The involvement of autoimmunity against retinal antigens in determining disease severity in toxoplasmosis

The involvement of autoimmunity against retinal antigens in determining disease severity in toxoplasmosis

Autor Vallochi, A. L. Google Scholar
Rios, L. D. Google Scholar
Nakamura, M. V. Google Scholar
Silveira, C. Google Scholar
Muccioli, C. Google Scholar
Martins, M. C. Google Scholar
Belfort, R. Google Scholar
Rizzo, L. V. Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Fundacao Zerbini
Resumo Purpose: Ocular lesions are frequent in various individuals infected with Toxoplasma gondii. Disease intensity in ocular toxoplasmosis varies greatly between patients. Autoimmunity has been suggested as a possible component to retinal destruction.Methods: Immunologic parameters in the response to retina antigens were evaluated in infected persons with and without ocular lesions and in non-infected controls. Subjects were divided into groups on the basis of titers of serum antibodies to T. gondii, presence and severity of ocular lesions, and clinical history.Results: Peripheral blood mononuclear cells from patients with mild disease responded to one or more retinal antigens with a significantly higher frequency than patients without disease or with severe disease. Interestingly, the cytokines produced by the proliferating mononuclear cells did not follow any specific patterns, except for the fact that IL-4 and IL-5 were seldom detected.Conclusions: Our results suggest that although the presence of an immune response towards autoantigens is not protective against the development of ocular lesions by the T. gondii, it may protect against the development of severe disease. (c) 2004 Elsevier B.V. All rights reserved.
Palavra-chave autoimmunity
IRBP
ocular toxoplasmosis
retinal antigens
S-Ag
Toxoplasma gondii
Idioma Inglês
Data de publicação 2005-02-01
Publicado em Journal of Autoimmunity. London: Academic Press Ltd- Elsevier B.V., v. 24, n. 1, p. 25-32, 2005.
ISSN 0896-8411 (Sherpa/Romeo, fator de impacto)
Publicador Elsevier B.V.
Extensão 25-32
Fonte http://dx.doi.org/10.1016/j.jaut.2004.11.003
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000227592600003
Endereço permanente http://repositorio.unifesp.br/handle/11600/28139

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