{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,2]],"date-time":"2026-11-02T17:56:29Z","timestamp":1793642189046,"version":"4.5.1"},"reference-count":60,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,2,23]],"date-time":"2026-02-23T00:00:00Z","timestamp":1771804800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      <jats:italic>Mycobacterium tuberculosis<\/jats:italic>\n                      (Mtb) causes active tuberculosis (TB) in approximately 10 million people annually, resulting in 1.6 million deaths. TB and helminthiasis have a significant geographical overlap, and helminth infections can trigger immunological responses that dampen Th1 immunity, which is essential for Mtb containment. While B cells are known to modulate T cell responses, their role during helminth\/TB co-infection remains unclear.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>This study aimed to analyze the effect of helminth exposure on T cell activation in a T and B cell co-culture system.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      T and B cells were isolated from healthy donor blood, stimulated with aCD3\/aCD28, and exposed to\n                      <jats:italic>Ascaris lumbricoides<\/jats:italic>\n                      protein antigens (ASC) or\n                      <jats:italic>Schistosoma mansoni<\/jats:italic>\n                      soluble egg antigen (SM).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      B cells reduced T cell proliferation, and SM exposure partly attenuated this inhibitory effect on CD4 T cells. ASC exposure did not affect T cell proliferation but increased soluble IL-15R\u03b1 and surface IL-15R\u03b1 and IL-2\/15R\u03b2 on CD4 T cells. Restimulation with recombinant human IL-15 revealed reduced and unsustained STAT5 activation in CD4 and CD8 T cells in ASC-exposed co-cultures. Additional analysis showed altered phosphorylation of STAT1, STAT3, and STAT6, indicating broader impairment of IL-15 responsiveness and a dampened Th1 activation profile. BCL6\/BLIMP-1 transcription factor expression of B cells in ASC-exposed co-cultures suggested a shift toward a more differentiated phenotype, such as plasma cell, memory B cells, or marginal zone MZ B cells, which are all typically BCL6\n                      <jats:sup>low<\/jats:sup>\n                      . The\n                      <jats:italic>in vivo<\/jats:italic>\n                      analysis of peripheral blood mononuclear cells from individuals in a helminth\/TB endemic region showed increased frequencies of CD38\n                      <jats:sup>hi<\/jats:sup>\n                      CD24\n                      <jats:sup>hi<\/jats:sup>\n                      B regulatory cells in helminth infected, and MZ B cells (IgM\n                      <jats:sup>high<\/jats:sup>\n                      unswitched B cells) in both helminth-infected and helminth\/TB co-infected individuals.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>ASC antigen exposure modulates T cell activation through dynamic regulation of the IL-15-pathway and STAT signaling. These findings suggest that ASC exposure may help prevent prolonged IL-15-driven responses, potentially limiting excessive inflammation during TB. B cells in ASC-exposed co-cultures exhibit transcriptional changes consistent with a shift away from the germinal center phenotype toward more differentiated states.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1766483","type":"journal-article","created":{"date-parts":[[2026,2,23]],"date-time":"2026-02-23T05:28:07Z","timestamp":1771824487000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Ascaris lumbricoides antigen exposure modulates T cell activation via regulation of IL-15R\u03b1 expression, STAT5 phosphorylation, and promotes differentiation of BCL6low B cells"],"prefix":"10.3389","volume":"17","author":[{"given":"Giggil","family":"Pushpamithran","sequence":"first","affiliation":[{"name":"Division of Inflammation and Infection, Department of Biomedical and Clinical Sciences, Faculty of Medicine and Health Sciences, Link\u00f6ping University","place":["Link\u00f6ping, 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