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Endogenous self-peptides derived from CNS antigens are presented on MHC class II molecules at the borders of the CNS and expand suppressive populations of CD4+ T cells.
Sialylated IgG protects against severe influenza by inducing the transcriptional repressor REST, which dampens the inflammatory response and preserves lung tissue function.
A preprint by Hor et al. shows that PD1 signalling regulates the maintenance of a high-affinity, stem-like T cell subset in tumour-draining lymph nodes.
A preprint by Villar-Vesga et al. shows that monocyte-derived cells in the central nervous system produce mitochondrial reactive oxygen species to promote neuroinflammation.
A preprint by Chung et al. presents a framework for the use of transcriptomic and epigenomic data to identify novel transcription factors driving CD8+ T cell states.
This Review discusses the different mechanisms of antibody-dependent enhancement (ADE) of infectious disease, including how antibodies can increase the pathogen load, protect bacteria from the immune system and amplify inflammation. The authors also highlight the role of autoantibodies and consider how a better understanding of ADE can be used to improve vaccines and treatments for infectious diseases.
Inflammasomes are signalling machines that drive inflammation. This Review highlights the signalling biology of inflammasomes and how we can use small molecules or biologics to block pathological inflammasome signalling to treat or prevent diverse human diseases.
Oral tolerance describes how the oral administration of harmless antigens (such as dietary proteins) leads to systemic immune unresponsiveness to these antigens. Its failure can lead to conditions such as food allergies. This Review from Cerovic, Pabst and Mowat explores new insights into the mechanisms of oral tolerance, discussing how ingested antigens enter and are processed in the intestine, the roles for unique antigen-presenting cells and the induction of immunosuppressive T cell populations. The authors also examine the maintenance of tolerance to bacterial antigens in the intestine, and they discuss the mechanisms behind the failure of oral tolerance and potential clinical interventions.
For effective central T cell tolerance, developing thymocytes must encounter a diverse range of self-antigens presented by various thymic cells. Here, the authors describe how medullary thymic epithelial cells, dendritic cells and B cells are uniquely adapted through promiscuous gene expression, strategic positioning and inflammatory signals, which shape the peptide–MHC ligandomes and extend self-antigen visibility in the thymic microenvironment.
