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Alloreactive T cell responses are considered the product of 'degenerate' recognition by T cells of many different complexes of peptide and major histocompatibility complex. New work shows instead that T cell receptor alloresponses are highly 'polyspecific' for such complexes.
Limited niche availability restricts the number of long-lived plasma cells that can reside in the bone marrow. New research describes homeostatic regulatory mechanisms that allow newly 'minted' plasma cells to gain entry to such niches.
Recruitment of lymphocytes to the lymph nodes requires L-selectin-mediated recognition of carbohydrate determinants presented by O-glycans. New work shows that N-glycans 'decorated' with the same determinants also contribute to lymphocyte homing.
Localized vitamin metabolism by dendritic cells generates homing cues that direct lymphocytes to specific tissues. Gut tropism is linked to vitamin A and now epidermal skin tropism is linked to vitamin D processing.
Epithelial cells responding to inflammatory stimuli can initiate class switching and antibody secretion in naive B cells. TSLP, BAFF and SLPI are epithelial cell–derived local regulators of effector B cell responses in mucosal environments.
The signaling adaptor Act1 is now shown in vivo to be essential for interleukin 17–mediated inflammation in the brain during experimental autoimmune encephalomyelitis and in gut epithelial cells during induced colitis.
'Promiscuous' gene expression in medullary thymic epithelial cells positive for the autoimmune regulator Aire is critical for central T cell tolerance. Expression of the tight-junction components claudin-3 and claudin-4 'marks' Aire+ epithelial cells in the postnatal thymus and their direct precursors in the embryo.
Regulatory T cells expressing the transcription factor Foxp3 are known to control autoreactivity during and subsequent to the development of the peripheral immune system. New evidence emphasizes the fact that those cells are constant and powerful guardians against the state of 'horror autotoxicus'.
T cell receptor activation requires the membrane-associated guanylate kinase CARMA1. A new study finds that a second such kinase, Dlgh1, is also required specifically for activation of the alternative p38 kinase pathway.
Cell fate 'decisions' involving multipotential progenitors seem to be 'dictated' by threshold activities of lineage-determining transcription factors. Such 'decisions' are now shown to be reinforced by the induction of secondary transcription factors that act in concert with the primary regulators.
Tolerance to self is engendered by multiple mechanisms. Lymph node stromal cells are now found to contribute to self-tolerance by their endogenous expression of peripheral tissue antigens.
New work shows that CARD9, the recently identified member of the caspase recruitment domain–containing family, directly interacts with the cytoplasmic protein Nod2 in the detection of intracellular bacteria.
Histone modification is an important means of 'fine tuning' gene expression. The Shigella flexneri dually specific phosphatase OspF shapes host inflammatory transcriptional responses by inducing epigenetic modifications.
Fungal infection is 'sensed' by host cell–expressed receptors. Two papers demonstrate that the C-type lectin receptor dectin-1 is required in vivo for cytokine production and killing of different fungal pathogens.
Loss of the aminopeptidase ERAAP produces a distinct repertoire of peptide–major histocompatibility complex class I complexes. That difference elicits frequencies of immune recognition in congenic mice similar to those in allogeneic immune responses.
Relapses and exacerbation of clinical symptoms are hallmarks of debilitating autoimmune diseases like multiple sclerosis. Osteopontin-induced survival of autoreactive T cells may be one mechanism underlying the clinical progression of autoimmune disease.
