FCE News: University of Alabama at Birmingham

Registration is now open for the 13th Annual Southeastern Immunology Symposium, taking place June 2–5, 2026, in Asheville, North Carolina. Go to sis-inc.org to review the agenda, register to attend, or submit your abstract. 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.

UAB would like to announce the expansion of 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. Other services include provision of viral recombinant antigens and B-cell tetramers to investigate B cell responses to infectious agents.

Learn more here: https://sis-inc.org/

FCE News: UT Southwestern Medical FCE

Thymic Hypoplasia in 22q11.2 Deletion Syndrome: Too Much Cartilage and Too Little Tissue

Pratibha Bhalla and Nicolai S.C. van Oers (UT Southwestern Medical Center)

22q11.2 deletion syndrome (22q11.2DS, aka DiGeorge syndrome) is the most common human chromosomal deletion, affecting 1/2150 individuals. Clinical presentations can include thymic hypoplasia/aplasia, hypoparathyroidism, cardiac defects and dysmorphic facial features. Thymic hypoplasia reduces T cell output, leading to patients having more infectious complication (van Oers and Sullivan, 2025). For decades, the thymic hypoplasia and more rarely, aplasia resulting from 22q11.2 deletion syndrome (22q11.2DS, aka DiGeorge syndrome) has been considered a thymic epithelial cell (TEC) problem: too few TECs educating too few T cells. Our recent studies suggest a strikingly different explanation, mesenchymal cells misguided into the wrong subsets in the thymus (Bhalla et al., 2025).

As the thymus begins to form during embryogenesis, neural crest–derived mesenchymal cells condense around the endodermal cells that delineate the 3rd pharyngeal pouch (Foster et al., 2008; Rodewald, 2008). The mesenchymal cells provide structural determinants as the thymus patterns, including the capsule, trabecular septae, and perivascular cells that support the establishment of the vasculature. Equally important, the mesenchymal cells drive endothelial-to-epithelial transitions, which TEC subsets forming thereafter. The two major processes driven by mesenchymal cells establish the unique 3-d stromal meshwork of the thymus, critical for T cell development (Bhalla et al., 2022b; Itoi et al., 2007; Nitta, 2022; Nitta and Takayanagi, 2020).
In mouse models of 22q11.DS, an abnormal expansion of embryonic mesenchymal-derived chondrocytes was found (Bhalla et al., 2025; Bhalla et al., 2022a). Driven by the Sox9 transcription factor, this mesenchymal subset produces cartilage-like extracellular matrix proteins and collagens. This creates a thymus that is smaller yet more dense due to the collagens and ECM proteins. This pathological accumulation of collagens and ECM proteins is evident in the murine embryos and in postnatal human thymuses from 22q11.2DS patients.

As a therapeutic strategy, drugs were tested for their ability to reduce collagen production and cross-linking. This led to the discovery that minoxidil, when administered in pregnant mice prior to the specification of the thymus, restored normal thymic tissue expansion in “22q11.2DS” murine embryos. Minoxidil, well-known for promoting hair growth and treating hypertensive conditions in humans, suppressed Sox9-driven chondrogenesis, and normalized collagen/ECM deposition in the thymus. Improvements in vascular patterning and positioning of the parathyroids were also noted. Taken together, the findings illustrate the importance of specific mesenchymal cell subsets in regulating thymus growth and expansion.
Together, these observations highlight a broader principle: the thymus is not just a collection of cells, but an architecturally complex organ that involves specific mesenchymal subsets.

References
Bhalla, P., N. Ahuja, A. Kumar, C. Xing, A. Moses, A. Shukla, K. Boetel, B.M. Evers, J.M. Shelton, M.T. de la Morena, C.A. Wysocki, O.B. Cleaver, and N.S.C. van Oers. 2025. Minoxidil restores thymic growth in 22q11.2 deletion syndrome by limiting Sox9+ chondrocyte expansion. Journal of Human Immunity 1:

Bhalla, P., Q. Du, A. Kumar, C. Xing, A. Moses, I. Dozmorov, C.A. Wysocki, O.B. Cleaver, T.J. Pirolli, M.L. Markert, M.T. de la Morena, A. Baldini, and N.S. van Oers. 2022a. Mesenchymal cell replacement corrects thymic hypoplasia in murine models of 22q11.2 deletion syndrome. J Clin Invest 132:

Bhalla, P., D.M. Su, and N.S.C. van Oers. 2022b. Thymus Functionality Needs More Than a Few TECs. Front Immunol 13:864777.

Foster, K., J. Sheridan, H. Veiga-Fernandes, K. Roderick, V. Pachnis, R. Adams, C. Blackburn, D. Kioussis, and M. Coles. 2008. Contribution of neural crest-derived cells in the embryonic and adult thymus. J Immunol 180:3183-3189.

Itoi, M., N. Tsukamoto, H. Yoshida, and T. Amagai. 2007. Mesenchymal cells are required for functional development of thymic epithelial cells. Int Immunol 19:953-964.

Nitta, T. 2022. Mesenchymal stromal cells in the thymus. Inflamm Regen 42:33.

Nitta, T., and H. Takayanagi. 2020. Non-Epithelial Thymic Stromal Cells: Unsung Heroes in Thymus Organogenesis and T Cell Development. Front Immunol 11:620894.

Rodewald, H.R. 2008. Thymus organogenesis. Annu Rev Immunol 26:355-388.

van Oers, N.S.C., and K. Sullivan. 2025. The Systemic Effects of 22q11.2 Deletion Syndrome on Immunity. J Human Immunity 2 e20250190:e20250190.

FCE News: Benaroya Research Institute

Benaroya Research Institute (BRI) is bringing together some of the leading voices from the local and national immunology research community for its third annual Immunology Symposium: New Horizons in Immunity and Disease on Tuesday, May 5. The event includes a full day of exciting presentations addressing some of the most relevant topics in immunology, as well as opportunities for collaboration and discussion among attendees.

This year’s keynote speakers are Jay Shendure, MD, PhD, a professor of genome sciences at the University of Washington, and Phil Greenberg, MD, a principal investigator at Fred Hutch Cancer Center. Please visit the BRI website to see the full list of speakers: https://www.benaroyaresearch.org/our-research/bri-scientific-symposium.

For those in the Seattle, Washington area who are interested in attending, visit the BRI website to register in advance. Please note that this event is an in-person opportunity only. We look forward to sharing what we learn during the event from speakers and attendees! If you have any questions, please email communications@benaroyaresearch.org.