Immunity to coccidiosis: T-cell control of infection with Eimeria vermiformis in mice does not require co-operation with inflammatory cells.

The necessity for co-operation between lymphocytes and myeloid-derived inflammatory cells in the mediation of anti-coccidial immunity was investigated using mice infected with Eimeria vermiformis. Reciprocal exchange of immune lymphocytes between H-2 compatible strains of contrasting susceptibility to infection (resistant BALB/B and susceptible C57BL/10) resulted in successful transfer of immunity in both homologous and heterologous exchanges. Recipients of immune cells, whatever their original response phenotype, expressed a high degree of immunity to infection, indicating that the differential susceptibility of the strains is a property of their lymphoid cells and is not attributable to their capacity to mount inflammatory responses. This conclusion was confirmed by the successful adoptive transfer of immunity into NIH mice previously exposed to 600 rad X-irradiation; at this level of irradiation inflammatory responsiveness is severely depressed. Additional confirmation that strain-response phenotype is lymphocyte dependent and that immune lymphocytes can mediate their effects against E. vermiformis without the intervention of inflammatory cells was obtained from studies on the mucosal mast cell response to infection. No correlation existed between the development of intestinal mastocytosis, an index of T-cell-mediated inflammatory responsiveness, and the expression of resistance to E. vermiformis in BALB/c (resistant), C57BL/10 (susceptible) and NIH (susceptible) mice.