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Platelets and phagocytes engage in bidirectional interaction in innate immunity and inflammation. Kupffer cell–platelet cooperation results in the rapid encasement of blood-borne bacteria and host protection.
Studies have linked the NLRP3 inflammasome pathway to the elaboration of sterile inflammation. CD36 serves a dual role by priming transcription of the gene encoding interleukin 1β (IL-1β) and inducing assembly of the NLRP3 inflammasome complex, which leads to the release of active IL-1β.
The generation of T cell–dependent humoral immunity is regulated by the miR-17∼92 cluster of microRNAs through their influence on the differentiation and function of follicular helper T cells.
Members of the SOCS (suppressor of cytokine signaling) family negatively regulate STAT transcription factors. The SOCS family member CIS is now shown to negatively regulate differentiation into the TH2 and TH9 subsets of helper T cells through negative regulation of STAT3, STAT5 and STAT6.
A third population of human T lymphocytes that express αβ T cell antigen receptors with restricted α-chain diversity has been identified. These cells recognize the lipid glucose monomycolate from Mycobacterium tuberculosis presented by CD1b.
The glycoprotein CD52 is an important target for clinical antibodies, but its receptor and function have remained a mystery. However, it now seems that CD52 may be released in soluble form by a subpopulation of human T cells and may thereby exert an as-yet-unrecognized regulatory function via the inhibitory molecule Siglec-10.
The mast cell–derived phospholipase PLA2G3 and fibroblast prostaglandin synthase contribute to a mast cell–fibroblast paracrine axis dependent on the prostaglandin PGD2 and its receptor DP1 that can enhance the maturation and mediator secretion of mast cells.
Either stimulation of the innate immune system or infection can result in transient focal inflammatory structures in the liver. Such structures can promote further proliferation of already activated cytotoxic T lymphocytes and enhance antipathogen immunity.
An algorithm developed with a systems-biology approach reconstructs some of the key regulatory events known to drive the development of cells of the mouse immune system and makes many other novel predictions for testing.
Repeated antigenic and inflammatory stimulation during chronic infection is thought to produce 'exhausted' T cells. However, persistent viruses also generate PD-1hi CD8+ T cells with proliferative and cytotoxic ability but 'censored' inflammatory function.
The newly identified steroid ligand of the receptor EBI2 (GPCR183), 7α,25-dihydroxycholesterol, is required for the positioning of splenic CD4+ dendritic cells in bridging channels to prime T cells for an efficient antibody response.
Interleukin 17 (IL-17) confers protection against Trypanosoma cruzi. Surprisingly, B cells are the relevant source, producing IL-17 via a unique pathway independent of the transcription factor RORγt, induced by T. cruzi trans-sialidase.
T cell activation requires an influx of amino acids. Slc7a5, an amino-acid transporter induced by the T cell antigen receptor, facilitates the influx of large neutral amino acids and in doing so promotes metabolic reprogramming necessary for T cell differentiation.
Obesity induces metabolic stress and is associated with inflammation. A cellular pathway now links SIRT2, a deacetylase involved in metabolic processes, to cytoskeleton remodelling and activation of the NLRP3 inflammasome.
Antibodies bound to pathogens that invade cells are sensed in the cytosol by the receptor TRIM21, which triggers innate signaling that leads to protective immunity.
The conversion of cells of the TH17 subset of helper T cells that previously expressed interleukin 17A (IL-17A) and the transcription factor RORγt into follicular helper T cells is needed to generate antigen-specific immunoglobulin A in gut mucosa, which suggests new connections in the cognate control of regional adaptive immunity.
Persistence is a poorly understood yet widespread outcome of viral infection. A study of RNA viruses in flies now shows that viral fragments endogenized as cDNA during the reverse transcription of retrotransposons provide immunity based on RNA-mediated interference in persistently infected cells.
The priming of naive T cells requires antigen presentation by activated dendritic cells, yet the optimal generation of effector and memory CD8+ T cells requires subsequent T cell–T cell interactions during the critical differentiation period.
The differentiation of monocytes is altered in cancer, which results in the unexpected conversion of a large proportion of monocytic myeloid-derived suppressor cells into polymorphonuclear myeloid-derived suppressor cells.
By increasing the range of epitopes presented to lymphocytes, determinant spreading allows a more diverse response to ensue. Now the cellular culprits responsible for determinant spreading in the central nervous system have been identified: they are specialized dendritic cells that recruit CD8+ T cells to an autoimmune 'crime'.
