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Additional immune functions of basophils have been identified in recent years. Mack and colleagues add to this growing list by showing that basophils enhance humoral memory responses by producing interleukins 4 and 6 in response to specific antigen.
The mechanisms responsible for establishing allelic exclusion remain enigmatic. New data indicate that stochastic interactions of antigen-receptor alleles with repressive nuclear compartments may contribute to the mechanisms that support allelic exclusion.
CIITA encodes the 'master regulator' of the expression of major histocompatibility complex class II genes. A new layer of complexity has been identified in the control of CIITA expression, which involves the formation of a complex three-dimensional chromatin structure promoted by interactions among many distant regulatory elements.
This report presents themes highlighted during the eclectic and stimulating Metchnikoff's Legacy in 2008 meeting hosted at the Institut Pasteur in April 2008 in honor of the 100th anniversary of the 1908 Nobel Prize.
Increasing evidence suggests that immune mechanisms underlie major inflammatory diseases that show no overt microbial etiology. In this context, a 4-day conference of clinical and nonclinical scientists convened in the United Arab Emirates to consider recent research developments in this fast-moving field.
Toll-like receptors trigger an innate immune response by activating signaling pathways that are dependent on IRAK kinases. According to Kawagoe et al., the least understood IRAK member, IRAK2, is required for the perpetuation of these signals.
The T cell receptor (TCR) is functionally coupled to a constellation of ten immunoreceptor tyrosine–based activation motifs (ITAMs). A new study suggests that this large number of ITAMs is mandatory for preventing autoimmunity.
B cell tolerance is achieved in part through secondary rearrangements that replace ('edit') exons encoding autoreactive antigen-receptor chains. New findings suggest that Foxo transcription factors are critical regulators of receptor editing by activating the transcription of recombination-activating genes.
Three new studies demonstrate that development of human TH-17 cells requires transforming growth factor-β and one or more proinflammatory cytokines, which are the same requirements as for mouse TH-17 development.
The intensity of cytokine-induced signaling by the kinase PI(3)K subunit p110δ proves to be an important regulator of T cell migration patterns. High PI(3)K activity functions through the nutrient and bioenergetic sensor mTOR to modulate the transcription factor KLF2 and thereby the repertoire of tissue-homing receptors expressed on effector T cells.
How engagement of surface T cell antigen receptors 'translates' into intracellular signal cascades remains vague. Genetic and biochemical experiments now allow modification of a model linking ligation of these receptors with CD3ɛ and other cytoplasmic signal-transduction 'machinery'.
Cross-presentation of antigens is essential for the responses of cytotoxic T cells to tumors and viruses. Two new papers offer insights into the subcellular compartment and types of dendritic cells that mediate cross-presentation.
Toll-like receptor signaling induces the production of proinflammatory cytokines and type I interferons. Inhibition of the kinase IRAK1 by the phosphatase SHP-1 provides reciprocal regulation of these pathways by dampening the former while enhancing the latter.
This report highlights the lively debate and discussions on lymphocyte plasticity and/or determinism that occurred at the second Ringberg Colloquium in February 2008 in the Bavarian hills near Tegernsee, Germany.
Every 2 years, scientists interested in immunomodulation meet to discuss new opportunities arising from interactions between basic science and clinical 'translation'. This report discusses the 8th International Conference on New Trends in Immunosuppression and Immunotherapy, 2008, in Berlin.
