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The TH1-TH2 paradigm, in which CD4+ T cells polarize into type 1 or type 2 helper cells, has been extended to other cells types. However, evidence now suggests that NK cells differentiate sequentially from immature type 2 to mature type 1 cells, a pathway that could apply to other lymphocytes.
Hypermutation and gene conversion appear to be distinct mechanisms that can explain somatic diversification of the antibody repertoire. Data in a recent Nature paper suggest unappreciated links between the two.
Most receptors transmit extracellular signals to the cytoplasm, but integrins can also be stimulated in the reverse direction. A recent pair of Science papers report that “inside-out” signaling from the TCR is mediated by a newly identified protein called SLAP-130 or Fyb.
Successful passage through several developmental checkpoints determines whether thymocytes survive, proliferate or differentiate. New data show that Wnt-frizzled–induced activation of TCF-1 or Lef-1, via their coactivator β-catenin, is critical during TCRB and TCRA gene rearrangement in thymocytes.
Individual lymphocytes express antigen receptors of a singular specificity. How this process, known as allelic exclusion, is established and maintained is unknown. Differences in subnuclear localization appear to contribute to enforcement of monoallelic receptor expression.
The pathogenesis of multiple sclerosis consists of an inflammatory and neurodegnerative phase. Better understanding of these stages has aided the development of specific therapeutic targets.
B cells can regulate many aspects of immune reactivity, as well as differentiate into antibody-producing cells. In SLE, a systemic autoimmune disease, recent research suggests enhanced B cell function is the defining pathogenic event.
The era of genomic-wide sequence analysis promises to yield new insights in global regulatory gene control. Comparative genome studies have identified a critical regulator of TH2 cytokine expression.
Dendritic cells can prime naïve lymphocytes. New data show how dendritic cells provide early activation cues by expression of IL-2, which may greatly enhance both T and B cell responses.
Although some cellular responses induced by TLRs are abolished in MyD88-deficient mice, TLR4, unlike TLR9, can still induce activation of NF-κB and MAPKs. The discovery of a cytoplasmic adapter protein for TLR4, called TIRAP, helps explain this phenomenon.
Type 1 diabetes is preventable in animal models and predictable in humans. The increase in our knowledge of basic immunology has allowed the initiation of large-scale clinical efforts to prevent diabetes.
Graves' disease and other autoimmune syndromes affecting the thyroid are the archetypes of organ-specific autoimmunity. Despite intensive research, the relative contribution of genetic and environmental factors to disease pathogenesis is not clear. Here, the latest developments in understanding the determinants of these diseases are discussed.
Identification of SH2D1A as the defective gene in X-linked lymphoproliferative syndrome highlighted the importance of SAP in the regulation of T cell activation. New data suggest an alternative explanation for how SAP controls signaling.
Certain types of regulatory T cells are preferentially induced at mucosal surfaces to maintain tolerance. However, the mechanisms involved in their induction are unclear. New evidence suggests DCs orchestrate this mucosal tolerogenic immune response.
