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Nat Med. 2007 Feb;13(2):139-45.

A brief history of T(H)17, the first major revision in the T(H)1/T(H)2 hypothesis of T cell-mediated tissue damage.

Author information

  • Interdepartmental Program in Immunology, Department of Neurology and Neurological Sciences, Beckman Center for Molecular Medicine, Stanford University, Stanford, California 94305, USA. steinman@stanford.edu

Erratum in

  • Nat Med. 2007 Mar;13(3):385.

Abstract

For over 35 years, immunologists have divided T-helper (T(H)) cells into functional subsets. T-helper type 1 (T(H)1) cells-long thought to mediate tissue damage-might be involved in the initiation of damage, but they do not sustain or play a decisive role in many commonly studied models of autoimmunity, allergy and microbial immunity. A major role for the cytokine interleukin-17 (IL-17) has now been described in various models of immune-mediated tissue injury, including organ-specific autoimmunity in the brain, heart, synovium and intestines, allergic disorders of the lung and skin, and microbial infections of the intestines and the nervous system. A pathway named T(H)17 is now credited for causing and sustaining tissue damage in these diverse situations. The T(H)1 pathway antagonizes the T(H)17 pathway in an intricate fashion. The evolution of our understanding of the T(H)17 pathway illuminates a shift in immunologists' perspectives regarding the basis of tissue damage, where for over 20 years the role of T(H)1 cells was considered paramount.

PMID:
17290272
[PubMed - indexed for MEDLINE]
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