{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T20:25:10Z","timestamp":1790195110730,"version":"4.1.0"},"reference-count":145,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"100","content-domain":{"domain":["www.science.org"],"crossmark-restriction":true},"short-container-title":["Sci. Immunol."],"published-print":{"date-parts":[[2024,10,25]]},"abstract":"<jats:p>\n                    Gastrointestinal (GI) B cells and plasma cells (PCs) are critical to mucosal homeostasis and the host response to HIV-1 infection. Here, high-resolution mapping of human B cells and PCs sampled from the colon and ileum during both viremic and suppressed HIV-1 infection identified a reduction in germinal center (GC) B cells and follicular dendritic cells (FDCs) during HIV-1 viremia. Immunoglobulin A\u2013positive (IgA\n                    <jats:sup>+<\/jats:sup>\n                    ) PCs are the major cellular output of intestinal GCs and were significantly reduced during viremic HIV-1 infection. PC-associated transcriptional perturbations, including type I interferon signaling, persisted in antiretroviral therapy (ART)\u2013treated individuals, suggesting ongoing disruption of the intestinal immune milieu during ART. GI humoral immune perturbations were associated with changes in the intestinal microbiome composition and systemic inflammation. These findings highlight a key immune defect in the GI mucosa due to HIV-1 viremia.\n                  <\/jats:p>","DOI":"10.1126\/sciimmunol.ado0090","type":"journal-article","created":{"date-parts":[[2024,10,25]],"date-time":"2024-10-25T13:58:06Z","timestamp":1729864686000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":7,"title":["Gastrointestinal germinal center B cell depletion and reduction in IgA\n                    <sup>+<\/sup>\n                    plasma cells in HIV-1 infection"],"prefix":"10.1126","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8793-5241","authenticated-orcid":true,"given":"Francesca","family":"Cossarini","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA."},{"name":"Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8274-1109","authenticated-orcid":true,"given":"Joan","family":"Shang","sequence":"additional","affiliation":[{"name":"Precision Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA."},{"name":"Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-7845-9984","authenticated-orcid":true,"given":"Azra","family":"Krek","sequence":"additional","affiliation":[{"name":"Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2624-2035","authenticated-orcid":true,"given":"Zainab","family":"Al-Taie","sequence":"additional","affiliation":[{"name":"Department of Genetics and Genomic 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