MHC class II articles from across Nature Portfolio

Podoconiosis is triggered by long term barefoot exposure to volcanic red clay soil. Here, Negash et al characterise the immune profile of podoconiosis patients to show this disease is associated with high levels of immune activation and inflammation.

Bead-based assays to assess the donor-specific antibody profile of solid organ transplant patients often produce discordant results relative to cell-based alternatives. In this study, the authors demonstrate that, for some MHC class-II-specific antibodies, discordance can be attributed to recognition of the MHC class-I-derived peptides bound to MHC class-II molecules.

Radiation induced gastrointestinal syndrome is a complication of radiotherapy and the tumor suppressor p53 is implicated in protection from gastrointestinal toxicity. Here Wang and colleagues show that p53 protection against radiation-induced gastrointestinal syndrome involves intestinal stem cell function and inhibition of inflammation triggered by radiation via the IL12- p40/MHC-II axis.

Protein glycosylation plays a vital role in antigen recognition and immune modulation. Here, the authors present a computational workflow for identifying glycosylated peptides from mass spectrometry-based immunopeptidome data and investigate the properties of glycosylated MHC associated peptides.

The analysis integrating immunoinformatics data mining models with large volumes of high-quality HLA-DQ specific immunopeptidomics data reveals trans-only HLA-DQ variants have a limited to no contribution to the overall HLA-DQ immunopeptidome.

A new study explores the links between diet and colorectal cancer risk by showing that changes to the intestinal microbiome in mice fed a high-fat diet result in attenuated MHC class II expression by intestinal stem cells and hence impaired immune surveillance of tumour initiation.

CD4⁺ T cell cytokines in the intestinal crypts balance intestinal stem cell renewal and differentiation.

In the current issue of Nature Immunology, Casanova and colleagues demonstrate that humans (and mouse models) with autosomal-recessive SPPL2a deficiency have a severe defect in conventional dendritic cell 2 survival and production of IL-12 and IL-23, and diminished IFN-γ secretion by mycobacterium-specific memory T cells, thus resulting in increased susceptibility to mycobacterial diseases.

Fragments of the protein α-synuclein, which accumulates in substantia nigra neurons in Parkinson disease, are expressed on the surface of these substantia nigra neurons and induce a form of autoimmunity that could account for the degeneration of these cells in the disease.