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T-LYMPHOCYTES IN EXPERIMENTAL LEISHMANIA AMAZONENSIS INFECTION: COMPARISON BETWEEN IMMUNIZED AND NAIVE BALB/C MICE
Afiliación
Universidade Federal da Bahia. Faculdade de Medicina. Hospital Universitário Professor Edgard Santos. Salvador, BA, Brasil
Universidade Federal da Bahia. Faculdade de Medicina. Hospital Universitário Professor Edgard Santos. Salvador, BA, Brasil
Universidade Feederal do Rio de Janeiro. Instituto de Microbiologia. Rio de Janeiro, RJ, Brasil
Universidade Federal da Bahia. Faculdade de Medicina. Hospital Universitário Professor Edgard Santos. Salvador, BA, Brasil
Universidade Federal da Bahia. Faculdade de Medicina. Hospital Universitário Professor Edgard Santos. Salvador, BA, Brasil
Universidade Feederal do Rio de Janeiro. Instituto de Microbiologia. Rio de Janeiro, RJ, Brasil
Universidade Federal da Bahia. Faculdade de Medicina. Hospital Universitário Professor Edgard Santos. Salvador, BA, Brasil
Resumen en ingles
Abstract. Highly susceptible naive BALB/c mice or mice
that had previously been immunized i.v. with solubilized
homologous antigen (partially resistant) were infected
with Leishmania amazonensis. Histologically, the main
differences between the two groups were lymphocytic
infiltration and macrophage activation. Assays of T-cell
function at 3 and 10 weeks after infection revealed that
purified T-cells did not proliferate following treatment
with leishmania antigen. A mitogenic anti-CD3 monoclonal
antibody (mAb) failed to activate T-cells after
3 weeks of infection as judged by proliferation and IL-2
secretion assays. After 10 weeks of infection, anti-CD3
mAb fully activated T-cells to proliferation and IL-2
secretion. On the other hand, T-cells released IL-3 in
response to leishmania antigen, anti-CD3 mAb and anti-
Thyl mAb at 3 and 10 weeks post-infection. Surprisingly,
a mitogenic anti-Thy 1 mAb (G7) fully activated Tcells
even at 3 weeks of infection as judged by proliferative
and IL-2 secretion assays. No significant differences
were found in the proliferative or interleukin secretory
responses of T-cells from animals that had been infected
in either the presence or the absence of prior immunization.
Since the Thyl triggering pathway has different
accessory cell and cytokine requirements than does the
CD3 : TCR lymphocyte activation pathway, it is possible
that immunization was more effective in changing the
cellular interactions of the T-lymphocyte than in altering
its intrinsic capabilities.
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