LACK-specific CD4(+) T cells that induce gamma interferon production in patients with localized cutaneous leishmaniasis during an early stage of infection |
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| Authors: | Bourreau Eliane Prévot Ghislaine Gardon Jacques Pradinaud Roger Hasagewa Hitoshi Milon Geneviève Launois Pascal |
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| Affiliation: | Immunologie des Leishmanioses. Service d'Epidémiologie, Institut Pasteur de Cayenne, 97306 Cayenne Cedex, France. |
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| Abstract: | The profile of cytokines induced by soluble leishmania antigen (SLA) and the Leishmania homologue of the mammalian receptor for activated C kinase (LACK), a candidate vaccine against leishmaniasis, and the cellular source of the cytokines produced in response to these antigens were analyzed in patients infected with Leishmania guyanensis. Gamma interferon (IFN-gamma) and interleukin-10 (IL-10) were produced in response to LACK. Although LACK-specific CD4(+) cells producing IFN-gamma were isolated only during the early phase of infection (less than 30 days following the onset of infection), cells producing IL-10 in response to LACK were detected in all patients. CD4(+) T cells producing IFN-gamma and IL-13 were produced in response to SLA in all patients. SLA- and LACK-specific T cells are effector memory cells, as they are CD45RA(-) CCR7(-) CD4(+) T cells. CD4(+) T cells producing IFN-gamma are CD62L(-), and CD4(+) T cells producing IL-10 are CD62L(+), indicating that these cells have different tissue-homing capacities. These findings show that SLA and LACK induce both type 1 (IFN-gamma) and type 2 (IL-10 or IL-13) cell responses. |
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