Springer Seminars in Immunopathology

, Volume 28, Issue 1, pp 3–16

Regulatory T cells in experimental autoimmune disease


DOI: 10.1007/s00281-006-0021-8

Cite this article as:
Suri-Payer, E. & Fritzsching, B. Springer Semin Immun (2006) 28: 3. doi:10.1007/s00281-006-0021-8


During the past 10 years, CD4+CD25+Foxp3+ regulatory T cells (Treg) have been extensively studied for their function in autoimmune disease. This review summarizes the evidence for a role of Treg in suppression of innate and adaptive immune responses in experimental models of autoimmunity including arthritis, colitis, diabetes, autoimmune encephalomyelitis, lupus, gastritis, oophoritis, prostatitis, and thyroiditis. Antigen-specific activation of Treg, but antigen-independent suppressive function, emerges as a common paradigm derived from several disease models. Treg suppress conventional T cells (Tcon) by direct cell contact in vitro. However, downmodulation of dendritic cell function and secretion of inhibitory cytokines such as IL-10 and TGF-β might underlie Treg function in vivo. The final outcome of autoimmunity vs tolerance depends on the balance between stimulatory signals (Toll-like receptor engagement, costimulation, and antigen dose) and inhibitory signals from Treg. Whereas most experimental settings analyze the capacity of Treg to prevent onset of autoimmune disease, more recent efforts indicate successful treatment of ongoing disease. Thus, Treg are on the verge of moving from experimental animal models into clinical applications in humans.


Foxp3 Regulatory mechanism Antigen specificity Targets Cure 

Copyright information

© Springer-Verlag 2006

Authors and Affiliations

  1. 1.Department of NeonatologyUniversity of Heidelberg, Children’s HospitalHeidelbergGermany
  2. 2.Division of Immunogenetics, D030German Cancer Research CenterHeidelbergGermany

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