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DOI 10.1590/s0365-05962012000600005

Медицинская библиотека · Anais brasileiros de dermatologia · 2012

OX40+ T lymphocytes and IFN-γ are associated with American tegumentary leishmaniasis pathogenesis.

Domingos Patrícia Luciana Batista, Viana Agostinho Gonçalves, Fraga Carlos Alberto de Carvalho, Bonan Paulo Rogério Ferreti

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

BACKGROUND

Leishmaniases are zoonoses considered a public health problem, representing a complex group of diseases with a broad clinical spectrum and epidemiological diversity. Leishmaniasis is caused by several species of protozoa of the genus Leishmania. The evolution of the pathology and the resolution of the leishmaniasis are dependent mainly on the Leishmania species involved, although the cytokine profile plays an important role in the development of the immune response.

OBJECTIVES

The purpose of our study was to evaluate the immune response of patients affected by lesions of cutaneous leishmaniasis by immunostaining of the OX40, CD20, IFN-γ and IL-4 proteins.

METHODS

The tissue samples were collected from indolent skin ulcers confirmed as cutaneous leishmaniasis of 41 patients aged between six and 90 years. The lesions were submitted to OX40, CD20, INF-γ and IL-4 immunolabeling.

RESULTS

We observed a statistically significant higher expression of IFN-γ compared with IL-4 (p=0.009). Besides, OX40 had higher expression when compared with CD20 (p<0.001).

CONCLUSION

The present study indicates that the immune response in lesions of cutaneous leishmaniasis is associated with a healing process, which can be explained by the higher expression of IFN-γ when compared with IL4 protein levels.

Для цитирования: Domingos Patrícia Luciana Batista, Viana Agostinho Gonçalves, Fraga Carlos Alberto de Carvalho, Bonan Paulo Rogério Ferreti. OX40+ T lymphocytes and IFN-γ are associated with American tegumentary leishmaniasis pathogenesis.. Anais brasileiros de dermatologia. 2012. DOI: 10.1590/s0365-05962012000600005.

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