Biomaterial Database

T-cell-dependent pathways in rheumatoid arthritis. 1997

G S Panayi

Rheumatology Unit, United Medical School, Guy's Hospital, London, UK.

Two theories, not necessarily mutually exclusive, attempt to explain the pathogenesis of rheumatoid arthritis. The mesenchymal hypothesis proposes that, after an initial event triggered by T cells, synovitis is maintained by autocrine and paracrine pathways involving macrophages and synovial fibroblasts. The T-cell hypothesis proposes that T cells are continuously involved in the pathogenesis of rheumatoid arthritis from its initiation phase through to the chronic stage. This paper reviews recent work in this area and concludes that there is substantial evidence in support of the T-cell hypothesis.

UI	MeSH Term	Description	Entries
D007596	Joints	Also known as articulations, these are points of connection between the ends of certain separate bones, or where the borders of other bones are juxtaposed.	Joint
D008954	Models, Biological	Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.	Biological Model,Biological Models,Model, Biological,Models, Biologic,Biologic Model,Biologic Models,Model, Biologic
D006801	Humans	Members of the species Homo sapiens.	Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D001172	Arthritis, Rheumatoid	A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.	Rheumatoid Arthritis
D001324	Autoantigens	Endogenous tissue constituents with the ability to interact with AUTOANTIBODIES and cause an immune response.	Autoantigen,Autologous Antigen,Autologous Antigens,Self-Antigen,Self-Antigens,Antigen, Autologous,Antigens, Autologous,Self Antigen,Self Antigens
D013585	Synovitis	Inflammation of the SYNOVIAL MEMBRANE.	Plica Syndrome,Synovial Plica Syndrome,Synovial Hypertrophy,Synovial Thickening,Hypertrophies, Synovial,Hypertrophy, Synovial,Plica Syndrome, Synovial,Synovial Hypertrophies,Synovial Thickenings,Synovitides,Thickening, Synovial,Thickenings, Synovial
D013601	T-Lymphocytes	Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.	T Cell,T Lymphocyte,T-Cells,Thymus-Dependent Lymphocytes,Cell, T,Cells, T,Lymphocyte, T,Lymphocyte, Thymus-Dependent,Lymphocytes, T,Lymphocytes, Thymus-Dependent,T Cells,T Lymphocytes,T-Cell,T-Lymphocyte,Thymus Dependent Lymphocytes,Thymus-Dependent Lymphocyte
D014158	Transcription, Genetic	The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.	Genetic Transcription
D016207	Cytokines	Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.	Cytokine