title: Endemically exposed asymptomatic individuals show no increase in the specific Leishmania (Viannia) panamensis-Th1 immune response in comparison to patients with localized cutaneous leishmaniasis.
abstract: In Colombia, most cases of human cutaneous leishmaniasis are caused by Leishmania (Viannia) panamensis. Interestingly, up to 30% of the exposed population do not suffer from clinical leishmaniasis although it is likely that they are continuously infected with Leishmania parasites. Since it is believed that the induction of efficient Th1 immune responses protects against Leishmania infections both in humans and in animal models, we determined if endemically exposed asymptomatics showed stronger Leishmania-specific Th1 immune responses than patients with active localized cutaneous leishmaniasis (LCL). We found that Montenegro skin test responses were slightly higher among asymptomatic individuals compared to patients suffering from LCL. However, PBMC from patients with LCL showed similar Leishmania-specific proliferative responses compared to PBMC from asymptomatic individuals. Furthermore, PBMC from both groups also secreted similar amounts of IFN-gamma, IL-12p40 and IL-10 after in vitro exposure to L. panamensis. No IL-4 was detected in the supernatants. Taken together our results suggest that lack of LCL development in endemically exposed asymptomatics cannot be explained by stronger systemic anti-Leishmania Th1 immune responses or decreased Th2 responses in these individuals in comparison to individuals who develop LCL. It may be possible that other mechanisms are responsible for resistance to cutaneous leishmaniasis in Colombia in endemically exposed asymptomatics.
authors.affiliation: Programa de Estudio y Control en Enfermedades Tropicales - PECET, Universidad de Antioquia, Medellín, Colombia. claudia.trujillo@mail.uni-wuerzburg.de
authors.forename: C M
authors.initials: CM
authors.lastname: Trujillo
authors.forename: S M
authors.initials: SM
authors.lastname: Robledo
authors.forename: J L
authors.initials: JL
authors.lastname: Franco
authors.forename: I D
authors.initials: ID
authors.lastname: Velez
authors.forename: K J
authors.initials: KJ
authors.lastname: Erb
authors.forename: P J
authors.initials: PJ
authors.lastname: Patiño
mesh_terms: D000293:Adolescent; D000328:Adult; D000818:Animals; D015703:Antigens, CD / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D002478:Cells, Cultured; D016207:Cytokines / Q000096:biosynthesis; D019353:Endemic Diseases; D005260:Female; D006801:Humans; D006968:Hypersensitivity, Delayed; D037181:Lectins, C-Type; D018334:Leishmania guyanensis / Q000254:growth & development / Q000276:immunology*; D016773:Leishmaniasis, Cutaneous / Q000276:immunology* / Q000469:parasitology / Q000473:pathology; D008213:Lymphocyte Activation; D008297:Male; D008875:Middle Aged; D012867:Skin / Q000276:immunology* / Q000469:parasitology / Q000473:pathology; D018417:Th1 Cells / Q000276:immunology*; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D016207:Cytokines; D037181:Lectins, C-Type; D000099192:CD69 Antigens