Volume 11 Issue 8, August 2010

Regulation of the inflammatory response is necessary for limiting tissue destruction and preventing autoimmunity. A recent discovery shows that CD11b activated by Toll-like receptors via inside-out signaling mediates degradation of the Toll-like receptor adaptors MyD88 and TRIF.

Mucosal-associated invariant T cells are evolutionarily conserved T lymphocytes with undefined antigen specificity. These cells are now shown to have a unique role in host defense by targeting highly conserved microbial antigens.

Type I interferons are produced by almost all nucleated cells in response to virus infection. MafB is now shown to modulate the efficiency of interferon production by setting a threshold for IRF3-dependent transcription.

Notch1 has an indispensable role in T cell development and NOTCH1 acts as a potent oncogene in T cell leukemia. New data now reveal the role of RNA-binding proteins in regulating the stability of Notch1 mRNA and the induction of T cell leukemia.

Mucosal-associated invariant T cells are evolutionarily conserved innate lymphocytes whose physiological function has remained unclear. Lantz and colleagues now demonstrate an important antimicrobial function for these cells.

PLZF is known to be a transcription factor for natural killer T cells. Now Hogquist and colleagues demonstrate that PLZF⁺ T cells regulate the size of the CD8⁺ memory T cell pool.

RNA-binding proteins are involved in post-transcriptional regulation. Turner and co-workers show that these proteins are also critical in thymopoiesis.

How Roquin controls expression of the inducible costimulator ICOS remains unclear. Heissmeyer and co-workers now show that Roquin binds to the 3' untranslated region of ICOS mRNA and interacts with proteins that confer post-transcriptional repression.

Integrins regulate the migration of leukocytes in inflammation. Cao and co-workers now show that CD11b is activated by Toll-like receptor–triggered inside-out signaling and feeds back to inhibit phosphorylation of the adaptors MyD88 and TRIF.

Type I interferons (IFN-α and IFN-β) are key to antiviral immunity. Kim and Seed now demonstrate that the transcription factor MAFB acts as a metastable switch to control expression of IFN-β.

Virulent Mycobacterium tuberculosis inhibits apoptosis of infected macrophages. Behar and co-workers show that inhibition of apoptosis prevents cross-presentation of M. tuberculosis antigens by dendritic cells and impedes initiation of T cell immunity.

Functional μ-immunoglobulin heavy chains pair with VpreB and λ5 to form precursor B cell antigen receptors. Jumaa and colleagues show that glycosylation at asparagine 46, a unique modification specific to the μ-heavy chain, is required for the function of such receptors.

Five specially commissioned reviews discuss how immune cells integrate a variety of environmental cues and intrinsic programs to create an efficient immune response.