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PHOSPHATIDYLSERINE EXPOSURE ON THE SURFACE OF LEISHMANIA AMAZONENSIS AMASTIGOTES MODULATES IN VIVO INFECTION AND DENDRITIC CELL FUNCTION
Affilliation
Universidade Federal do Rio de Janeiro. Instituto de Ciências Biomédicas. Programa de Ciências Morfológicas. Rio de Janeiro, RJ, Brasil / Universidade Federal do Rio de Janeiro. Campus UFRJ Macaé. Pólo Universitário, Macaé, RJ, Brasil / University of Texas Medical Branch. Institute for Human Infections and Immunity. 3Department of Microbiology and Immunology. Galveston, TX, USA.
University of Texas Southwestern Medical Center. Department of Pharmacology. Dallas, TX, USA.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia Celular. Rio de Janeiro, RJ, Brasil / Universidade de São Paulo. Instituto de Ciências Biomédicas. Departamento de Parasitologia.São Paulo, SP, Brasil.
University of Texas Southwestern Medical Center. Department of Pharmacology. Sealy Center for Vaccine Development. Center for Biodefense and Emerging Infectious Diseases. 7Department of Pathology. Dallas, TX, USA /
University of Texas Southwestern Medical Center. Department of Pharmacology. Dallas, TX, USA.
Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Biologia Celular. Rio de Janeiro, RJ, Brasil / Universidade de São Paulo. Instituto de Ciências Biomédicas. Departamento de Parasitologia.São Paulo, SP, Brasil.
University of Texas Southwestern Medical Center. Department of Pharmacology. Sealy Center for Vaccine Development. Center for Biodefense and Emerging Infectious Diseases. 7Department of Pathology. Dallas, TX, USA /
Abstract
Leishmania amazonensis parasites can cause diverse forms of leishmaniasis in humans and
persistent lesions in most inbred strains of mice. In both cases, the infection is characterized by a
marked immunosuppression of the host. We previously showed that amastigote forms of the
parasite make use of surface-exposed phosphatidylserine (PS) molecules to infect host cells and
promote alternative macrophage activation, leading to uncontrolled intracellular proliferation of
the parasites. In this study, we demonstrated that treatment of infected mice with an PS-targeting
monoclonal antibody ameliorated parasite loads and lesion development, which correlated with
increased proliferative responses by lymphocytes. In addition, we observed an enhanced dendritic
cell (DC) activation and antigen presentation in vitro. Our data imply that the recognition of PS
exposed on the surface of amastigotes plays a role in down-modulating DC functions, in a matter
similar to that of apoptotic cell clearance. This study provides new information regarding the
mechanism of immune suppression in Leishmania infection.
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