2003
DOI: 10.1016/s0020-7519(03)00179-6
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Intradermal inoculations of low doses of Leishmania major and Leishmania amazonensis metacyclic promastigotes induce different immunoparasitic processes and status of protection in BALB/c mice

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Cited by 42 publications
(38 citation statements)
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“…These mice are susceptible to infection by various Leishmania species, including L. major and L. amazonensis as presented here (7,17). The standard method for following infection in this in vivo model is based on estimation of parasite loads by labor-intensive microscopic enumeration of sacrificed animals or caliper-based measurements of the size or thickness of lesions that have developed at the site of infection, such as the footpad, ear dermis, or tail base (7,22).…”
mentioning
confidence: 88%
“…These mice are susceptible to infection by various Leishmania species, including L. major and L. amazonensis as presented here (7,17). The standard method for following infection in this in vivo model is based on estimation of parasite loads by labor-intensive microscopic enumeration of sacrificed animals or caliper-based measurements of the size or thickness of lesions that have developed at the site of infection, such as the footpad, ear dermis, or tail base (7,22).…”
mentioning
confidence: 88%
“…Although leishmaniasis is an intracellular infection, the contribution of CD8 + T-cells as immune correlates of disease at primary infection remained to be addressed [28,29] until the data from low dose experimental challenge in both Balb/c and C57BL/6 mice was extrapolated. The data from Balb/c mice infected by low dose challenge was controversially CD8 + T-cell dependent, but these mice were able to elevate Th1 type immune response and control the primary and secondary infection [30][31][32]. However data from C57BL/6 mice clearly shed light on CD8 + T-cells as contributors to CL control.…”
Section: Humoral Immune Response Evaluation By Elisa As Th1/th2 Deviamentioning
confidence: 99%
“…At the onset of a primary infection with L. major, parasites multiply at the site of infection, and lymphocytes from infected mice produce IFN-␥, IL-10, IL-4, and IL-13, clearly indicating no obvious bias toward Th1 or Th2 immunity. Mice infected with very low doses of parasites never develop cutaneous lesions, and these mice do not become immune to subsequent infection, indicating that lesion development plays an important role in the acquisition by BALB/c mice of what is termed "concomitant immunity" (14).…”
Section: Cr3mentioning
confidence: 99%