Immunity to coccidiosis: adoptive transfer in NIH mice challenged with Eimeria vermiformis

Abstract

The development of a reliable model for the adoptive transfer of immunity to coccidiosis (infection with Eimeria vermiformis in NIH mice) is described. More than 10(8) of a mixture of spleen and mesenteric lymph node (MLN) cells, given either intravenously or intraperitoneally, were required to transfer a significant degree of protection. Dividing cells, present in the donors at 10 or 14 days after priming, but not at 5 or 19 days, were shown to be the effectors. When examined separately, MLN cells were found to be superior to spleen cells, and the injection of as few as 5 x 10(7) was capable of substantially reducing the oocyst output from a challenge inoculum. The recipients of cells from primed mice had earlier, and sometimes higher, titres of specific antibodies in the serum but, overall, there was no correlation between these titres and protection. Further characterization of the cells responsible for adoptively transferring immunity to this infection should now be possible.

Genetic Dissection of Primary and Secondary Responses to a Widespread Natural Pathogen of the Gut,Eimeria vermiformis

“…Controls received PBS, pH 7.2, with no cells. Recipient mice were challenged with E. vermiformis 24 h after adoptive transfer, as described by Rose et al (38,42). Fig.…”

“…The development of immunity to E. vermiformis can be demonstrated by adoptive transfer of mesenteric lymph node cells (MLNC) to irradiated naive recipients (38,42) or T-cell-deficient recipients (A. L. Smith and A. C. Hayday, unpublished data) (see below). Although complete protection is rarely achieved, naive recipients of MLNC from mice 8 to 12 days after primary infection are invariably more resistant to infection than mice inoculated with cells from naive mice or mice mock inoculated with PBS (38; A. L. Smith and A. C. Hayday, unpublished observations).…”

Coccidia: A review of recent advances on immunity and vaccine development

“…In chickens, both spleen cells and PBL were capable of transferring antibody and cell mediated responses, resulting in decreased oocyst output in recipients (Rose & Hesketh, 1982). Depletion of T h -and T c/s -cells, using anti-L3T4 (T h ) and anti-Lyt2 (T c/s ), eliminated the ability of the cells to adoptively transfer immunity to E. vermiformis (Rose et al, 1988a). In murine coccidiosis, elimination of T-helper cells, but not T-cytotoxic cells abrogated passive transfer of protection (Rose et al, 1988a).…”

“…Depletion of T h -and T c/s -cells, using anti-L3T4 (T h ) and anti-Lyt2 (T c/s ), eliminated the ability of the cells to adoptively transfer immunity to E. vermiformis (Rose et al, 1988a). In murine coccidiosis, elimination of T-helper cells, but not T-cytotoxic cells abrogated passive transfer of protection (Rose et al, 1988a). A partial in vivo depletion of mouse T-cells using the anti-Thyl.2 (pan T) mAb resulted in an abrogation of protective immunity to E. falciformis and extended the patent period (Stiff & Vasilakos, 1990).…”

T-cell alpha beta + and gamma delta + deficient mice display abnormal but distinct phenotypes toward a natural, widespread infection of the intestinal epithelium.

“…However, because nu/nu animals harbor defects in ct3 T cells, y6T cells, and epithelia (the target for infection), these data do not define any one cell type critical to the host response. Nonetheless, a major role for a:+ T cells was indicated by other studies, such as those where immunity was conferred on naive mice by transfer of mesenteric lymph node (MLN) CD4+ T cells from infected mice (19,20). At the same time, the potential involvement of both acxB T cells and y5+ cells was suggested by dynamic changes in both cell types during infection (21).…”