Journal
CELL REPORTS
Volume 28, Issue 12, Pages 3047-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2019.08.037
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Funding
- Penn Center for AIDS Research [P30 AI 045008]
- Veterans Affairs (VA) Merit Award [IMMA-020-15F]
- NIH [R01AI134879, R00AG040149, S10OD020072]
- Welch Foundation [F1785]
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CXCR5 is a key marker of follicular helper T (T-FH) cells. Using primary lymph nodes (LNs) from HIVinfected patients, we identified a population of CXCR5(-) CD4(+) T cells with T-FH -cell-like features. This CXCR5(-) subset becomes expanded in severe HIV infection and is characterized by the upregulation of activation markers and high PD-1 and ICOS surface expression. Integrated analyses on the phenotypic heterogeneity, functional capacity, T cell receptor (TCR) repertoire, transcriptional profile, and epigenetic state of CXCR5(-) PD-1(+)ICOS(+) T cells revealed a shared clonal relationship with TFH cells. CXCR5(-) PD-1(+)ICOS(+) T cells retained a poised state for CXCR5 expression and exhibited a migratory transcriptional program. TCR sequence overlap revealed a contribution of LN-derived CXCR5(-) PD-1(+)ICOS(+) T cells to circulating CXCR5(-) CD4(+) T cells with B cell help function. These data link LN pathology to circulating T cells and expand the current understanding on the diversity of T cells that regulate B cell responses during chronic inflammation.
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