CD4-positive T cells articles from across Nature Portfolio

Regulatory T cells, and to certain extent other T cell subsets, limit the immune response to avoid harmful inflammation and tissue damage. Here authors identify a surface molecule, Lrig1, that is directly responsible for the suppressive function in regulatory T cells and in Il-17-producing helper T cells.

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.

Here, the authors show that short-term consumption of energy-dense diets deficient in fiber, similar to eating patterns for many people today, results in a transient depression of the mucosal and systemic immune systems such that susceptibility to bacterial infection is increased.

In inflammation, some regulatory T (T_reg) cells lose FoxP3 expression and become exT_reg cells. Ley and colleagues mapped mouse T_reg and exT_reg cell transcriptomes to a human peripheral blood mononuclear cell single-cell RNA-sequencing dataset with surface markers (CITE-seq) and identify human exT_reg cells as cytotoxic CD4⁺ T cells.

A study in Immunity reports that a high-fat diet in mice leads to the loss of PPARγ⁺ T_reg cells in the skin, which exacerbates psoriasis mediated by IL-17-producing γδ T cells.

A preprint by Ramanan et al. examines the roles of accessory transcription factors in regulating subsets of colonic regulatory T cells, independently of the microbiota and T cell specificity.

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.

New research demonstrates that regulatory T cells in gut and joint tissues differ in their response to and ability to control TNF-mediated inflammation.

Bystander activation that leads to expression of IL-9 in effector T_H9 cells is induced by a TCR-independent, STAT-dependent mechanism and may represent a new strategy for therapeutic intervention to treat T_H9-induced pathologies in vivo.