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However, there is great complexity in the clinical picture with infections, autoimmunity, and inflammation occurring. Emerging evidence suggests that qualitative T cell dysfunction occurs, and the goal of this study was to utilize single-cell RNA-seq to better define altered gene expression patterns to inform on the mechanisms associated with recurrent infections.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We utilized single-cell RNA-seq to define distinct populations in 22q11.2 Deletion Syndrome (\n                      <jats:italic>N<\/jats:italic>\n                      \u2009=\u200913) and controls (\n                      <jats:italic>N<\/jats:italic>\n                      \u2009=\u200911) as well as within a subcohort of patients with 22q11.2 Deletion Syndrome and recurrent infections.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>When we analyzed differentially expressed genes, we identified a signature of type I interferons across all cell types. Within the T cell compartment, and particularly within the follicular helper T cells, we identified a senescence signature. The alterations found in T cells were most substantial in the patients with recurrent infection.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>While T cell numbers can often normalize in patients with 22q11.2 Deletion Syndrome, our data indicate significantly altered function as defined by differentially expressed genes and aligned with what is known about T cell senescence. The effect was greatest in the patients with recurrent infection. This would be expected to impact T cell function and may account for ongoing symptoms, reduced B cell maturation, and possibly the risk of immune dysregulation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1007\/s10875-026-01987-2","type":"journal-article","created":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T00:14:36Z","timestamp":1770077676000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Follicular Helper T Cells and B Cell Maturation in Patients with 22q11.2 Deletion Syndrome and Recurrent Infections"],"prefix":"10.1007","volume":"46","author":[{"given":"Nouf","family":"Alsaati","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Katherine","family":"Beigel","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kelly","family":"Maurer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sarah E.","family":"Henrickson","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Montana","family":"Knight","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Audrey","family":"Green","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Victoria","family":"Giunta","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniel E.","family":"McGinn","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bekah","family":"Wang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"T. 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