Mecanismos celulares y bioquímicos involucrados en la fisiopatogenia de la púrpura trombocitopénica autoinmune / Cellular and biochemical mechanisms involved in physiopathogenesis of autoimmune thrombocytopenic purpura
Gac. méd. Méx
;
138(5): 461-472, sep.-oct. 2002.
Artículo
en Español
| LILACS
| ID: lil-333690
RESUMO
Autoimmune thrombocytopenic purpura (ATP) is a bleeding disorder caused by excessive destruction of antibody-coated platelets. It is known that platelet destruction takes place in macrophages of reticulo-endothelial system, but immunological mechanisms involved in such destruction are unknown. The objective of this article is to review the literature concerning pathogenesis of ATP to have controlled experimental conditions some animal laboratory models have been used. The (NZW X BXSB) F1 mice have been studied as autoimmune disease model and Harrington mouse as an immune purpura model. Studies in humans suggest that there are some differences in pathogenesis of acute or chronic ATP, particularly in reactive T cells. For example, in chronic form there are high levels of The (CD4+) activity concomitant with low levels of T suppressor (CD8+) activity, while in acute form there is no dominance of any particular T cell activity or CD4+ is even decreased. Mitogen lymphocyte proliferation is increased in chronic ATP but decreased in acute form.
Texto completo:
Disponible
Índice:
LILACS (Américas)
Asunto principal:
Púrpura Trombocitopénica Idiopática
Límite:
Animales
/
Humanos
Idioma:
Español
Revista:
Gac. méd. Méx
Asunto de la revista:
Medicina
Año:
2002
Tipo del documento:
Artículo
País de afiliación:
México
Institución/País de afiliación:
Centro Nacional de la Transfusión Sanguínea/MX
/
UNAM/MX
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