{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T06:05:19Z","timestamp":1789452319131,"version":"build-2803163510"},"reference-count":51,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T00:00:00Z","timestamp":1789430400000},"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>Introduction<\/jats:title>\n                    <jats:p>Programmed cell death protein-1 (PD-1) functions as a pivotal immune checkpoint, essential for maintaining peripheral immune tolerance, and serves as a significant therapeutic target in cancer immunotherapy. Nevertheless, the relationship between PD-1 deficiency and baseline alterations in T-cell receptor (TCR) repertoire organization, as well as the susceptibility to lupus-like autoimmunity, remains inadequately elucidated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      In this study, we integrated immune repertoire sequencing with bulk RNA sequencing of peripheral blood mononuclear cells (PBMCs) to delineate the organization of the TCR\u03b2 repertoire and genotype-associated transcriptional changes in PD-1-deficient mice. To assess autoimmune susceptibility following an environmental immune challenge, we utilized a\n                      <jats:italic>Campylobacter jejuni<\/jats:italic>\n                      (CJ-S131)-induced lupus-like autoimmune model.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Our findings revealed that PD-1-deficient mice exhibited alterations in TCR\u03b2 repertoire diversity, complementarity-determining region 3 (CDR3) length distributions, TRBV\/TRBJ segment usage, V-D-J recombination patterns, and clonotype abundance. Through transcriptomic analysis, we identified significant alterations in the expression of genes linked to lymphocyte development and the maintenance of the T-cell receptor (TCR) repertoire. Concurrently, our predicted regulatory-network analysis highlighted FOXC1, E2F1, GATA2, and MEF2A as potential upstream transcription factors implicated in subsets of these transcriptional changes. PD-1 deficiency was correlated with modified proportions of T cells, natural killer (NK) cells, B cells, and the CD4\n                      <jats:sup>+<\/jats:sup>\n                      CD25\n                      <jats:sup>+<\/jats:sup>\n                      CD127\n                      <jats:sup>low\/\u2212<\/jats:sup>\n                      putative regulatory T-cell population. Additionally, PD-1-deficient splenocytes demonstrated heightened proliferative responses upon polyclonal stimulation. In the context of CJ-S131-induced autoimmune challenge, PD-1-deficient mice exhibited elevated levels of lupus-associated autoantibodies and more severe lupus-like renal pathology.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>Collectively, our findings suggest that PD-1 deficiency is linked to disrupted TCR\u03b2 repertoire organization, extensive immune dysregulation, and an increased vulnerability to infection-induced lupus-like autoimmunity.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1911666","type":"journal-article","created":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T05:36:02Z","timestamp":1789450562000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["PD-1 deficiency reshapes the TCR\u03b2 repertoire and T-cell developmental programs 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