ON THE COVER
Immunohistochemical triple staining of IL-33 (green), Iba1 (red), and GFAP (yellow) in the fovea of an 82-year-old female donor diagnosed with age-related macular degeneration. Blue: DAPI (49,6-diamidino-2-phenylindole) staining of the nuclei. Image kindly provided by Dr. Menno van Lookeren Campagne.
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Brief Definitive Report
Chan et al. describe a combination of alleles with hypomorphic and activating mutations in the T cell signaling molecule ZAP-70 in a patient with autoimmunity.
Zhu et al. report the identification of CD112R as a new coinhibitory receptor of the TIGIT–DNAM-1 family for human T cells.
Butyrophilins are proteins secreted during lactation and thought to influence immune function. Sarter et al. generated butyrophilin-2a2–deficient mice to show enhanced effector T cell responses, antitumor responses, and exacerbated EAE due to the impaired APC modulation of T cell immunity.
Xi et al. demonstrate that IL-33 is a key regulator of retinal inflammation and degeneration.
RAG-mediated DNA double-strand breaks activate a cell type–specific checkpoint to inhibit pre–B cell receptor signals
B-lineage cells reconcile the competing needs of proliferation and genome stability.
Type I IFN promotes NK cell expansion during viral infection by protecting NK cells against fratricide
Madera et al. show that NK cells unable to receive type I IFN signals during MCMV infection have defective expansion and memory cell formation, possessing increased susceptibility to apoptosis due to NK cell–mediated fratricide.
The miR-23∼27∼24 clusters control differentiation of effector T cells. In particular, miR-24 targets IL-4 and miR-27 targets GATA3, thus collaborating in the control of Th2 immunity.
IL-1–induced Bhlhe40 identifies pathogenic T helper cells in a model of autoimmune neuroinflammation
Lin et al. show that Bhlhe40 expression identifies encephalitogenic CD4+ T helper cells and define a pertussis toxin–IL-1–Bhlhe40 pathway active in experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis.
Klein et al. show that Ptch2 loss in either the niche or in hematopoietic cells drives myeloproliferation and accelerates JAK2V617F-driven pathogenesis, causing transformation of nonlethal chronic MPNs into aggressive lethal leukemias.