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Comparison of the humoral and cellular immune responses to two preparations of Cryptosporidium parvum CP15/60 recombinant protein.

This study compares the immune responses produced by immunising mice and rabbits with two preparations of the recombinant 15/60 kDa protein of Cryptosporidium parvum. Genomic C. parvum DNA was amplified and the recombinant protein was synthesized as a fusion protein with glutathione-S-transferase in Escherichia coli and in the eukaryotic system of baculovirus/insect cells. Both recombinant proteins induced similar levels of serum antibodies against the fusion recombinant protein, but the eukaryotic recombinant protein triggered a stronger humoral response to C. parvum. Similarly, increased lymphoproliferation occurred only after stimulation of spleen cells from mice immunised with the eukaryotic recombinant protein. This suggests that the eukaryotic protein is a better candidate for immunological studies on cryptosporidiosis.

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Cellular immune mechanisms in Coxsackievirus group B, type 3 induced myocarditis in Balb/C mice.

Coxsackie B viruses are a common cause of viral myocarditis in humans. A murine model of the human disease has been developed using Coxsackievirus group B, type 3 and inbred Balb/c mice. Infection of T lymphocyte deficient mice does not result in significant myocarditis indicating the importance of T cells in this disease. The virus can be isolated from the hearts of T cell deficient and normal mice in equal concentrations. Virus elimination presumably is mediated by virus specific neutralizing antibody induced in both groups. T lymphocytes, natural killer cells and macrophage obtained from normal virus infected mice are all capable of lysing myofibers in vitro. Maximum lysis is obtained with the cytolytic T cells. When these cell populations or Coxsackievirus immune antibody were adoptively transferred into T lymphocyte deficient animals infected with the virus, only animals given T cells developed significant myocarditis.

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