1887

Abstract

R to infection by spp. involves cellular (Plant and Glynn, 1974) and humoral immune responses (Di Pauli, 1972). Differences in delayed hypersensitivity permit the classification of animals into susceptible and resistant strains (Vas, Roy and Robson, 1973) whilst differences in antibody response allow classification into high- and low-responder strains (McDevitt and Sela, 1965).

Plant and Glynn (1974) calculated the LD50 of strain C5 in six different strains of mice after subcutaneous injection. Strains of mice could easily be separated into those sensitive to less than 10 and those resistant to more than 10 micro-organisms. The most susceptible were BALB/C mice, which had an LD50 of less than 10, whilst the most resistant mice belonged to the CBA strain, which had an LD50 of 10. The explanation for this difference is at the moment unclear.

Crossreactivity between human tissue and bacterial antigens is thought to be responsible for the development of rheumatic fever after infection with group-A β-haemolytic streptococci (Kaplan, Meyeserian and Kushner, 1961), though antistreptococcal antibodies have not produced cardiac lesions in experimental animals. Similarly, susceptibility to infection with in mice may be due to partial tolerance of the pathogen caused by crossreactivity to a self component (Rowley and Jenkin, 1962).

Previous reports have demonstrated that cellular immune responses to can be linked to the genetic status of the mouse strain (Plant and Glynn, 1974) but a significant antibody increase was not obtained when the animals were inoculated with relatively small doses of live micro-organisms. Antibody responses could not be studied when larger inoculating doses were used because the animals of the susceptible strains died within a few days.

We have studied the antibody response of CBA and BALB/C mice, to large doses of inactivated bacteria, and investigated the crossreaction between the micro-organism and surface antigens of spleen and lymph-node cells obtained from high- and low-responder strains as a possible explanation for the differing antibody responses.

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/content/journal/jmm/10.1099/00222615-13-1-11
1980-02-01
2019-10-14
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