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The transcriptional repressor Bcl-6 operates in many hematopoietic lineages. Melnick and colleagues show that Bcl-6 with a mutant BTB corepressor interaction domain selectively impairs B cell effector function.
NKp46+ innate lymphoid cells are important for the control of gut microbes, but their development is unclear. Belz and colleagues show that they develop from lymphoid tissue–inducer cells in a Notch- and T-bet-dependent manner.
During pathogen infection, antibodies can be carried into the cell, where they are detected by the cytosolic antibody receptor TRIM21. McEwan and colleagues show that the recognition of intracellular antibodies by TRIM21 activates immunological signaling.
Thymic stromal lymphopoietin promotes type 2 allergic immune responses via the transcription factor STAT5. Ziegler and colleagues show that ablation of STAT5 in DCs prevents type 2 but not type 1 immunity.
Retrotransposons are often thought of as 'selfish' genetic elements that replicate themselves without any obvious benefit to the host genome. Saleh and colleagues demonstrate that retrotransposons can be involved in generating silencing RNA species to regulate viral replication.
The production of type I interferon is regulated by the master transcription factor IRF7. Kim and colleagues show that OASL1 specifically recognizes IRF7 mRNA and inhibits its translation and the production of type I interferon.
The CARM1–MALT1–Bcl-10 complex links ligation of the antigen receptor to NF-κB activation. Thome and colleagues show that MALT1 paracaspase activity requires monoubiquitination at Lys644. Lymphomas with Lys644 mutants have diminished survival.
Tarlinton and colleagues show that the antiapoptotic protein Mcl1 is essential for plasma cell survival and is induced by BCMA signaling in bone marrow, but not spleen, plasma cells.
Vignali and colleagues show that a full complement of ITAMs is required in the TCR-CD3 complex for TCR-driven T cell proliferation, whereas a low number of functional ITAMs is sufficient for cytokine secretion.
Villadangos and colleagues show that lung resident memory CD8+ T cells selectively maintain expression of IFITM3, a protein that confers broad resistance to viral infection.
Plasma cells are antibody 'factories', which places considerable metabolic stress on these cells. Cenci and colleagues show that long-lived plasma cells and sustained antibody production require autophagy activation.
Gabrilovich and colleagues show that monocytic myeloid-derived suppressor cells (MDSCs) differentiate into polymorphonuclear MDSCs in individuals with tumors, demonstrating a demonstrating a distinct regulation of myeloid cell development in cancer.
CD4+ and CD8+ T cells are considered distinct functional lymphocyte subsets. Cheroutre and Mucida and their colleagues show that mature gut-associated CD4+ T cells lose ThPOK expression and reactivate CD8 cytolytic effector programs.
Sekiya and colleagues demonstrate that the Nr4a nuclear receptors, which are encoded by immediate-early genes upregulated by TCR stimulation in thymocytes, have an essential role in regulatory T cell development.
CD4+ and CD8+ T cells are considered distinct functional lymphocyte subsets. Cheroutre and Mucida and their colleagues show that mature gut-associated CD4+ T cells lose ThPOK expression and reactivate CD8 cytolytic effector programs.
Innate lymphoid cells are cytokine-producing cells that contribute to tissue homeostasis. Spits and colleagues identify a human innate cell population that expresses T-bet and IFN-γ and is prevalent in Crohn's disease.
Unlike vaccination, infection by a live pathogen often impairs dendritic cell function. Iwasaki and colleagues show that during infection with influenza virus, signaling via the IL-1 receptor is both required and sufficient for the priming of CD8+ T cells.
Autoreactive CD8+ T cells are prevalent in multiple sclerosis. Goverman and colleagues identify tumor necrosis factor–inducible nitric oxide synthase (TNF-iNOS)-producing dendritic cells that cross-present myelin antigen to activate naive CD8+ T cells in the central nervous system.