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Unlike conventional T cells, “naïve” nonclassical MHC class I T cells have an effector cell phenotype. This may be a result of their distinct thymic selection program.
CD4 is almost universally required for HIV to enter cells. A mutable disulfide bond of CD4, however, can influence the permissiveness of cells to HIV infection.
The resolution of an immune response was thought to coincide with the clearance of infection. However, the kinetics of CD8+ T cell decline may be programmed far before the antigen load lightens.
TSLP is now revealed to be an important regulator of DC-mediated control of TH2-based human allergic responses, identifying a potentially new species-specific function for this cytokine.
IgE-FcεRI complex formation represents a critical step in the initiation of allergic responses. Conformational changes involving the Cε2 domain may underlie the persistent activation of FcεRI-bearing cells.
Biofilms offer cover for many pathogenic bacteria. A recent paper in Nature reveals that lactoferrin is an innate tool that inhibits biofilm formation.
The identity of the thymic epithelium precursor has been elusive.A marker is now shown to identify a population of cells that can give rise to a functional thymus.
Although cytokines and STATs are accepted as being integral to TH1 differentiation, T-bet had emerged as a possible master control switch. Fresh data forces a reexamination of the factors that control TH cell development.
Classical opsonins are serum proteins that coat microorganisms and particles so as to enhance uptake by macrophages. A recent Nature paper has identified a macrophage-derived opsonin for apoptotic cells.
The α-defensins from Paneth cells in intestinal crypts need processing to be fully functional. Unlike for mice, the cleaving enzyme for human HD5 turns out to be trypsin.
Some strains of mice fail to mount an efficient NK cell response to MCMV infection. With the use of deletion mutants, the in vivo basis for MCMV resistance to killing by NK cells is revealed.
In some autoimmune diseases, antibodies form that recognize other self-antibodies or DNA. A recent report in Nature implicates the Toll-like receptor 9 and innate immunity as a possible key to understanding the initiation of this process.
Synapse formation in the immune system and the nervous system have common features. The identification of neuropilin-1, a neuronal receptor, as participating in naïve T cell–DC contact helps emphasize the molecular similarities between these systems.
CD1 presents lipid antigens to T cells. Intrinsic properties of microbial lipids, such as alkyl chain length, may be essential determinants of their efficient presentation to T cells.
The pTα cytoplasmic chain was initially thought to be dispensable for T cell development. A reanalysis of the pTα cytoplasmic tail now shows this domain plays a critical role in pre-TCR signaling.
What does Coxsackie virus have to do with diabetes? Evidence is emerging that insulin-producing β cells are highly susceptible to acute infection by Coxsackie virus if their production of interferon is inhibited, resulting in diabetes.
Lack of proper tools hampers early diagnosis and treatment of antigen-specific autoimmune diseases. A new strategy that makes use of peptide-MHC reagents could control recent-onset diabetes in mice.
Patients with severe asthma accumulate inflammatory cells in their airway walls. Studies with MMP2-deficient mice now show that an inability of these cells to egress from the lung can be fatal.
The current paradigm is that reactive oxygen species produced by leukocytes directly kill bacteria. Data in a recent Nature article belie that simplicity.
