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The molecular events behind T cell quiescence are poorly understood. Evidence is now emerging that the transcription factor LKLF can potentially programme cells to a resting state in a c-Myc–dependent manner.
Unlike the BCR, the TCR cannot undergo affinity maturation. However, T cells respond with greater sensitivity to antigen during an immune response. New evidence suggests T cells undergo avidity maturation to enhance T cell responsiveness in the absence of changes in intrinsic affinity.
Immunological synapse formation is essential for T cell activation. A recent paper in Science reports that immunological and neurological synapses utilize a common molecule, agrin.
γδ T cells are the misunderstood siblings of the antigen receptor family. A recent paper in Nature that describes the crystal structure of a γδ TCR should initiate a clearer understanding of these enigmatic cells.
BLyS and family are known to affect B cells in a positive fashion. Knock-outs of BLyS receptors indicate some new functions, including negative regulation by one BLyS receptor, TACI.
Expression of mIgM was thought to be essential for the differentiation of B cells expressing antibodies of other classes. New evidence suggests isotype class switching to IgA can occur in the absence of mIgM.
T cells, move over. B cells are now reported, in a recent paper in Nature, to have their own immunological synapses with APCs. Only this time the antigen is whole and B cells don't keep it to themselves.
Our current understanding of lymphocyte migration across the endothelium includes four steps: attachment, rolling, arrest and diapedesis. New evidence suggests the involvement of another step, chemorheotaxis.
Genetic ablation experiments have shown that Vav is critical for TCR signaling. Evidence is now emerging that the Vav family of signaling molecules play a critical role in antigen receptor signaling in B cells as well as in T cells.
Multiple error-prone DNA polymerase appear to contribute to immunoglobulin somatic hypermutation. Genetic and biochemical data now indicate that DNA polymerase η may be responsible for the generation of some of the strand-biased hotspot A mutations in the immunoglobulin loci.
The events that enable polarization of T cells and migration across the vasculature to the target are largely unknown. New evidence suggests that PKC-β(I) may be pivotal in controlling this process.
Adjuvants and inflammation inhibit TCR ligation-induced apoptosis of T cells. Bcl-3 may enhance the increased T cell survival by positive regulation of NF-κB transcription factors.
NK cell receptors either activate or inhibit the fratricidal tendencies of NK cells. Structural analysis of receptor-ligand complexes of both types of receptors reveals striking similarities in form, despite the diverse function.
Differentiation of periperal T cells into TH1 and TH2 subsets is a crucial part of a normal immune response. Evidence is emerging that a signaling pathway involving the SAP molecule may play an important role in this differentiation process.
Activation, proliferation and differentiation of CD8+ cytotoxic T cells must be carefully regulated. New evidence suggests that antigen and costimulation may be enough to trigger the program.
The disappearance of CD4+ T cells during an HIV infection sets the stage for the characteristic immunodeficiency. But how do the virally infected cells protect themselves long enough to manufacture more HIV virions? A recent paper in Nature suggests that Nef may be part of the answer.
