Reviews & Analysis

The Toll-like receptor (TLR) family targets pathogen-derived molecules in regions unlikely to change under selection pressures. For TLR5, which recognizes the protein flagellin, the function of the targeting motif is key.

Mast cells are not only important in IgE-associated disorders but also contribute to host defense against bacteria. One way they do this is by enhancing T cell recruitment and lymph node enlargement during bacterial infection.

TLR ligands mediate adjuvant effects. Unlike lipopolysaccharide, poly(I:C) is capable of using a TLR-Trif–independent pathway to induce costimulatory molecule upregulation on antigen-presenting cells.

Although natural killer T cells are activated during infection, it is not clear how this process occurs. Closer examination indicates that recognition of endogenous ligands and interleukin 12, rather than bacterial products, may drive the activation process.

The importance of cross-priming in vivo is controversial because its relative contribution in the presence of conventional priming is unclear. However, data from the examination of a conserved tyrosine residue in the cytoplasmic tail of MHC class I favor the cross-priming hypothesis.

Patients with type 2 Hermansky-Pudlak syndrome are immunodeficient. Mutations in AP-3 that prevent movement of lytic granules along microtubules in CD8⁺ T cells help explain these patients' susceptibility to infection.

Tim-3, a member of the T cell immunoglobulin mucin family, is expressed by T_H1 cells. Analysis of Tim-3–Tim3 ligand signaling now shows this pathway is intimately involved in the counter-regulation of T helper type 1 immune responses.

The LFA-1 integrin is known to mediate adhesion between T cells and antigen-presenting cells. New evidence, however, is provided for its role in transmitting signals that promote T cell activation and differentiation.

Peptide chemokines were initially thought to govern effector T cell migration to inflamed tissues. Several studies now show that the leukotriene B₄ is intimately involved in T cell homing.

A recent pair of Nature papers potentially provide some of the missing pieces to the puzzle of how antigens are cross-presented.

Dendritic cells require a special 'license' to present exogenous antigens to CD8⁺ T cells. Such permission may be provided by type I interferons during viral infections.

Certain infectious diseases, autoimmune disorders and cancers are associated with T cell receptor ζ chain down-regulation. Interferon-γ production by T helper type 1 cells seems to be pivotal in this process.

Mutations now reveal fresh clues about the in vivo function of AID. Interactions with other proteins seem to influence subsequent mutation and DNA rearrangement.