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γδT cells do not play a major role in controlling infection in experimental cysticercosis

Published online by Cambridge University Press:  01 October 1999

S. A. TOENJES
Affiliation:
Department of Biology, P.O. Box 7325, Wake Forest University, Winston-Salem, NC 27109, USA
R. J. SPOLSKI
Affiliation:
Department of Biology, P.O. Box 7325, Wake Forest University, Winston-Salem, NC 27109, USA
K. A. MOONEY
Affiliation:
Department of Biology, P.O. Box 7325, Wake Forest University, Winston-Salem, NC 27109, USA
R. E. KUHN
Affiliation:
Department of Biology, P.O. Box 7325, Wake Forest University, Winston-Salem, NC 27109, USA
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Abstract

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Protective immunity against larval Taenia crassiceps has been shown to rely on T cells; however, the roles of the specific subsets of T cells during infection are not known. To investigate a possible role for γδT cells, this study investigated larval infection in δ-chain knock-out C57BL/6 (deltaKO) and wild-type C57BL/6 mice. It was found that deltaKO mice and C57BL/6 mice were equally susceptible to infection suggesting γδT cells do not play a major role in protective immunity. Cytokine production by concanavalin A (ConA)-stimulated spleen cells from infected deltaKO mice and C57BL/6 mice were determined. All infected mice demonstrated an increased IL-10 production suggesting a Th1-inhibitory function. Cells from infected deltaKO mice and C57BL/6 mice did not show increases in IL-4 production. Heavily-infected C57BL/6 mice showed a decrease in IFN-γ production compared to deltaKO mice. These observations suggest that an increase in IL-10 production best correlates with a non-protective immune response. To make comparisons between in vitro cytokine production and systemic immune responses, cytokine levels in serum were determined. C57BL/6 mice and deltaKO mice showed increases in serum levels of IL-4 and IFN-γ at 52 days post-infection. The systemic immune response of these mice, therefore, is a mixed Th1/Th2-type response and γδT cells are apparently not responsible for the systemic increases in these cytokines.

Type
Research Article
Copyright
1999 Cambridge University Press