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Endemically exposed asymptomatic individuals show no increase in the specific Leishmania (Viannia) panamensis-Th1 immune response in comparison to patients with localized cutaneous leishmaniasis.

作者信息

Trujillo C M, Robledo S M, Franco J L, Velez I D, Erb K J, Patiño P J

机构信息

Programa de Estudio y Control en Enfermedades Tropicales - PECET, Universidad de Antioquia, Medellín, Colombia.

出版信息

Parasite Immunol. 2002 Sep-Oct;24(9-10):455-62. doi: 10.1046/j.1365-3024.2002.00488.x.


DOI:10.1046/j.1365-3024.2002.00488.x
PMID:12654087
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.

摘要

相似文献

[1]
Endemically exposed asymptomatic individuals show no increase in the specific Leishmania (Viannia) panamensis-Th1 immune response in comparison to patients with localized cutaneous leishmaniasis.

Parasite Immunol. 2002

[2]
Distinct innate and acquired immune responses to Leishmania in putative susceptible and resistant human populations endemically exposed to L. (Viannia) panamensis infection.

Scand J Immunol. 2000-5

[3]
Immunocytochemical and histopathologic characterization of lesions from patients with localized cutaneous leishmaniasis caused by Leishmania panamensis.

Am J Trop Med Hyg. 1996-10

[4]
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Clin Exp Immunol. 1999-4

[5]
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[6]
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[7]
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[8]
[Immunopathology of American tegumentary leishmaniasis].

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[9]
Local Delivery of the Toll-Like Receptor 9 Ligand CpG Downregulates Host Immune and Inflammatory Responses, Ameliorating Established Leishmania (Viannia) panamensis Chronic Infection.

Infect Immun. 2017-2-23

[10]
Th1/Th2 immune responses are associated with active cutaneous leishmaniasis and clinical cure is associated with strong interferon-gamma production.

Hum Immunol. 2009-6

引用本文的文献

[1]
A Mouse Model of Ulcerative Cutaneous Leishmaniasis by to Investigate Infection, Pathogenesis, Immunity, and Therapeutics.

Front Microbiol. 2022-6-13

[2]
Epitopes in Humans Naturally Resistant to the Disease: Working Toward a Synthetic Vaccine.

Front Cell Infect Microbiol. 2021-6-7

[3]
Asymptomatic infection with American cutaneous leishmaniasis: epidemiological and immunological studies.

Mem Inst Oswaldo Cruz. 2016-10

[4]
Dynamic analysis of Th1/Th2 cytokine concentration during antiretroviral therapy of HIV-1/HCV co-infected patients.

BMC Infect Dis. 2012-4-25

[5]
Macrophages participate in host protection and the disease pathology associated with Leishmania braziliensis infection.

BMC Infect Dis. 2012-3-29

[6]
Murine model of chronic L. (Viannia) panamensis infection: role of IL-13 in disease.

Eur J Immunol. 2010-10

[7]
CD26 expression on CD4+T cells in patients with cutaneous leishmaniasis.

Clin Exp Immunol. 2008-7

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