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Natural killer (NK) activity, detected by the lysis of Yac-1 target cells, was examined in splenic and mesenteric lymph node (MLN) cells throughout the course of infection with Eimeria vermiformis in BALB/c and C57B1/6 (B6) mice. These strains are, respectively, relatively resistant and susceptible to primary infections, which render them equally, and completely, resistant to challenge. Resting levels of NK activity were higher in B6 than in BALB/c, and B6 responded earlier in the course of infection than BALB/c, but splenic peak values were higher in BALB/c; the pattern of response in MLN cells was similar in both strains, but the peak was higher in BALB/c. At the time (7 days p.i.) of peak NK response in BALB/c mice there was, depending upon the choice of NK-resistant/lymphokine-activated killer (LAK)-sensitive target cells, either little (P388D1), or no (P815) splenic LAK activity. Challenge of immunized BALB/c mice did not evoke a detectable NK response. Although the higher NK activity in BALB/c mice correlated with greater control of primary infection, depletion of NK activity (demonstrated in splenic cells) in vivo by treatment with anti-asialo GM1 antibodies did not greatly affect the course of infection. Furthermore, this treatment did not augment the exacerbation of infection produced by treatment with anti-interferon-gamma (IFN-gamma) MoAb, indicating that, at least in this system, NK cells are not a fundamentally important source of this controlling cytokine of eimerian infections. The results suggest that NK cells may not greatly influence the outcome of coccidial infections.

Original publication

DOI

10.1111/j.1365-2249.1994.tb06080.x

Type

Journal article

Journal

Clinical and experimental immunology

Publication Date

08/1994

Volume

97

Pages

273 - 279

Addresses

Department of Immunology and Pathology, Institute for Animal Health, Newbury, UK.

Keywords

Killer Cells, Natural, Killer Cells, Lymphokine-Activated, Animals, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Eimeria, Coccidiosis, Disease Models, Animal, G(M1) Ganglioside, Female, Immunity, Innate, Interferon-gamma