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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.
Proteins are digested into peptides for presentation by MHC to T cells. A recent paper in Science reports that some lipids also undergo processing in order to be presented by the unconventional class I protein CD1.
New data shows that NADPH oxidase activation by Rac2 involves an insert-dependent interaction between Rac2 and cyt b. This unique activation mechanism has far-reaching implications for the regulation of related signaling systems.
In addition to the TCR and classical MHC class I, MHC class 1–like molecules can interact with a variety of receptors that play a role in T cell activation. Engagement of NKG2D on CMV-specific αβ CD8+ cells by MIC was found to provide them with a costimulatory signal and augment their cytotoxic response.
Notch is heavily involved in T cell lineage commitment . . . or is it? New data indicates that neither CD4 nor CD8 cell maturation is Notch1-dependent, whereas Notch1 is critical for earlier steps in T cell development.
What determines whether immune responses against a self-peptide can evoke an anaphylactic response? New evidence describes anaphylaxis that appears to be governed by thymic expression of the self-antigen.