Immunogenicity of the P-8 amastigote antigen in the experimental model of canine visceral leishmaniasis

被引:37
|
作者
Carrillo, E.
Ahmed, S.
Goldsmith-Pestana, K.
Nieto, J.
Osorio, Y.
Travi, B.
Moreno, J.
McMahon-Pratt, D. [1 ]
机构
[1] Yale Univ, Dept Epidemiol & Publ Hlth, New Haven, CT 06520 USA
[2] WHO, Collaborating Ctr Leishmaniasis, Inst Salud Carlos III, Madrid 28220, Spain
[3] CIDEIM, Cali, Colombia
[4] CSIC, Ctr Invest Biol, E-28040 Madrid, Spain
关键词
Leishmania; canine; cytokine; immunogenicity; P-8;
D O I
10.1016/j.vaccine.2006.10.036
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The P-8 proteoglycolipid complex (P-8 PGLC), an amastigote antigen of Leishniania pifanoi, has been demonstrated to induce protection in mouse models, as well as to induce Tc1/Th1-like cellular responses in American cutaneous leishmaniasis patients. Because the immunization with P-8 PGLC in the murine model does not appear to be genetically restricted, we have studied the reactivity of the P-8 PGLC in Leishmania infantunt infected dogs. In this study, it is shown that PBMC from experimentally infected dogs (asymptomatic, oligosymptomatic) significantly proliferated in response to soluble leishmanial antigen (SLA) or the P-8 PGLC. Further, quantification of the gene expression induced by the stimulation with P-8 in asymptornatically infected dogs showed an up-regulation of IFN-gamma and TNF-alpha, which were three to 4-fold higher than that induced by soluble Leishmania antigen (SLA). While no measurable induction of IL-10 was observed, low levels of IL-4 mRNA were observed in response to both P-8 and SLA antigens. Thus, our studies establish that P-8 is recognized by infected canines and elicits a potentially curative/protective Th1-like immune response. The identification of Leishmania antigens that elicit appropriate immune responses across different host species (humans, canine) and disease manifestations (cutaneous or visceral) could be an advantage in generating a general vaccine for leishmaniasis. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1534 / 1543
页数:10
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