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T helper type 1 cells (TH1 cells) serve a dominant function in T cell–mediated colitis. New work reports that interleukin 17A, an effector cytokine required for the development of autoimmune tissue inflammation, directly inhibits TH1 development by suppressing the expression of key TH1-associated genes and therefore regulates TH1 cell–mediated colitis.
Regulatory T cells have the remarkable ability to suppress immune responses driven by different types of effector T cells. Two recent studies, documenting important functions for T-bet and IRF4 in regulatory T cells, demonstrate that this ability requires the expression of transcription factors typically associated with effector T cell function.
T cell antigen receptor (TCR)-transgenic models have been enormously influential in studies of T cell development in the thymus, particularly in terms of positive and negative selection. New transgenic mice produced with TCR genes cloned from regulatory T cells show that TCR specificity does 'instruct' regulatory T cell fate, within limits.
The 3020insC mutation in Nod2 is associated with Crohn's disease, but how it influences disease pathogenesis is unknown. A new study shows that the 3020insC mutant protein fails to activate a key transcription factor that drives interleukin 10 expression, resulting in reduced production of this anti-inflammatory cytokine.
T cell expansion and contraction during the immune response to pathogens are regulated by a wide variety of cell-intrinsic and cell-extrinsic factors. A new study identifies a role for CTLA-4 signaling and activation of the Foxo3 transcription factor in modulating T cell populations.
How the immune system responds to local infection and establishes protective immunity in susceptible tissues remains unclear. Two new studies show that local tissue-resident dendritic cells prime cytotoxic T lymphocyte responses and that memory cytotoxic T lymphocytes remain in the tissue to provide antiviral immunity.
Little is known about how pathogenic T cells gain access to the uninflamed brain in multiple sclerosis and experimental autoimmune encephalomyelitis. A new study reports that interleukin 17–producing T helper cells enter the uninflamed central nervous system through the choroid plexus by a CCR6-CCL20–dependent mechanism.
How immunoglobulin gene loci are specifically targeted by activation-induced cytidine deaminase while the rest of the genome avoids potentially mutagenic events is becoming clearer.
Antibody responses are critical for host protection against many pathogens. By reporting what actually occurs in vivo, two new studies provide important clues about follicular helper T cells that are dedicated to providing help to B cells.
Two papers published recently in Science exploit new transgenic mouse systems to explore the path that activated CD8+ T cells take on the way to memory differentiation.
Although the development of natural killer T cells is a T cell antigen receptor–dependent process, the signaling pathways involved are poorly defined. New data demonstrate that the calcineurin–transcription factor NFAT pathway exerts a critical influence on this process by controlling the transcription factor Egr2.
The intrinsic stability of mRNA is important in the regulation of gene expression. New data show that the intrinsic stability of tumor necrosis factor–induced mRNA transcripts strongly influences the coordinated expression of genes that promote distinct phases of the inflammatory response.
Factors influencing progenitor cell 'choice' between lymphoid and myeloid lineage fates are incompletely understood. New work implicates the transcription factor Mef2c as one component needed to promote lymphoid and suppress myeloid lineage differentiation.
