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A pathogenic role for T cell–derived IL-22BP in inflammatory bowel disease
- Source :
- Science. 354:358-362
- Publication Year :
- 2016
- Publisher :
- American Association for the Advancement of Science (AAAS), 2016.
-
Abstract
- Intestinal inflammation can impair mucosal healing, thereby establishing a vicious cycle leading to chronic inflammatory bowel disease (IBD). However, the signaling networks driving chronic inflammation remain unclear. Here we report that CD4+ T cells isolated from patients with IBD produce high levels of interleukin-22 binding protein (IL-22BP), the endogenous inhibitor of the tissue-protective cytokine IL-22. Using mouse models, we demonstrate that IBD development requires T cell–derived IL-22BP. Lastly, intestinal CD4+ T cells isolated from IBD patients responsive to treatment with antibodies against tumor necrosis factor–α (anti–TNF-α), the most effective known IBD therapy, exhibited reduced amounts of IL-22BP expression but still expressed IL-22. Our findings suggest that anti–TNF-α therapy may act at least in part by suppressing IL-22BP and point toward a more specific potential therapy for IBD.
- Subjects :
- CD4-Positive T-Lymphocytes
0301 basic medicine
medicine.medical_treatment
T cell
Inflammation
Endogeny
Inflammatory bowel disease
Antibodies
Mice
03 medical and health sciences
0302 clinical medicine
medicine
Animals
Humans
Intestinal Mucosa
Immunity, Mucosal
Multidisciplinary
biology
Tumor Necrosis Factor-alpha
business.industry
Binding protein
Receptors, Interleukin
Inflammatory Bowel Diseases
medicine.disease
digestive system diseases
3. Good health
Disease Models, Animal
030104 developmental biology
Cytokine
medicine.anatomical_structure
Immunology
biology.protein
Tumor necrosis factor alpha
Immunotherapy
medicine.symptom
Antibody
business
030215 immunology
Subjects
Details
- ISSN :
- 10959203 and 00368075
- Volume :
- 354
- Database :
- OpenAIRE
- Journal :
- Science
- Accession number :
- edsair.doi.dedup.....701bf72e0aa56f02a98d277c9338aa49