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Chromatin Landscape of IL-4-expressing CD4 T cells in the lung and lung-draining lymph nodes

ABSTRACT: Using bulk-, single cell-, ATAC-, and TCR repertoire sequencing, this study reveals that helminth infection causes the expansion of distinct IL-4-competent CD4+ T cells in the lung and lung-draining lymphoid tissues, providing insight into tissue-specific mechanisms of type-2 cytokine regulation and the lineage commitment of T-helper 2 (Th2) and T follicular helper (Tfh) cells. IL-4 competent CD4+ T cells were stratified into three groups: lymphoid-restricted T follicular helper (Tfh) cells; nonlymphoid resident T-helper 2 (Th2) cells; and transitional cells that share identity with both tissue compartments. Differences in transcriptome, locus accessibility, and the enrichment of distinct transcription factor motifs suggested that IL-4 competency was likely achieved via distinct mechanisms among lymphoid- and lung-resident CD4+IL-4+ populations. These findings reveal a complex relationship between lymphoid- and nonlymphoid-resident CD4+ T cell populations in settings of type-2 immunity.

ORGANISM(S): Mus musculus

PROVIDER: GSE155208 | GEO | 2021/05/17

REPOSITORIES: GEO

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Transcription profiling of IL-4-expressing CD4 T cells in the lung and lung-draining lymph nodes

Project description:Using single cell RNA-sequencing and whole-genome targeted transcription profiling, this study reveals that helminth infection causes the expansion of distinct but clonally related IL-4-competent CD4+ T cells in the lung and lung-draining lymphoid tissues providing insight into tissue-specific mechanisms of type-2 cytokine regulation and the lineage commitment of T-helper 2 (Th2) and T follicular helper (Tfh) cells.

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Gene expression in TFH cells

Project description:After activation, CD4+ helper T (Th) cells differentiate into distinct effector subsets. Although chemokine (C-X-C motif) receptor 5-expressing T follicular helper (Tfh) cells are important in humoral immunity, their developmental regulation is unclear. Here we show that Tfh cells had a distinct gene expression profile and developed in vivo independently of the Th1 or Th2 cell lineages. Tfh cell generation was regulated by ICOS ligand (ICOSL) expressed on B cells and was dependent on interleukin-21 (IL-21), IL-6, and signal transducer and activator of transcription 3. However, unlike Th17 cells, differentiation of Tfh cells did not require transforming growth factor b (TGF-b) or Th17-specific orphan nuclear receptors RORa and RORg in vivo. Finally, naive T cells activated in vitro in the presence of IL-21 but not TGF-b signaling preferentially acquired Tfh gene expression and promoted germinal-center reactions in vivo. This study thus demonstrates that Tfh is a distinct Th cell lineage.

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