Regulation of the primary immune response to ovalbumin in mice: activation of T cells mediating delayed-type hypersensitivity, nonspecific help, and specific help, and their sensitivity to radiation

Lubet, M.T.; Kettman, J.R.

Journal of Immunology 123(1): 426-433

1979


ISSN/ISBN: 0022-1767
PMID: 87480
Document Number: 140062
The immune response to ovalbumin (OVA) in mice is controlled by at least 4 genes. In this study the site of action of the genes regulating the response to OVA was investigated. To this end, helper T -OVA was studied. When mice were immunized with limiting doses of TNP-OVA, anti-TNP antibodies were elicited but anti-OVA antibodies were not. OVA-specific helper T cells were apparently not the limiting factor in the anti-OVA antibody responses. Helper T cell functions were also measured in in vitro assays. Two kinds of helper T cell activity were measured. Nonspecific healper T cell activity (the bystander effect) was determined by measuring the ability of OVA-primed spleen cells to help the anti-sheep red blood cells (SRBC) antibody response in cultures stimulated with SRBC and TNP-OVA. Antigen-specific helper activity was determined by measuring the ability of OVA-primed spleen cells to help the anti-TNP antibody response in cultures stimulated with TNP-OVA. In vivo-priming doses of OVA that do not elicit a delayed-type hypersensitivity (DTH) response or a primary antibody response apparently prime for nonspecific and antigen-specific helper T cells. The genes regulating the immune response to OVA apparently do not control activation of helper T cells. These T cell subpopulations that recognize OVA can be further distinguished by virtue of their sensitivity to radiation. The DTH effector cells and cells responsible for nonspecific help were not sensitive to 1000R. The specific helper activity was sensitive to 1000R. The subsets that were not sensitive to radiation were distinguished by their independent activation by OVA.

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