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TLR 2 and TLR 4 in Cutaneous Leishmaniasis Caused by Leishmania major
Author(s) -
Tolouei S.,
Hejazi S. H.,
Ghaedi K.,
Khamesipour A.,
Hasheminia S. J.
Publication year - 2013
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12105
Subject(s) - lesion , innate immune system , flow cytometry , cutaneous leishmaniasis , leishmania major , immunology , immune system , wound healing , gene expression , biology , medicine , inflammation , leishmania , leishmaniasis , pathology , gene , world wide web , computer science , parasite hosting , biochemistry
Cutaneous leishmaniasis ( CL ) is a self‐healing skin disease which rarely for unknown reason(s) the lesion develops to a non‐healing form. It seems that the initial contact of L eishmania parasites with the host innate immune system is an important step in the outcome of the disease. Recent studies suggested that toll‐like receptors ( TLR s) play a role in L eishmania recognition. In this study, the level of TLR 2 and TLR 4 was checked in patients with healing form of lesion and compared with that of patients with non‐healing form of lesion caused by L eishmania major . Gene expression of TLR 2 and TLR 4 in peripheral blood‐derived macrophages, before and after stimulation with live L . major promastigotes, was evaluated using quantitative real‐time reverse transcription PCR and flow cytometry. The results showed that the mean relative gene expression and difference membrane expression of TLR 2 in macrophages of patients with healing form of lesion were significantly higher than patients with non‐healing form of lesion ( P < 0.0001 and P = 0.0034), respectively, and the mean relative gene expression and difference in protein expression of TLR 4 in macrophages of patients with healing form of lesion were significantly higher than that of patients with non‐healing form of lesion ( P = 0.021 and P = 0.002), respectively. The data suggested a possible role for TLR 2 and TLR 4 in the outcome of CL lesion. Further studies are needed to understand more about the detail role of the immune factors in leishmaniasis.