Skip to Main Content

Advertisement

Issues

  • Cover Image

    Cover Image

    issue cover

    ON THE COVER
    Wang et al. show that the transcription factor Batf is required for the induction of gut-homing receptors on T cells in response to retinoic acid. The image shows CD4+ (blue) and CD8+ (red) T cells in the small intestinal villi in wild-type mice.
    See page 475

  • PDF Icon PDF LinkTable of Contents
  • PDF Icon PDF LinkEditorial Board
ISSN 0022-1007
EISSN 1540-9538
In this Issue

Brief Definitive Report

A primary immunodeficiency syndrome caused by loss-of-function mutations in the IL-21 receptor exhibits impaired B, T, and NK cell function.

Synovial IgG-expressing B cells from patients with rheumatoid arthritis show specificity for citrullinated autoantigens.

High-affinity antibodies reenter germinal centers (GCs) and limit antigen access, thus causing sustained directional evolution in GCs toward higher-affinity antibody production.

Endothelial cell ablation of the lymphotoxin-β receptor results in failure to develop peripheral lymph nodes and normal high endothelial venues, which impairs lymphocyte homing.

Article

Induction of gut-homing receptors in T cells in response to retinoic acid requires the transcription factor BATF.

IL-1R1 signaling drives T cell activation in the CNS via effects on DC activation.

IL-27 promotes the differentiation of monocytes to HIV-resistant macrophages by down-regulating host factor SPTBN1.

Innate lymphoid type 2 cells maintain eosinophils and alternatively activated macrophages in visceral fat via the production of IL-5 and IL-13.

STAT3-mediated induction of Reg3γ enhances bacteriostatic and bactericidal activity to pulmonary Staphylococcus aureus.

Genetic deficiency for endoglin leads to increased metastatic capability by weakening the endothelial cell barrier.

p63 is up-regulated in melanoma and prevents nuclear accumulation of p53.

Cytotoxic T cells increase leukemia stem cell numbers in a murine model of chronic myeloid leukemia.

Blocking TGFβ signaling after chemotherapy accelerates hematopoietic reconstitution and delays the return of cycling HSCs to quiescence.

Correction

Close Modal
This Feature Is Available To Subscribers Only

Sign In or Create an Account

Close Modal
Close Modal