Sharp pain in the head
According to the "T cell centric" theory of RA, activation of CD4+ cells would trigger and maintain the inflammatory process in the rheumatoid joint (slide). sharp pain in the head Left rib cage pain. Interestingly, although large numbers of CD4+ cells persist in the synovium throughout the disease course, they appear to be inactive in the chronic phase of the disease. For example, expression of surface antigens (such as IL2 and transferrin receptors), and secretion of specific cytokines (e. g. sharp pain in the head Rheumatic arthritis. , IL2, IL4 and g-IFN), that are associated with an activated T cell state are very low (slide). Slide RA. patho. sharp pain in the head Chronic pelvic pain. propogation. syn. 2 In contrast, cytokines known to be produced primarily by "effector" cells (macrophages) and connective tissue cells (fibroblasts) are expressed in abundance in RA synovium and synovial fluid, as measured by ELISA or mRNA studies. These cytokines include IL1, IL6, TNF, IL8 and GM-CSF. According to the alternative theory (the "macrophage-fibroblast theory") of RA, these two cell types appear to be largely responsible for creating a self-perpetuating state of chronic inflammation in which T cell participation may no longer be critical. In this scenario, the activated macrophage continuously secretes IL-1 and TNF which maintain the synovial fibroblast in an activated state (slide). The fibroblast, in turn, secretes large amounts of: a) cytokines - IL6, IL8 and GM-CSF; b) prostaglandins; and c) protease enzymes. GM-CSF feeds back to promote the maturation of newly recruited monocytes to macrophages. IL-8 and IL-6 contribute to the recruitment and/or activation of yet other cell populations, while the prostaglandins and proteases act directly to erode and destroy nearby connective tissues such as bone and cartilage. This process is elaborated further below. (top of section)Inflammatory mediators in RA In addition to activating synovial cells to secrete inflammatory mediators (slide), IL-1 and TNF also have profound systemic effects (slide). For example, increased systemic levels of TNF and IL-1 are associated with fever, muscle wasting and decreased appetite. Some of these effects are mediated via the induction of IL-6 synthesis. Mature plasma cells that secrete rheumatoid factor are another prominent cellular component of rheumatoid synovium. The stimulus for maturation of B cells to immunoglobulin-secreting plasma cells has classically been ascribed to CD4+ T cells; however, as already noted, CD4+ T cells are not activated in the chronic phase of rheumatoid arthritis. IL-6, however, is a potent stimulus for maturation of B cells to plasma cells. Thus, synovial fibroblasts are likely providing the "T cell independent" stimulus for continuous plasma cell activation and rheumatoid factor production. IL-6 also suppresses albumin synthesis by the liver and stimulates acute phase protein synthesis (slide).
Sharp pain in the head
Pain || Chest pains || Arthritis in horses || Osteoarthritis cures