Volume 12 Issue 11, November 2011

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Type 2 cytokine–producing innate lymphoid cells are present in human and mouse lungs, where they contribute to both type 2 immune responses and tissue repair.

The MHC class I–like molecule TL selects high-affinity effector memory T cells to man the barriers in the intestinal mucosa.

The kinase LRRK2 is a risk factor for inflammatory bowel disease. New data show that LRRK2 blocks the transport of NFAT to the nucleus and that LRRK2 deficiency results in enhanced susceptibility to experimental colitis in mice.

How the kinase PKC-θ is targeted to the immunological synapse and is activated once there remains unclear. A targeting motif in PKC-θ and the previously unsuspected kinase GLK identified in two separate papers now explains this.

Cytokine-producing innate lymphoid cells are found at mucosal surfaces. Artis and Wherry and their colleagues show that innate 'nuocyte-like' cells accumulate in virus-infected lungs and contribute to the repair of tissues.

Mice have lineage-negative IL-7Rα⁺ (innate lymphoid) cells that contribute to type 2 immunity. Spits and colleagues identify a similar CRTH2⁺CD161⁺ population in human lungs and gut that produces IL-13 after stimulation.

The adaptor LRRK2 has been identified as a major susceptibility factor for Crohn's disease. Lenardo and colleagues show that LRRK2 negatively regulates activation of the transcription factor NFAT independently of NFAT phosphorylation.

The cellular sources of IL-9 in lung inflammation remain unknown. Stockinger and colleagues use an IL-9 reporter to show IL-9 production is restricted to innate lymphoid cells during papain-induced lung inflammation.

Production of MHC class I epitopes involves the proteasome and multiple peptidases. Bernstein and colleagues show that angiotensin-converting enzyme (ACE) contributes to the generation of this peptide repertoire by trimming carboxyl termini.

Establishing effector memory cells at mucosal barriers is critical for immune protection against pathogens. Cheroutre and colleagues show that interactions between thymus leukemia antigen and CD8αα contribute to the generation of CD8αβ⁺ effector memory T cells.

Efficient T cell priming occurs in organized lymphoid tissues. Turley and colleagues show that activated T cells induce nitric oxide production by lymph node stromal cells, thus limiting T cell proliferation.

The kinase PKC-θ translocates to the center of the immune synapse, but the molecular basis of this interaction is unclear. Altman and colleagues identify a conserved proline-rich motif in the V3 domain of PKC-θ required for its association with CD28 and localization to the immunological synapse.

The enzyme that directly activates the kinase PKC-θ during T cell antigen receptor signaling is still unknown. Tan and colleagues show that the serine-threonine kinase GLK is a direct activator of PKC-θ.

Antigen recognition by surface immunoglobulin triggers downstream signaling and endocytosis of B cell antigen receptors. Pierce and colleagues show that distinct kinase-activation patterns distinguish surface receptor signaling from that of internalized receptors.