5 research outputs found
Role of CD8+ T cells in endogenous interleukin-10 secretion associated with visceral leishmaniasis
Role of CD8+ T cells in endogenous interleukin-10 secretion associated with visceral leishmaniasis
This study examined the role and source of endogenous interleukin-10
(IL) secretion in visceral leishmaniasis (VL). The amounts of
endogenous and Leishmania specific IL-10 and interferon-g (IFN)
secreted by peripheral blood mononuclear cells (PBMC) from VL patients
were compared. The correlation coefficient between endogenous IL-10
secretion and Leishmania specific IFN-g was -0.77, suggesting a major
role for endogenous IL-10 secretion in VL. The effects of CD4+ and CD8+
T cell clones, isolated from a treated VL patient, on IL-10 secretion
were assayed by mixing the clones with autologous, inactivated PBMC.
The CD8+ clones mediated increased levels of IL-10 secretion in the
presence of PBMC alone suggesting that CD8+ T cells may mediate
endogenous IL-10 secretion
Immunotherapy for visceral leishmaniasis: Ability of factors produced during anti-leishmania responses of skin test positive adults to inhibit peripheral blood mononuclear cell activities associated with visceral leishmaniasis
The course of human Leishmania chagasi infections appears to be
determined by the balance between type 1 (T1) CD4+ and CD8+ T
suppressor (Ts) cell activities. Skin test positive adults living in
hyperendemic areas who have no history of visceral leishmaniasis (VL)
have T1 CD4+ T cell immunodominant responses against L. chagasi. The
cytokines they secrete during anti-leishmania responses are a probable
source of cytokines which inhibit the CD8+ Ts cells associated with VL.
The ability of supernatants generated from peripheral blood mononuclear
cells derived from skin test positive adults to reverse immune
responses which appear to be mediated by CD8+ Ts cells was assessed in
three sets of screening assays. The supernatants displayed three
candidate factors. One, which could be explained by Leishmania antigens
in the supernatant, decreased high endogenous IL-10 secretion
characteristic of one class of VL patients. A second activity decreased
high endogenous proliferation characteristic of the same class of
patients without decreasing antigen specific proliferation. The third
activity inhibited or killed CD8+ T cells but not CD4+ T cells. These
activities might be useful in treating VL