IL-17 and the Th17 lineage in systemic lupus erythematosus.
Curr Opin Rheumatol
; 20(5): 519-25, 2008 Sep.
Article
in En
| MEDLINE
| ID: mdl-18698171
ABSTRACT
PURPOSE OF REVIEW Systemic lupus erythematosus etiology includes both genetic and environmental factors. Evidence suggests that many genetic loci in humans and mouse models contribute to the occurrence and clinical presentation of lupus. This large array of different genes affects many aspects of immune cell function, including the activation and functional differentiation of B cells, T cells, dendritic cells and other immune cells. In particular, the T-cell components that contribute to systemic lupus erythematosus pathogenesis are incompletely defined. RECENT FINDINGS:
A major paradigm shift in understanding how CD4+ T cells contribute to autoimmunity recently occurred with the discovery of a new T-cell population that produces the cytokine IL-17 (IL-17A), termed 'Th17'. Although Th17 cells contribute to autoimmune disease in rheumatoid arthritis and Crohn's disease, their role in systemic lupus erythematosus is far less clear.SUMMARY:
In this review, we focus on an emerging role for the cytokine IL-17 and the cells that produce it in contributing to lupus in particular based on recent findings in animal models.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
T-Lymphocytes
/
Autoimmunity
/
Cell Lineage
/
Interleukin-17
/
Lupus Erythematosus, Systemic
Type of study:
Prognostic_studies
Limits:
Animals
/
Humans
Language:
En
Journal:
Curr Opin Rheumatol
Journal subject:
REUMATOLOGIA
Year:
2008
Document type:
Article
Affiliation country:
United States
Publication country:
EEUU
/
ESTADOS UNIDOS
/
ESTADOS UNIDOS DA AMERICA
/
EUA
/
UNITED STATES
/
UNITED STATES OF AMERICA
/
US
/
USA