Author:
T. Silveira Fernando,B. Campos Marliane,F. Müller Silvia,K. Ramos Patrícia,V. Lima Luciana,V. dos Santos Thiago,Maria Gomes Claudia,D. Laurenti Márcia,Lucia da Matta Vania,Eduardo Corbett Carlos
Abstract
American cutaneous leishmaniasis (ACL) is one of the most complex parasitic diseases from a clinical-immunopathological point of view due to the great heterogeneity of Leishmania species responsible for the disease. Currently, fifteen Leishmania species of the subgenera Leishmania, Viannia and Mundinia may give rise to ACL in Latin America. In Brazil, seven species are associated to the disease, but L. (V.) braziliensis and L. (L.) amazonensis stand out for producing the broadest clinical-immunopathological spectrum: localized cutaneous leishmaniasis [LCL: DTH+/++], borderline disseminated cutaneous leishmaniasis [BDCL: DTH+/−], mucocutaneous or mucosal leishmaniasis [MCL/ML: DTH++++], and anergic diffuse cutaneous leishmaniasis [ADCL: DTH−]. Although human genetic profile plays important factor in the immunopathogenesis of ACL, it deserves to be highlighted the crucial role of species-specific antigens of L. (V.) braziliensis and L. (L.) amazonensis [lipophosphoglycans, phosphatidylserine, proteophosphoglycans, glycoprotein-63 and CD200 – a macrophage activation inhibitor molecule] in the modulation of T-cell immune response (CD4+/CD8+) that will define the infection evolution.
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