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Lymphocyte adhesion requires rapid responses. Lymphocytes from mice deficient in the Rap effector molecule RAPL lack this property and are therefore deficient in their immune responses.
The B cell transmembrane glycoprotein modulates immune signaling. Mice containing specific Cd22 mutations show that the extracellular glycan-binding function is regulatory and indicate unexpected complexity in CD22-ligand interactions.
The innate inflammatory immune response must be finely tuned to avoid excessive damage to the host. One molecule, A20, is intricately involved in dampening inflammatory signals mediated by both tumor necrosis factor and multiple Toll-like receptors.
The physical location of key proteins may turn out to significantly influence the differentiation tack that a cell takes. If clusters of antigen receptors include interferon-γ receptors in their midst, the fate of that T cell may be tipped.
A comprehensive overview, three review articles and a perspective examine how the innate immunity influences the outcome of the adaptive immune response.
