Antirheumatoid drug has specific act on the T-cell is
(Abatacept) (514-Lippincott's pharmacology 4th)Abatacept is a costimulation -modulator that inhibits the activation of T-cells (629- Katzung 11th)* ABATACEPT - T. lymphocytes needs two interactions to become activated (1) The antigen- presenting cells (i.e. Macrophages or B cells) must interact with the receptor on the T cell (2) The CD80/CD86 protein on the antigen presenting cell must interact with the C.D 28 protein on the T.cell. the result activated T. lymphocytes responsible for the release of pro inflammatory cytokines and maintenance of inflammation in RAAbatacept is a soluble recombinant fusion protein made up of the extracellular domain of human CTLAA and it competes with CD28 for binding on CD80/ CD86 protein thereby preventing full T-cell activationUses- in moderate to severe RA who had an inadquate respose to DMARDs such as mothotrexate or TNa inhibitors* RITUXIMAB - B- lymphocyte are derived from the bone marrow and are necessary for efficient immune response however in RA, B-cell can perpetuate the inflammatory process in the synovium by1. activating T-lymphocytes 2. producing autoantibodies such as anti CCP (anti-cyclic citrullinated peptide antibody) and rheumatoid factor and3. producing pro-inflammatory cytokines such as TNF a and IL-1Rituximab is a genetically engineered chimeric murine (human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B.lymphocytes resulting in B.cell depletionRituximab has been shown to reduce joint erosion and joint space narrowing in these patientsRituximab is a chimeric monoclonal antibody that targets CD20-B lymphocytes (632-Katzung 11th)Etanercept. Infliximab - TNFa- inhibitorsLEFLUMQMIDE - Immunomodulatory agent* Leflunomide is rapidly converted in tfye body to an active metabolite which inhibits dihydroarotate dehydrogenase and pyrimidine synthesis in actively dividing cells. Antibody production by B. cell may be depressed (204-KDP 6th)* Teratogenic in experimental animals and therefore is contraindicated in pregnancy and in women of child bearing potentialLeflunomide inhibits - T-cell proliferatin and production of autoantibodies by B-cellsImportant Points* COX-2 inhibitors show similar analgesic and anti inflammatory activity compared to traditional NSAIDs. They do not affect platelets - Like NSAIDs. COX-2 inhibitors may cause the development of ARF due to renal vasoconstriction. COX-2 inhibitors have the potential for increasing the risk of myocardial infarction*** DMARDs - the effects may take 6 weeks to 6 months to become evident although some biologies are effective within 2 weeks; generally they are slow-acting compared with NSAIDS
Etanercept
Infliximab
Rituximab
Abatacept
Immunomodulator