Abstract
T helper (TH) cells can assume different phenotypes characterized by the secretion of distinct effector molecules. Interferon-gamma producing TH1 and IL-4 producing TH2 cells have long been recognized as important mediators of host defense, whereas regulatory T cells are known to suppress T cell responses. Recently, TH17 cells were characterized as a novel CD4(+) subset that preferentially produces IL-17, IL-17F, and IL-22 as the signature cytokines. TH17 cells appear to play a critical role in sustaining the inflammatory response and their presence is closely associated with autoimmune disease, which makes them an attractive therapeutic target. In this review, we focus on the mechanisms that regulate the differentiation of naive T cells into TH17 cells and on TH17 effector cytokines, as they represent opportunities for therapeutic intervention.
MeSH terms
-
Animals
-
CD4-Positive T-Lymphocytes / immunology
-
CD4-Positive T-Lymphocytes / metabolism
-
Cytokines / immunology
-
Cytokines / metabolism*
-
Humans
-
Inflammation / therapy
-
Interferon-gamma / immunology
-
Interferon-gamma / metabolism
-
Interleukin-17 / immunology
-
Interleukin-17 / metabolism*
-
Interleukin-23 / immunology
-
Interleukin-23 / metabolism
-
Receptors, Cytokine / immunology
-
Receptors, Cytokine / metabolism
-
STAT3 Transcription Factor / immunology
-
STAT3 Transcription Factor / metabolism
-
T-Lymphocyte Subsets / immunology
-
T-Lymphocyte Subsets / metabolism
-
T-Lymphocytes, Helper-Inducer / immunology*
-
T-Lymphocytes, Helper-Inducer / metabolism*
-
T-Lymphocytes, Regulatory / immunology
-
T-Lymphocytes, Regulatory / metabolism
-
Transforming Growth Factor beta / immunology
-
Transforming Growth Factor beta / metabolism
Substances
-
Cytokines
-
Interleukin-17
-
Interleukin-23
-
Receptors, Cytokine
-
STAT3 Transcription Factor
-
Transforming Growth Factor beta
-
Interferon-gamma