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Intracellular bacteria in cancer cells promote the recruitment of neutrophils and their polarization towards an immunosuppressive phenotype via a cGAS-STING-dependent pathway.
A new study shows that inflammation spreads from psoriatic skin to joint disease through the migration of skin myeloid precursors to the joints, where they can become inflammatory macrophages unless they are kept in check by resident regulatory fibroblasts.
Respiratory viral infections can weaken the immune system and carry a risk of severe bacterial secondary infections. A research article in Science Immunology shows that segmented filamentous bacteria in the gut can enhance the antibacterial function of alveolar macrophages in the lungs and provide protection against secondary infections.
Besides killing infected or transformed cells, interferon-activated natural killer cells can kill T follicular helper cells and may contribute to poor antibody responses in some individuals infected with SARS-CoV-2.
A study in Nature reports that heterotypic T cell clusters identifed in clinical samples of melanoma metastases are biologically relevant to tumour control and might have therapeutic potential.
Sanchez-Garcia et al. report that systemic hypoxia-induced epigenetic reprogramming of neutrophil progenitors in the bone marrow reduces their effector function to limit lung tissue damage.
Amyotrophic lateral sclerosis is associated with CD4+ T cells that are specific for the C9orf72 autoantigen and preferentially produce IL-4, IL-5 and IL-10.
A study in Science Immunology reports that regulatory T cells in the skin modulate neuronal tone directly through their production of the opioid enkephalin.
B cells that expand following infection with EBV can colonize the brain, where they recruit activated T cells that have potential to cause neuronal damage, thereby providing a mechanism to explain the link between EBV and increased MS risk.