Rheumatoid arthritis factor

WPG-PA carrying IgG has been also applied to the isolation of the rheumatoid factor from sera of rheumatoid arthritis patients [128]. Some other applications of WPG-PA are the following. 

HBV, hepatitis B HCV, hepatitis C IAP, inhibitor of apoptosis protein DBM, IAP binding motifs INCA, inhibitory CARD NASH, non-alcoholic steatohepatitis PCD, programmed cell death PCI, pan-caspase inhibitor OA, osteoarthritis RA, rheumatoid arthritis Smac, second mitochondria-derived activator of caspases TRAIL, tumor necrosis factor-related apoptosis-inducing ligand. 

Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown aetiology with some autoimmune features. Current thinking favours the hypothesis that interplay between genetic factors, sex hormones, and possibly an infectious agent or another immune activating agent initiates an autoimmune pathogenic mechanism that culminates in a disease with inflammatory and destructive features. 

It is an autoantibody whose autoantigen is the Fc portion of IgG. Rheumatoid factors may be of any immunoglobulin isotype but it is IgM rheumatoid factor that is commonly measured in rheumatoid arthritis. Classification criteria for rheumatoid arthritis include only one serological test, namely rheumatoid factor. However, it is not diagnostic test rather it may be confirmatory when a number of other clinical features are present. 

Human tumor necrosis factor (TNF) (Fig. 1) is a hormone-like proinflammatory peptide belonging to the group of cytokines. It is mainly produced by cells of the immune system in response to infection, inflammation, or cell damage. Disregulated TNF is an important factor in many pathological situations, like sqDsis, rheumatoid arthritis, inflammatory bowel disease (Crohn s disease), and Cachexia. The cytotoxic activity of TNF is of interest in development of new antitumoral strategies. 

Reye s Syndrome RGS Protein Rhabdomyolysis Rheumatoid Arthritis Rheumatoid Factor Rho... 

Identify risk factors for developing rheumatoid arthritis. 

Scott DL. Prognostic factors in early rheumatoid arthritis. Rheumatology (Oxford) 2000 39(Suppl l) 24-29. 

Nanki T, Hayashida K, El-Gabalawy HS, et al. Stromal cell-derived factor-l-CXC chemokine receptor 4 interactions play a central role in CD4+ T cell accumulation in rheumatoid arthritis synovium. J Immunol 2000 165(11) 6590-6598. 

Kanbe K, Takemura T, Takeuchi K, Chen Q, Takagishi K, Inoue K. Synovectomy reduces stromal-cell-derived factor-1 (SDF-1) which is involved in the destruction of cartilage in osteoarthritis and rheumatoid arthritis. J Bone Joint Surg Br 2004 86(2) 296-300. 

Reactive nitrogen species are another factor of free radical damage in rheumatoid arthritis, although their role is less studied than that of oxygen radicals. Stichtenoth and Frolich [242] pointed out that the inhibition of nitric oxide synthesis had beneficial effects in humans. Mazzetti et al. [243] found that IL-1(3 stimulated NO production in RA chondrocytes. We demonstrated that NO synthase of RA neutrophils generated the enhanced amount of peroxynitrite [234]. Nitric oxide and oxygen radicals are also important inducers of death of human osteoarthritic synoviocytes [244]. 

Feldmann, M., Elliott, M.J., Woody, J.N., Maini, R.N. 1997. Anti-tumor necrosis factor alpha therapy of rheumatoid arthritis. Advances in Immunology 64, 283-350. 

Anaemia often becomes a characteristic feature of several chronic diseases, such as rheumatoid arthritis. In most instances this can be linked to lower than normal endogenous serum EPO levels (although in some cases a deficiency of iron or folic acid can also represent a contributory factor). Several small clinical trials have confirmed that administration of EPO increases haematocrit and serum haemoglobin levels in patients suffering from rheumatoid arthritis. A satisfactory response in some patients, however, required a high-dose therapy that could render this therapeutic approach unattractive from a cost benefit perspective. 

Secondary OA is associated with a known cause such as rheumatoid arthritis or another inflammatory arthritis, trauma, metabolic or endocrine disorders, and congenital factors. 

Major risk factors include current smoker, low body weight (<127 lb in postmenopausal women), history of osteoporotic fracture in a first-degree relative, and personal history of low-trauma fracture as an adult. Other independent risk factors include age, high bone turnover, low body mass index (<19 kg/m2), rheumatoid arthritis, and glucocorticoid use. Decision tools may help identify individuals who should undergo BMD testing, such as the Osteoporosis Risk Assessment Instrument and the Simple Calculated Osteoporosis Risk Estimation. 

Interleukin 1 (IL-1) is produced mainly by activated monocytes-macropha-ges, and its principal action is to stimulate thymocytes. A pleiotropic cytokine, IL-1 induces the expression of a large diversity of cytokines such as IL-6, leukaemia inhibitory factor (LIF), and other proinflammatory molecules (Di-marello 1994). IL-1 and TNF-a carry out as part of their function increasing the expression of NF-/cB and JNK (c-Jun N-terminal kinase). The importance of IL-1 in OCS is demonstrated because the IL-1-receptor-deficient mouse is resistant to ovariectomy (OVX)-induced bone loss (Lorenzo et al. 1998). The importance in pathological bone loss is also illustrated by the fact that treatment with IL-1 receptor antagonist slows down bone erosion for patients affected with rheumatoid arthritis (Kwan et al. 2004). IL-1 increases osteoclast differentiation rather than mature osteoclast activity, and infusion of IL-1 into mice induces hypercalcemia and bone resorption. Finally, IL-1 and TNF-a... 

Kang, C. P. et al., The influence of a polymorphism at position -857 of the tumour necrosis factor alpha gene on clinical response to etanercept therapy in rheumatoid arthritis, Rheumatology (Oxford), 44, 547, 2005. 

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