T-helper 17 cells articles from across Nature Portfolio

A study in mice to identify mechanisms through which a mucosal Klebsiella pneumoniae vaccine elicits Th17 tissue resident memory cells in the lungs reveals a major role for IL-1a signaling and highlights the utility of IL-1a as a mucosal adjuvant.

Periodontitis is closely linked with inflammatory bowel disease (IBD) and may have overlapping characteristics. Here the authors show that a periodontal pathogen P. gingivalis promotes intestinal inflammation by affecting the microbiome metabolite linoleic acid and Th17/Treg cell balance in the intestine.

Regulatory T (T_reg) cells are functionally heterogeneous, yet how each T_reg cell subset exerts its suppressor function remains unresolved. Lin et al. identify IL-27 as a key T_reg cell effector molecule selectively required for gut T_H17 cell regulation.

IL-17 secreting Th17 cells have established roles in numerous immune-pathologies but paradoxically are required homeostatically in the maintenance of the intestinal barrier. Here the authors establish Raftlin-1 in the recruitment of phospholipids that are linked to the emergence of pathogenic Th17 cells in animal models of bowel inflammation.

Lazarevic and colleagues show that the transcription factor EGR2 controls a transcriptional program specific to pathogenic T_H17 cells in the CNS.

Interleukin 26 (IL-26) has been shown to have antimicrobial and pro-inflammatory effects. Here the authors establish a role for IL-26 in the generation of IL-17A producing Th17 CD4⁺ T cells and suggest it involves epithelial cross talk in skin lesions of psoriasis patients.

The mechanisms by which T_H17 cells can either protect barrier tissues or initiate autoimmunity remain unknown. Here we identify the transcription factor EGR2 as a key determinant of T_H17 cell pathogenicity. EGR2 was found to govern T_H17 cell migration, regulate the expression of pathogenicity-associated genes, and facilitate the recruitment of other immune cells in the central nervous system.

Commensal-specific T cells promote the regeneration of damaged sensory nerves in the skin, through an IL-17-dependent pathway.

T_H17 cells combat infection but can also drive pathological inflammation. A T_H17 cell NLRP3–caspase-8–caspase-3–GSDME axis is now shown to release the alarmin IL-1α without triggering cell death.

Extrathymic MHCII⁺Rorc⁺ Aire-expressing cells that share characteristics with type 3 innate lymphoid cells (ILC3s) internalize C. albicans and present its antigens, priming the development of Candida-specific T_H17 cells.