Table of contents


From the editors

p319 | doi:10.1038/nri2332

Top

Research Highlights

Vaccines: Explaining alum: immunologists' dirty little secret | PDF (158 KB)

p320 | doi:10.1038/nri2317

Mast cells: Food allergy unplugged | PDF (304 KB)

p321 | doi:10.1038/nri2329

Immunotherapy: A mismatch that works | PDF (277 KB)

p321 | doi:10.1038/nri2330

T-cell activation: The waves behind the TGN1412 storm | PDF (313 KB)

p322 | doi:10.1038/nri2320

Antigen presentation: Prime time: insights into cross-presentation | PDF (234 KB)

p322 | doi:10.1038/nri2323

In brief

MHC molecules | B-cell signalling | T-cell development | PDF (97 KB)

p323 | doi:10.1038/nri2334

Inflammation: Stopping before the damage is done | PDF (110 KB)

p324 | doi:10.1038/nri2324

NKT cells: NKT cells join the IL-17 gang | PDF (234 KB)

p324 | doi:10.1038/nri2325

Tumour immunology: Tumour surveillance by NKG2D | PDF (216 KB)

p324 | doi:10.1038/nri2328

In brief

Haematopoiesis | Antiviral immunity | PDF (90 KB)

p325 | doi:10.1038/nri2331

T cells: Tuning T cells through the aryl hydrocarbon receptor | PDF (226 KB)

p326 | doi:10.1038/nri2319

In the news

Antibiotics from alligators! | PDF (78 KB)

p326 | doi:10.1038/nri2333

Erratum: In Brief: T-cell development

p325 | doi:10.1038/nri2321

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Reviews

Immunobiology of the TAM receptors

Greg Lemke & Carla V. Rothlin

p327 | doi:10.1038/nri2303

The TAM receptors — TYRO3, AXL and MER — are emerging as important regulators of innate immune responses. Here, the authors describe their roles in inhibiting inflammation driven by antigen-presenting cells, in promoting phagocytosis of apoptotic cells and in stimulating maturation of natural killer cells.

TH17 cells in development: an updated view of their molecular identity and genetic programming

Chen Dong

p337 | doi:10.1038/nri2295

The study of T helper 17 (TH17) cells is one of the fastest-moving fields in immunology. Here, Chen Dong discusses our current understanding of this TH-cell lineage and examines some of the issues that remain to be resolved in this field.

Resolving inflammation: dual anti-inflammatory and pro-resolution lipid mediators

Charles N. Serhan, Nan Chiang & Thomas E. Van Dyke

p349 | doi:10.1038/nri2294

Episodes of acute inflammation must be resolved to avoid tissue damage and chronic disease. Three families of lipid mediators — lipoxins, resolvins and protectins — actively promote the resolution of inflammation through multiple mechanisms, as discussed in this Review.

CCR7 and its ligands: balancing immunity and tolerance

Reinhold Förster, Ana Clara Davalos-Misslitz & Antal Rot

p362 | doi:10.1038/nri2297

In this Review, Reinhold Förster and colleagues highlight recent advances in the understanding of how CC-chemokine receptor 7 (CCR7) and its two ligands, CCL19 and CCL21, contribute to both immunity and tolerance.

NLRs at the intersection of cell death and immunity

Jenny P.-Y. Ting, Stephen B. Willingham & Daniel T. Bergstralh

p372 | doi:10.1038/nri2296

In this Review, Jenny Ting and colleagues discuss the role of the NLR (nucleotide-binding domain, leucine-rich repeat containing) family proteins in various forms of cell death, including two newly recognized types of cell death — pyroptosis and pyronecrosis.

Molecular pathogenesis of T-cell leukaemia and lymphoma

Iannis Aifantis, Elizabeth Raetz & Silvia Buonamici

p380 | doi:10.1038/nri2304

Recent studies of T-cell leukaemia have provided insight into the molecular mechanisms responsible for the induction and progression of this disease. As discussed here, many of the genes that are dysregulated in T-cell leukaemia are known to be involved in T-cell development.

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Perspective

Opinion

Not always the bad guys: B cells as regulators of autoimmune pathology

Simon Fillatreau, David Gray & Stephen M. Anderton

p391 | doi:10.1038/nri2315

Accumulating evidence suggests that B cells can regulate immune responses. Here, the authors present a model to explain how B cells may regulate autoimmune pathology by secreting interleukin-10 in response to Toll-like receptor triggering and thereby mediate immune suppression.

See also: Correspondence by Rieger & Bar-Or

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