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Precursor cells entering the thymus have non-T cell potential, yet T cell development is clearly favored. A mechanism dedicated to repressing conflicting myeloid cell fate early during the establishment of T cell identity has now been found.
Successful interviewing can be best attributed to a combination of careful research and preparation, along with the ability to connect with employers on a personal level and demonstrate value.
Mice immunized with influenza virus in the presence of rapamycin, which blocks the formation of germinal centers, make mostly IgM antibodies that protect against infection with multiple subtypes of influenza virus, including avian viruses.
Paired immunoglobulin-like receptors (PIRs) recognize β2-microglobulin. Munitz and colleagues show that PIR-A and PIR-B have opposing roles in eosinophil development in response to interleukin 5 in the bone marrow.
The adaptor ASC is required for caspase-1 activation via the NLRP3 and AIM2 inflammasomes. Mitsuyama and colleagues show that signaling dependent on the kinases Syk and Jnk controls ASC speck formation through ASC phosphorylation.
Induction of type I interferon is a central event of antiviral immune responses. Fikrig and colleagues show that the transcription factor ELF4 is recruited by STING and translocates to the nucleus to control transcription of type I interferon genes.
Hematopoietic deficiency in the Notch target Hes1 results in severe defects in the T cell lineage. Bhandoola and colleagues show that Hes1 constrains myeloid gene-expression programs in T cell progenitors.
Lymphocyte function is regulated by phosphatidylinositol-dependent pathways. Uzel and colleagues identify a cohort of immunodeficient patients with hyperactive phosphatidylinositol-3-OH kinase activity due to mutant p110δ subunits, which results in enhanced senescence of cells of the immune system.
Jameson and colleagues show that the establishment of resident memory CD8+ T cells in nonlymphoid tissues requires transcriptional downregulation of the trafficking molecule S1P1, mediated by induced loss of the transcription factor KLF2.
Long-lived tissue-resident memory T cells (TRM cells) confer fast, robust protection after pathogen rechallenge. Gebhardt and colleagues show that skin TRM cells arise from KLRG1– cells that differentiate in situ in response to IL-15 and TGF-β.
Antibody responses are impaired during HIV-1 infection. Cicala and colleagues show that the HIV-1 glycoprotein gp120 directly impairs B cell function by promoting expression of TGF-β and the inhibitory receptor FcRL4.