Abstract
T cells, in particular CD4+ T cells, have been implicated in mediating many aspects of autoimmune inflammation. However, current evidence suggests that the role played by CD4+ T cells in the development of rheumatoid inflammation exceeds that of activated proinflammatory T-helper (Th)1 effector cells that drive the chronic autoimmune response. Subsets of CD4+ T cells with regulatory capacity, such as CD25+ regulatory T (Treg) cells and Th2 cells, have been identified, and recent observations suggest that in rheumatoid arthritis the function of these regulatory T cells is severely impaired. Thus, in rheumatoid arthritis, defective regulatory mechanisms might allow the breakdown of peripheral tolerance, after which the detrimental Th1-driven immune response evolves and proceeds to chronic inflammation. Here, we review the functional abnormalities and the contribution of different T cell subsets to rheumatoid inflammation.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Abatacept
-
Animals
-
Anti-Inflammatory Agents / therapeutic use
-
Antibodies, Monoclonal / therapeutic use
-
Arthritis, Rheumatoid / immunology
-
Arthritis, Rheumatoid / therapy
-
Autoimmune Diseases / immunology*
-
Autoimmune Diseases / therapy
-
Bystander Effect
-
CD4-Positive T-Lymphocytes / immunology
-
CD8-Positive T-Lymphocytes / immunology
-
Humans
-
Immunoconjugates / therapeutic use
-
Immunologic Factors / therapeutic use
-
Inflammation / immunology*
-
Inflammation / therapy
-
Lymphokines / physiology
-
Mice
-
Mice, Transgenic
-
Receptors, Antigen, T-Cell, alpha-beta / analysis
-
T-Lymphocyte Subsets / immunology
-
T-Lymphocytes / immunology*
-
Th1 Cells / immunology
-
Tumor Necrosis Factor-alpha / antagonists & inhibitors
Substances
-
Anti-Inflammatory Agents
-
Antibodies, Monoclonal
-
Immunoconjugates
-
Immunologic Factors
-
Lymphokines
-
Receptors, Antigen, T-Cell, alpha-beta
-
Tumor Necrosis Factor-alpha
-
Abatacept