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Clinical and genetic heterogeneity of rheumatoid arthritis

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Klimiuk P. A., Weyand C. M., Sierakowski S., Goronzy J. J.

Postępy Higieny i Medycyny Doświadczalnej

2000

vol. 54

issue 6

845-853

The diagnostic category of rheumatoid arthritis, a syndrome of chronic inflammatory disease of the synovial membrane and of extraarticular tissues, covers a broad spectrum of clinical phenotypes. Here we propose that distinct combinations of disease risk genes produce heterogeneity of rheumatoid disease. Recognition of this genetic and clinical heterogeneity has immediate implications as it provides the opportunity to develop selective therapies for the different variants of disease.

The role of T cells in rheumatoid arthritis

100%

Weyand C. M., Bryl E., Goronzy J. J.

Archivum Immunologiae et Therapiae Experimentalis

2000

vol. 48

issue 5

429-435

In rheumatoid arthritis (RA), T cells infiltrate into the synovial membrane where they initiate and maintain activation of macrophages and synovial fibroblasts, transforming them into tissue-destructive effector cells. The diversity of the disease process and the formation of complex lymphoid microstructures indicates that multiple T cell activation pathways are involved. This model is supported by the association of distinct disease patterns with different variants and combinations of HLA class II molecules. T cell pathology in RA, however, is not limited to the joint. Affected patients have major abnormalities in the T cell pool with a marked contraction in T cell receptor diversity and an outgrowth of large clonal populations. Clonally expanded CD4+ T cells lose expression of the CD28 molecule and gain expression of perforin and granzyme. Consequently, the functional profile of expanded CD4+CD28null T cells is fundamentally changed and is shifted towards tissue-injurious capabilities. CD4+CD28null T cells are particularly important in patients with extraarticular manifestations of RA, where they may have a direct role in vascular injury. Understanding the mechanisms underlying the loss of T cell diversity and the emergence of pro-inflammatory CD4+CD28- T cell clonotypes may have implications for other autoimmune syndromes.

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1 Archivum Immunologiae et Therapiae Experimentalis

1 Postępy Higieny i Medycyny Doświadczalnej

2 2000

2 Goronzy J. J.

2 Weyand C. M.

1 Bryl E.

1 Klimiuk P. A.

1 Sierakowski S.

Search results

Clinical and genetic heterogeneity of rheumatoid arthritis

The role of T cells in rheumatoid arthritis