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IS THERE ANY DIFFERENCE IN THE IN SITU IMMUNE RESPONSE IN ACTIVE LOCALIZED CUTANEOUS LEISHMANIASIS THAT RESPOND WELL OR POORLY TO MEGLUMINE ANTIMONIATE TREATMENT OR SPONTANEOUSLY HEAL?
Cell-mediated immunity
Cutaneous leishmaniasis
Host-parasite interaction
Immunohistochemistry
Immunopathology
In situ immune response
Macrophages
Spontaneous healing
Treatment relapse
Author
Affilliation
Oswaldo Cruz Foundation. Oswaldo Cruz Institute. Laboratory of Immunoparasitology. Rio de Janeiro, RJ, Brazil.
National Institute of Cancer. Service of Oncological Dermatology. Rio de Janeiro, RJ, Brazil.
Oswaldo Cruz Foundation. Oswaldo Cruz Institute. Laboratory of Immunoparasitology. Rio de Janeiro, RJ, Brazil.
Oswaldo Cruz Foundation. Evandro Chagas National Institute of Infectious Diseases. Laboratory of Clinical Research and Surveillance in Leishmaniasis. Rio de Janeiro, RJ, Brazil.
Oswaldo Cruz Foundation. Evandro Chagas National Institute of Infectious Diseases. Laboratory of Clinical Research and Surveillance in Leishmaniasis. Rio de Janeiro, RJ, Brazil.
Oswaldo Cruz Foundation. Evandro Chagas National Institute of Infectious Diseases. Laboratory of Clinical Research and Surveillance in Leishmaniasis. Rio de Janeiro, RJ, Brazil.
Oswaldo Cruz Foundation. Evandro Chagas National Institute of Infectious Diseases. Laboratory of Clinical Research and Surveillance in Leishmaniasis. Rio de Janeiro, RJ, Brazil.
Oswaldo Cruz Foundation. Evandro Chagas National Institute of Infectious Diseases. Laboratory of Clinical Research and Surveillance in Leishmaniasis. Rio de Janeiro, RJ, Brazil.
Oswaldo Cruz Foundation. Evandro Chagas National Institute of Infectious Diseases. Laboratory of Clinical Research and Surveillance in Leishmaniasis. Rio de Janeiro, RJ, Brazil.
Oswaldo Cruz Foundation. Oswaldo Cruz Institute. Laboratory of Immunoparasitology. Rio de Janeiro, RJ, Brazil.
National Institute of Cancer. Service of Oncological Dermatology. Rio de Janeiro, RJ, Brazil.
Oswaldo Cruz Foundation. Oswaldo Cruz Institute. Laboratory of Immunoparasitology. Rio de Janeiro, RJ, Brazil.
Oswaldo Cruz Foundation. Evandro Chagas National Institute of Infectious Diseases. Laboratory of Clinical Research and Surveillance in Leishmaniasis. Rio de Janeiro, RJ, Brazil.
Oswaldo Cruz Foundation. Evandro Chagas National Institute of Infectious Diseases. Laboratory of Clinical Research and Surveillance in Leishmaniasis. Rio de Janeiro, RJ, Brazil.
Oswaldo Cruz Foundation. Evandro Chagas National Institute of Infectious Diseases. Laboratory of Clinical Research and Surveillance in Leishmaniasis. Rio de Janeiro, RJ, Brazil.
Oswaldo Cruz Foundation. Evandro Chagas National Institute of Infectious Diseases. Laboratory of Clinical Research and Surveillance in Leishmaniasis. Rio de Janeiro, RJ, Brazil.
Oswaldo Cruz Foundation. Evandro Chagas National Institute of Infectious Diseases. Laboratory of Clinical Research and Surveillance in Leishmaniasis. Rio de Janeiro, RJ, Brazil.
Oswaldo Cruz Foundation. Evandro Chagas National Institute of Infectious Diseases. Laboratory of Clinical Research and Surveillance in Leishmaniasis. Rio de Janeiro, RJ, Brazil.
Oswaldo Cruz Foundation. Oswaldo Cruz Institute. Laboratory of Immunoparasitology. Rio de Janeiro, RJ, Brazil.
Abstract
Localized cutaneous leishmaniasis caused by Leishmania braziliensis can either respond well or poorly to the treatment or heal spontaneously; It seems to be dependent on the parasite and/or host factors, but the mechanisms are not fully understood. We evaluated the in situ immune response in eighty-two active lesions from fifty-eight patients prior to treatment classified as early spontaneous regression (SRL-n = 14); treatment responders (GRL-n = 20); and non-responders (before first treatment/relapse, PRL1/PRL2-n = 24 each). Immunohistochemistry was used to identify cell/functional markers which were correlated with the clinical characteristics. PRL showed significant differences in lesion number/size, clinical evolution, and positive parasitological examinations when compared with the other groups. SRL presented a more efficient immune response than GRL and PRL, with higher IFN-γ/NOS2 and a lower percentage of macrophages, neutrophils, NK, B cells, and Ki-67+ cells. Compared to SRL, PRL had fewer CD4+ Tcells and more CD163+ macrophages. PRL1 had more CD68+ macrophages and Ki-67+ cells but less IFN-γ than GRL. PRL present a less efficient immune profile, which could explain the poor treatment response, while SRL had a more balanced immune response profile for lesion healing. Altogether, these evaluations suggest a differentiated profile of the organization of the inflammatory process for lesions of different tegumentary leishmaniasis evolution.
Keywords
CD163Cell-mediated immunity
Cutaneous leishmaniasis
Host-parasite interaction
Immunohistochemistry
Immunopathology
In situ immune response
Macrophages
Spontaneous healing
Treatment relapse
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