Interleukin-1@b Selectively Expands and Sustains Interleukin-22^+ Immature Human Natural Killer Cells in Secondary Lymphoid Tissue
Among human natural killer (NK) cell intermediates in secondary lymphoid tissue (SLT), stage 3 CD34^-CD117^+CD161^+CD94^- immature NK (iNK) cells uniquely express aryl hydrocarbon receptor (AHR) and interleukin-22 (IL-22), supporting a role in mucosal immunity. The mechanisms controlling proliferation and differentiation of these cells are unknown. Here we demonstrate that the IL-1 receptor IL-1R1 was selectively expressed by a subpopulation of iNK cells that localized proximal to IL-1@b-producing conventional dendritic cells (cDCs) within SLT. IL-1R1^h^i iNK cells required continuous exposure to IL-1@b to retain AHR and IL-22 expression, and they proliferate in direct response to cDC-derived IL-15 and IL-1@b. In the absence of IL-1@b, a substantially greater fraction of IL-1R1^h^i iNK cells differentiated to stage 4 NK cells and acquired the ability to kill and secrete IFN-@c. Thus, cDC-derived IL-1@b preserves and expands IL-1R1^h^iIL-22^+AHR^+ iNK cells, potentially influencing human mucosal innate immunity during infection.
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