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Published at www.nejm.org November 4, 2009 (10.1056/NEJMe0909225)

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In this issue of the Journal, Glocker et al.¹ provide the first substantial support for a functional role for the immunosuppressive cytokine interleukin-10 in the pathogenesis of inflammatory bowel disease in humans. By performing genetic-linkage and candidate-gene analysis of two unrelated consanguineous families with children who have a severe, progressive, poorly treatable form of Crohn's disease that occurs in the first year of life, the investigators identified homozygous, recessive loss-of-function mutations in the interleukin-10 receptor genes, IL10RA and IL10RB, which most likely contributed to the patients' disease. A third distinct mutation in IL10RA was found in an unrelated patient. . . . [Full Text of this Article]

Source Information

From the Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD.

This article (10.1056/NEJMe0909225) was published on November 4, 2009, at NEJM.org.

This article has been cited by other articles:

• (2009). Interleukin-10 Receptor Mutations and Severe Inflammatory Bowel Disease. JWatch Gastroenterology 2009: 2-2 [Full Text]