Published in Nature Immunology
The mechanisms that drive responses to PD-1-blocking immunotherapy in some but not all patients have been puzzling. A new study suggests that the balance of PD-1 expression levels between CD8+ T cells and Treg cells might provide an answer.
Published in Nature Immunology
Two studies reveal a role for the transcriptional regulator BATF3 as a T cell–intrinsic factor mediating effective memory responses. This finding opens future avenues of investigation and opportunities to enhance cellular immunotherapy.
Published in Nature Immunology
BATF3 is a member of the AP-1 transcription factor family. Kastenmüller and colleagues show that BATF3 is needed to promote memory CD8+ T cell responses. Activated CD8+ T cells transiently upregulate BATF3, which in turn suppresses expression of proapoptotic BIM to promote cell survival.
Published in Nature Immunology
Treg cells are essential for immune homeostasis, but the transcription factors controlling their cellular identity are incompletely understood. Schumann and colleagues use pooled and arrayed CRISPR screens and scRNA-seq to describe key gene networks in human Treg cells.
Published in Nature Immunology
The pathways controlling T follicular helper (TFH) cell development are only partially understood. Allen and colleagues demonstrate the importance of the T cell receptor, with low tonic signaling promoting TFH cell development and high tonic signaling opposing it.
Published in Nature Immunology
Luster and colleagues show that Treg cells that reside in lung mucosa can respond to IL-33 upon allergen exposure and suppress innate cell responses. IL-33-activated ST2+ Treg cells secrete IL-35, which suppresses IL-17 production by γδ T cells and lessens eosinophil recruitment into the lung.
Published in Nature Immunology
SARS-CoV-2-specific CD4+ and CD8+ T cell epitopes are found in both convalescent patients and virus-naive volunteers and are indicative of heterologous recognition shared with seasonal cold viruses.
Published in Nature Immunology
The lung endothelial cell–derived angiocrine Rspondin3 activates Wnt–β-catenin signaling in interstitial macrophages, leading to a metabolic–epigenetic reprogramming of interstitial macrophages that drives anti-inflammatory responses and attenuates endotoxin-induced lung injury.
Published in Nature Immunology
Humans with inherited defects in DOCK8 expression are prone to allergic, type 2 CD4+ T cell responses. Mandl and colleagues reveal an important role for cell death in driving such type 2 signals during infection.
Published in Nature Immunology
Sepsis is a biphasic disease characterized by an initial inflammatory phase, followed by a prolonged immunosuppression phase. Puthalakath and colleagues utilize a CRISPR-mediated mutagenesis screen to identify TREML4 as a regulator of sepsis-induced immunosuppression.
