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Although CD4+ T cell help is required for effective pathogen control, persistent antiviral CD4+ T cell help can, paradoxically, impair the generation of neutralizing antibody responses and thus potentially limit protective immunity.
CD4+ T cells reportedly program CD8+ T cells to develop into suitable memory cells during the primary immune response. However, new data indicate that the maintenance of CD8+ memory T cells requires continuous exposure to bystander CD4+ T cells.
Members of the PIAS family can negatively regulate the cytokine-activated Jak-STAT pathway in vitro. One member of this family, PIAS1, is a nonredundant and physiologic regulator of certain STAT1-dependent interferon-induced genes.
Many patients with Crohn disease, an inflammatory bowel disorder, carry mutations in NOD2. The finding that NOD2 normally dampens Toll-like receptor 2–mediated inflammation may explain this association.
A handful of agonist peptide–MHC complexes can evoke a sustained signal from the T cell receptor. A combination of mathematical models and imaging experiments suggests a key function for CD4 and endogenous (self) peptides in the generation of this sensitive response.
Granulomas are thought to be immunological barriers that effectively contain mycobacteria. This hypothesis is now challenged by data that show granulomas are dynamic entities permissive to bacterial latency and reinfection.
Antimicrobial peptides are essential effectors of gut immunity. The cryptdin-related sequence peptides represent a newly identified large family of antimicrobial peptides that form dimers to increase diversity.
How do cells fend off intracellular viruses that slip in below extracellular defensive 'radar screens'? The identification of a cytoplasmic RNA helicase that signals through CARD interactions links viral detection to the interferon-β induction pathway.
A hierarchy of stem cells has been identified within leukemias, providing a more complex view of how these self-renewing populations parallel the normal stem cell compartment. As the resemblance between normal and malignant stem cells deepens, new opportunities for understanding and treating malignancy emerge.
For lymphocytes to function properly, they must move to and recognize precise anatomical locations. To do so, lymphocytes must decipher cues from a panoply of competing traffic signals.
