Table of contents


From the editors

p411 | doi:10.1038/nri2100

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Research Highlights

T cells: Human TH17 cells take centre stage

p413 | doi:10.1038/nri2108

Immune regulation: Terminating inflammatory responses

p414 | doi:10.1038/nri2104

Tumour immunology: DCs under the influence

p414 | doi:10.1038/nri2105

In the news

Chitin might hold key to asthma

p414 | doi:10.1038/nri2114

In brief

Reproductive immunology | Evolution | T-cell development

p415 | doi:10.1038/nri2112

Immunodeficiency: Modelling Omenn syndrome

p416 | doi:10.1038/nri2106

Antigen presentation: Planning your route from the start

p416 | doi:10.1038/nri2107

Asthma and allergy: Opposing roles for osteopontin

p417 | doi:10.1038/nri2109

Innate immunity: Pannexin-1: the missing link?

p418 | doi:10.1038/nri2110

Immune regulation: MicroRNAs and the immune response

p418 | doi:10.1038/nri2111

In brief

Natural killer cells | Autoimmunity | Immune regulation

p419 | doi:10.1038/nri2113

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Focus on: Cytokines & cytokine therapies

FOREWORD

Cytokines and interventional immunology

David A. Hafler

p423 | doi:10.1038/nri2101

PROGRESS

TH1 cells control themselves by producing interleukin-10

Anne O'Garra & Paulo Vieira

p425 | doi:10.1038/nri2097

Recent studies have shown that the anti-inflammatory cytokine interleukin-10 can be produced by T helper 1 cells. In this Progress article, Anne O'Garra and Paulo Vieira discuss the implications of these studies and the outstanding questions that they now raise.

REVIEWS

Cytokines in the pathogenesis of rheumatoid arthritis

Iain B. McInnes & Georg Schett

p429 | doi:10.1038/nri2094

In a rheumatoid joint, a hierarchical network of cytokines controls immunological processes that promote autoimmunity, chronic inflammation and tissue destruction in rheumatoid arthritis. As proposed in this Review, defining these functional hierarchies may present new opportunities for treating the disease.

TGFbeta signalling in control of T-cell-mediated self-reactivity

Yuri P Rubtsov & Alexander Y Rudensky

p443 | doi:10.1038/nri2095

This Review describes the recent advances in our understanding of the role of TGFbeta (transforming growth factor-beta) signalling in the regulation of T-cell differentiation in the thymus and periphery, with particular emphasis on TGFbeta-mediated control of self-reactive T cells.

SOCS proteins, cytokine signalling and immune regulation

Akihiko Yoshimura, Tetsuji Naka & Masato Kubo

p454 | doi:10.1038/nri2093

In this Review, Akihiko Yoshimura and collegues discuss the most recent advances in our understanding of suppressor of cytokine signalling (SOCS) proteins in the regulation of immunity, their involvement in human diseases and the therapeutic implications of targeting this family of cytokine regulators.

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Reviews

The role of junctional adhesion molecules in vascular inflammation

Christian Weber, Line Fraemohs & Elisabetta Dejana

p467 | doi:10.1038/nri2096

Recent studies have elucidated important roles for members of the junctional adhesion molecule (JAM) family in controlling vascular permeability and leukocyte transmigration. Christian Weber and colleagues highlight the role of JAMs as gate keepers in inflammation and vascular pathology.

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Perspectives

Opinion

Signalling through TEC kinases regulates conventional versus innate CD8+ T-cell development

Leslie J. Berg

p479 | doi:10.1038/nri2091

A number of different non-conventional T-cell lineages with innate phenotypes have been identified. As outlined here, it seems likely that 'innate' T cells develop as a result of interactions with non-classical MHC molecules expressed by haematopoietic cells in the thymus.

Innovation

Integrating epitope data into the emerging web of biomedical knowledge resources

Bjoern Peters & Alessandro Sette

p485 | doi:10.1038/nri2092

In this age of information, keeping up with the literature can be overwhelming for any researcher. The generation of the IEBD – the first epitope-related database that makes complex and context-dependent information on immune epitopes readily accessible and searchable – may help

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