|Ryszard Rutkowski, Tadeusz Moniuszko|
T cell response is initiated by T-cell receptor (TCR) binding to antigen (I signal) but it also requires interactions between costimulatory molecules on antigen presenting cells and T lymphocyte surface (II signal). TCR/CDz complex stimulation, in the absence of co-stimulation, results in lymphocytes T anergy or apoptosis. The induction of costimulatory signal depends on interaction between CD80/CD86 and CD28/CTLA-4 molecules. CD80 and CD86 are expressed on monocytes/macrophages, dendritic cells, Langerhans cells, fibroblasts, eosinophils, thymocytes, lymphocytes T and B, bronchial and gastric epithelial cells and tumor cell lines.
There is no expression of CD80 or it is very low on resting APC, whereas CD86 are constitutively expressed on the surface of antigen presenting cells. When APC are stimulated, B7.2 expression is maximal after 6-8 hours, followed by B7.1 after about 24 to 48 hours. CD80 and CD86 expression is increased in autoimmune diabetes, contact dermatitis, sarcoidosis, colitis ulcerosa, Crohn's disease, atopic dermatitis, allergic rhinitis or bronchial asthma what proves their special role in pathomechanisms of inflammation. In animal models of experimental allergic encephalomyelitis, bronchial asthma, rheumatoid arthritis, systemic lupus erythematosus, psoriasis, thyreoiditis, neoplasmatic diseases or transplant rejection the treatment with anti-CD80 and/or CD86 can modulate their clinical course.
Alergia Astma Immunologia, 2001, 6(2), 87-94
keywords: CD80 (B7.1), CD86 (B7.2), kostymulacja, odczyn zapalny, choroby alergiczne, CD80 (B7.1), CD86 (B7.2), costimulation, inflammatory process, allergic disease
pages: from 87 to 94
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