Featured
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Article |
Phosphorylation and linear ubiquitin direct A20 inhibition of inflammation
The authors define molecular mechanisms by which distinct domains of the ubiquitin editing enzyme A20 contribute to the regulation of inflammation and cell death.
- Ingrid E. Wertz
- , Kim Newton
- & Vishva M. Dixit
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Article |
Immune homeostasis enforced by co-localized effector and regulatory T cells
Autoantigen-presenting dendritic cells are shown to interact with both effector and regulatory T cells, and effector-produced IL-2 activates the transcription factor STAT5 in regulatory T cells, which in turn upregulates suppressive molecules and prevents autoimmunity.
- Zhiduo Liu
- , Michael Y. Gerner
- & Ronald N. Germain
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Letter |
T-cell exhaustion, co-stimulation and clinical outcome in autoimmunity and infection
CD8 T-cell exhaustion, although a negative prognostic indicator during persistent infections, is shown to be associated with a good outcome in autoimmune and inflammatory diseases.
- Eoin F. McKinney
- , James C. Lee
- & Kenneth G. C. Smith
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Letter |
BACH2 represses effector programs to stabilize Treg-mediated immune homeostasis
Diverse autoimmune and allergic diseases are associated with polymorphisms in a locus encoding the transcription factor BACH2; here, BACH2 is shown to be a broad regulator of immune activation that stabilizes the differentiation of Treg cells by repressing commitment of CD4+ T cells to alternate cell fates.
- Rahul Roychoudhuri
- , Kiyoshi Hirahara
- & Nicholas P. Restifo
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Letter |
Negligible impact of rare autoimmune-locus coding-region variants on missing heritability
A search for variants in coding exons of 25 genome-wide association study risk genes in a large cohort of autoimmune patients finds that rare coding-region variants at known loci have a negligible role in common autoimmune disease susceptibility, arguing against the previously proposed rare-variant synthetic genome-wide association hypothesis.
- Karen A. Hunt
- , Vanisha Mistry
- & David A. van Heel
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Letter |
Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1
Transcriptional profiling of developing TH17 cells identifies serum glucocorticoid kinase 1 (SGK1) as an essential node downstream of IL-23 signalling, and transcriptional analysis shows that a modest increase in salt concentration induces SGK1 expression, promotes IL-23 receptor expression and enhances TH17 cell differentiation, accelerating the development of autoimmunity.
- Chuan Wu
- , Nir Yosef
- & Vijay K. Kuchroo
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Letter |
Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells
Increased salt concentrations are shown to induce murine and human TH17 cells by a mechanism that depends on activation of p38/MAPK, NFAT5 and SGK1; mice kept on a high-salt diet develop a more severe experimental autoimmune encephalomyelitis due to increased induction of TH17 cells.
- Markus Kleinewietfeld
- , Arndt Manzel
- & David A. Hafler
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Comment |
The worm returns
Joel V. Weinstock explains why several clinical trials are deliberately infecting people with helminths to treat autoimmune diseases.
- Joel V. Weinstock
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Letter |
Regulatory B cells control T-cell autoimmunity through IL-21-dependent cognate interactions
IL-21- and CD40-dependent cognate interactions with T cells are identified as key drivers for the generation of IL-10-producing regulatory B cells, which can protect against autoimmune disease.
- Ayumi Yoshizaki
- , Tomomitsu Miyagaki
- & Thomas F. Tedder
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Outlook |
Perspective: Clues, not conclusions
Scientists have some way to go before they can prove that COPD should be treated as an autoimmune disease, says Steven R. Duncan.
- Steven R. Duncan
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Outlook |
Nutrition: The vitamin D complex
Many COPD patients are deficient in vitamin D, a condition that can lead to bone problems as well as difficulty breathing. Can dietary supplements be of help?
- Thea Singer
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News & Views |
Licensed in the lungs
In multiple sclerosis, the body's own immune cells attack the brain and spinal cord. But how they get there from peripheral tissues has been a mystery. Surprisingly, the lungs might be a key transit point. See Letter p.675
- Richard M. Ransohoff
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Letter |
Endogenous antigen tunes the responsiveness of naive B cells but not T cells
Mature B cells encounter antigens during development that induce anergy or functional unresponsiveness; this large reservoir of dormant autoreactive B cells may serve as a pool of extended antibody specificity for purposes of protective immunity, as well as the source of pathogenic autoantibodies that characterize rheumatic diseases such as systemic lupus erythematosus.
- Julie Zikherman
- , Ramya Parameswaran
- & Arthur Weiss
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Letter |
Response to self antigen imprints regulatory memory in tissues
Thymus-derived regulatory T cells are activated by recognition of peripheral self antigen, persist in the target tissue on cessation of antigen exposure, and respond to re-exposure to self antigen with enhanced functional activity.
- Michael D. Rosenblum
- , Iris K. Gratz
- & Abul K. Abbas
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Research Highlights |
Taming psoriasis with vitamin D
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Research Highlights |
Immunology: Killer cells help
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Letter |
Functionally defective germline variants of sialic acid acetylesterase in autoimmunity
Sialic acid acetylesterase (SIAE) is an enzyme that is involved in B-cell activation and is required to maintain immunological tolerance in mice. It is shown here that rare, inherited and functionally defective SIAE variants are associated with a variety of autoimmune diseases in humans. The study provides one of the first examples of the importance of rare genetic variants in complex diseases, such as those involving autoimmunity.
- Ira Surolia
- , Stephan P. Pirnie
- & Shiv Pillai