Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
TLR4 somehow manages to activate both MyD88- and TRIF-dependent signaling. According to Medzhitov and colleagues, TLR4 engages MyD88 and TRIF sequentially at the cell surface and in endosomes, respectively, thereby providing access to distinct pools of signaling proteins.
The bone marrow contains specialized microenvironments that maintain blood cells and supply the requisite factors for their development. Newly identified bone marrow–resident dendritic cells create unique niches for mature B cells.
The homing of lymphocytes to secondary lymphoid organs occurs at specialized blood vessels, the high endothelial venules. Autotaxin, a phospholipid-producing enzyme secreted by high endothelial venule endothelium, is a new participant found to facilitate the entry of lymphocytes into secondary lymphoid organs.
Activation of the transcription factor NF-κB by Toll-like receptors must be controlled to avoid excessive inflammation. The tripartite-motif protein family member TRIM30α has now been shown to mediate a negative regulatory feedback mechanism curtailing such responses.
Basophils have long been suspected to be potent inducers of T helper type 2 differentiation. Sokol and colleagues now demonstrate that basophils are required for adoption of the T helper type 2 fate in vivo in response to allergens with protease activity.
Both activation and termination of transcription factor NF-κB signaling require ubiquitin modification of pathway components. The E3 ligase Itch teams up with the NF-κB inhibitor A20 to edit the composition of ubiquitin chains on the signaling adaptor RIP, thereby limiting inflammatory responses.
Two groups demonstrate proteolytic activity for MALT1, a component of the signaling pathway mediating antigen receptor–dependent stimulation of the transcription factor NF-κB, and identify its first substrates.
Naive T cells can spend hours 'sampling' dendritic cells before making a stable conjugate with a single dendritic cell. It is the antigen 'dose' that determines how long this process takes.
Kruppel-like factor 2 is now shown to regulate chemokine receptor expression in lymphocytes, which leads to their homing to nonlymphoid organs after they leave the thymus.
Lymphocytes depend on endothelial adhesion molecules such as ICAM-1 and VCAM-1, upregulated with inflammation, to facilitate transmigration across junctional barriers. New data show that ALCAM replaces VCAM-1 in the CNS during the development of neuroinflammatory diseases such as multiple sclerosis.
Inducible regulatory T cells respond to TGF-β by upregulating Foxp3 expression. Tone and colleagues identify an enhancer site in Foxp3 that binds transcription factors Smad3 and NFAT, suggesting a means by which TGF-β regulates Foxp3 expression.
