immunology
The 5th International Symposium of Clinical Immunology, 22-23 May 2026 in Japan
The 5th International Symposium of Clinical Immunology Date: Friday 22 – Saturday 23 May 2026 in Maihama, Japan Venue: Hotel Okura Tokyo Bay Meeting Style: Hybrid Mode (in-person and online).
Please visit: https://icongroup.co.jp/isci2026/
Member Society NEWS: American Society for Histocompatibility and Immunogenetics (ASHI)
New ASHI Educational Offering – Leadership Essentials Webinar Series
The ASHI Leadership Essentials Webinar Series (LEWS) is a new professional development program dedicated exclusively to the topics and challenges faced by laboratory supervisors and managers. These sessions focus on the day-to-day operational, administrative, and leadership responsibilities unique to these roles. LEWS is designed for HLA professionals in current or emerging leadership roles, including laboratory supervisors, managers, technical leads, quality managers, and laboratory directors.
Click here for more information: https://www.ashi-hla.org/page/LEWS
