Journal of Clinical and Cellular Immunology
Open Access
ISSN: 2155-9899
ISSN: 2155-9899
Charles J. Malemud
Foley Medical Building, 2061 Cornell Road, Cleveland, Ohio 44106-5076
Tanzania
Review Article
Apoptosis Resistance in Rheumatoid Arthritis Synovial Tissue
Author(s): Charles J. MalemudCharles J. Malemud
The pathogenesis of rheumatoid arthritis (RA) evolves from deregulated cellular and humoral immunity resulting in a chronic and systemic inflammatory response. Perpetuating the sustained inflammation in RA synovial joints requires the migration and retention of activated T-lymphocytes, B-lymphocytes, mast cells, neutrophils and antigen presenting cells. The synovial tissue becomes hyperplastic as a result of unrestrained synoviocyte proliferation and the resistance of synoviocytes, immune and inflammatory cells to apoptosis. Synoviocyte proliferation is mainly sustained by the elevated levels of pro-inflammatory cytokines in the RA synovial joint milieu. Thus, proinflammatory cytokines, including tumor necrosis factor-α, interleukin-(IL)-1β and IL-6, IL-17, interferon-γ, among others, predominantly activate the stress-activated protein kinase/mitogen-activated protein k.. View More»
DOI:
10.4172/2155-9899.S3-006