Format

Send to

Choose Destination
See comment in PubMed Commons below
Curr Opin Rheumatol. 2014 Mar;26(2):204-10. doi: 10.1097/BOR.0000000000000036.

T cell subsets and their role in the pathogenesis of rheumatic disease.

Author information

1
aUniversity of Arkansas, Little Rock, Arkansas bUniversity of Michigan, Ann Arbor, Michigan, USA.

Abstract

PURPOSE OF REVIEW:

T lymphocytes are critical to the pathogenesis of systemic rheumatic diseases. Understanding of the roles of T cells in disease has been enriched by the description of highly distinct effector subsets of CD4 T lymphocytes. The purpose of this review is to describe selected advances in the biology of T lymphocytes that are pertinent to the pathogenesis or treatment of rheumatic diseases.

RECENT FINDINGS:

Knowledge is expanding about not only pathogenic effector T cell subsets, such as the TH17 cells, but also of regulatory T cells (Treg), the functions of which are defective, but correctable, in several rheumatic diseases. Although the initial agent that demonstrated a role for T cells in rheumatoid arthritis was CTLA4-Ig (abatacept), use of this biologic is now expanding to other rheumatic diseases. Moreover, effects of other biologics are now understood to in part be mediated by effects on T cell subsets. Experimental model systems in rodents continue to be valuable testing grounds for future approaches to treatment of human disease. Meanwhile, the roles of effector T cell subsets are becoming clearer in conditions such as Sjogren's syndrome and scleroderma. Finally, rheumatic diseases, including rheumatoid arthritis and spondyloarthropathies, have been critical for identification of new innate-like T cell subsets.

SUMMARY:

Imbalances in the numbers and functions of specific T cell subsets are key pathogenic derangements in systemic rheumatic diseases, and these insights are leading to changes in clinical practice.

PMID:
24445478
DOI:
10.1097/BOR.0000000000000036
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wolters Kluwer
    Loading ...
    Support Center