Immunity to coccidiosis: genetic influences on lymphocyte and cytokine responses to infection with Eimeria vermiformis in inbred mice

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Abstract
Cellular and cytokine responses to infection with Eimeria vermiformis were compared in BALB/c (resistant) and C57BL/6 (B6‐susceptible) inbred mice. Cellular responses in the mesenteric lymph node (MLN) occurred sooner after primary infection in the resistant BALB/c strain. In contrast, proliferative responses occurred earlier after challenge in B6 mice. Resting levels of CD4 + ve and CD8 + ve T‐lymphocytes in the MLN differed between the two strains but the relative numbers of each subset remained relatively constant throughout primary infection. MLN cells taken at intervals after infection were assayed for release of the cytokines IFN‐gamma, IL‐5 and IL‐10 after culture in vitro with the mitogen Concanavalin A (Con‐A) or with parasite antigen. With either stimulus cells from resistant BALB/c mice released IFN‐gamma and IL‐5 earlier after infection than did B6 cells. The strains had a comparable absolute ability to produce IFN‐gamma but BALB/c cells released more IL‐5 than did B6, levels declining, rather than increasing, during primary infection in the latter. Only cells from BALB/c mice released IL‐10 during infection. Cells taken after a secondary infection released relatively little cytokine after pulsing in vitro. These data suggest that the difference in response phenotype between the two strains when infected with E. vermiformis reflect a kinetic, rather than a qualitative, difference in ability to mount protective T‐helper (Th) cell subset responses. No evidence was found for a Th2‐mediated interference with ability to release IFN‐gamma, the cytokine most closely associated with protective immunity.

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