Lymphocyte differentiation articles from across Nature Portfolio

Interactions between Semaphorin-3A (SEMA3A) and Neuropilin-1 (NRP1) and Plexin-A1 and Plexin-A4 have been shown to affect T cell development. Here the authors investigate how these interactions affect CD8⁺ T cells in tumour immunity, showing that NRP-1, Plexin-A1 and Plexin-A4 are upregulated on T cells allowing tumour derived SEMA3A to inhibit CD8⁺ T cell migration and function.

The heterogeneity in naive CD8⁺ T cells is essential for diverse immune responses. Here the authors show that variations in developmental self-reactivity of CD8⁺ T cells influence their differentiation into T_c17 cells in inflammatory conditions.

Studies in mice show that effector T regulatory cells in the gut are most functional in the lamina propria, but this homeostatic niche is disrupted in inflammation, suggesting a spatial mechanism of tolerance to commensal microorganisms.

Loss of function mutation studies has provided insights into regulatory T-cell biology. Here Cardinez et al explore the effects of a murine Ikbkb (IKK2) gain of function model and show IKK2 activity results in the expansion of regulatory T cells with partial effector function and suggest an IKK2 dose-dependent relation between psoriatic immunopathology and psoriatic arthritis.

Regulation of thymocyte development by RNA-binding proteins is not fully characterized. Here the authors show the RBP ARPP21 interacting with the Rag1 3’-UTR to promote Rag1 expression, TCR rearrangement and an increased diversity of the TCR repertoire and that ARPP21 is down regulated by TCR stimulation.

In this Review, Wilfahrt and Delgoffe discuss how T cells integrate nutrient sensing with activating stimuli to shape their differentiation and sensitivity to metabolites.

A study in Science reports 10 individuals with pre-TCRα deficiency who have late-onset or no clinical phenotype, which suggests that αβ T cells can develop through a pre-TCRα-independent, non-canonical rescue pathway.

The transcription factor NFAT5 regulates T cell exhaustion, a dysfunctional state caused by chronic exposure to antigen and other signals, during cancer but not during chronic viral infection.