A role for Th17 cells in the regulation of tertiary lymphoid follicles.

Immune responses propagate in secondary lymphoid organs (SLOs), such as the spleen and lymph nodes. These highly organized structures are typified by distinct B-cell follicles and T-cell zones, and are orchestrated by interactions between the TNF superfamily molecules expressed on hematopoietic cells and their receptors on mesenchymal cells and the subsequent cytokines and chemokines that are elicited. During chronic immune responses, cellular effectors of the immune response can infiltrate target tissue and organize anatomically into de novo B-cell follicles and T-cell areas, a phenomenon called lymphoid neogenesis or the formation of tertiary lymphoid organs (TLOs). Critical to the development of SLOs are lymphoid-tissue inducer (LTi) cells, that is innate lymphoid cells that arise from common precursor cells within the fetal liver. Of interest, Th17 cells, a subset of CD4(+) T cells most associated with autoimmune pathogenesis, share many developmental and effector markers with LTi cells. Here, we compare and contrast LTi and Th17 cells, and review recent evidence that Th17 cells and Th17 cytokines, such as IL-17 and IL-22, contribute to the development of ectopic lymphoid structures in chronic-ally inflamed tissue.