Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Autophagy has been suggested—on the basis of in vitro studies—to be involved in defense against bacterial challenge. A study in drosophila now shows the importance of autophagy in vivo and links a pattern recognition receptor to the autophagy pathway.
The production of inflammatory interleukin 1β after uptake of silica crystals and alum salt or amyloid-β occurs by a process that involves lysosomal destabilization and release of cathepsin B that activates the NLRP3 inflammasome.
New findings show that ERAAP, an endoplasmic reticulum aminopeptidase involved in antigen processing, helps mice survive encounters with a feline-derived parasite.
Host immunity requires cytotoxic lymphocytes that are able to move toward their targets but are also able to stop after identifying target cells and then establish stable cell-cell contact. A new study shows that separate phosphorylation sites in HS1, an actin cytoskeleton–remodeling factor, can regulate both processes.
A key regulator of the balance of signals that activate effector mechanisms versus those that restrain them, β-arrestin 2 mediates the inhibition of natural killer cell cytotoxicity.
Transcription factors of the Ets family are important for mammalian development. A genetic screen now finds that the Ets family member Erg is essential for definitive hematopoiesis and adult hematopoietic stem cell function.
Neutrophils can respond to many chemotactic signals, but how these cells 'prioritize' such signals to react to invading pathogens has remained unclear. The phosphatase PTEN seems to be critical in directing the migration of neutrophils toward their end target in a complex milieu of competing signals.
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.
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'.