Journal
EXPERT REVIEW OF CLINICAL IMMUNOLOGY
Volume 12, Issue 4, Pages 417-425Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1586/1744666X.2016.1133295
Keywords
endothelial cells; CD80/CD86; costimulatory molecules; abatacept; T lymphocytes; CTLA-4-Ig; Rheumatoid arthritis; B lymphocytes; macrophages; osteoclasts
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Funding
- Bristol-Myers Squibb
- Actelion
- Horizon
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Rheumatoid arthritis (RA) is characterized by chronic joint inflammation as well as by extra-articular involvement. The immunopathology of RA is polygenic and involves different cell populations. Patients with an inadequate response to non-biologic disease- modifying antirheumatic drugs (DMARDs) should integrate their therapy with biologic DMARDs. Biologic DMARDs can target several inflammatory cytokines, or CD20+ B cells, or can modulate T-cell co-stimulation and activation. The cytotoxic T lymphocyte-associated antigen 4 immunoglobulin fusion protein (CTLA-4-Ig: abatacept) that selectively modulates the CD28:CD80/86 co-stimulation signal appears a biologic DMARD interacting with T cells but also with other cell populations involved in RA pathophysiology. Activated B lymphocytes, macrophages, osteoclasts and endothelial cells express the costimulatory molecules (CD80/86) and are downregulated by CTLA-4 blockade. The relatively low frequency and severity of safety issues related to CTLA-4-Ig treatment seems further to confirm the targeted downregulatory action exerted by the fusion protein, which is mainly focussed on activated immune/inflammatory cells.
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