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Lymphocytes from patients with neoplastic disease were tested for sensitization to encephalitogenic factor (EF) by the macrophage migration inhibition test. Sensitization to EF was demonstrated in 71% of patients with various forms of neoplastic disease. Sensitization to EF was also demonstrated for 31% of subjects with no evidence of neoplastic disease; these included patients with warts, chronic bronchitis and hernias. In contrast, healthy subjects showed no sensitization to myelin basic protein. These observations suggest that sensitization to EF may not be confined to patients with neoplastic disease. Lymphocytes from hamsters bearing a transplanted virus induced tumour were sensitized to EF prepared from both human and hamster brain. Sensitization was also seen in hamsters infected with influenza virus but not in animals with acute tubular necrosis produced by glycerol treatment. The development of an animal model system provides a method for the investigation of possible mechanisms of sensitization.
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The parameters of migration inhibition test of leucocytes isolated both from the peripheral blood, spleen and lymph nodes of monkeys Cercopithecus aethiops were determined. Concentration of measles virus that does not produce nonspecific migration inhibition of leucocyte obtained from sero-negative animals was also defined.
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Migration of peripheral leucocytes collected from Theileria annulata carrier cattle was inhibited in the presence of piroplasmal antigen. The degree of inhibition was antigen density dependent. The same antigen did not inhibit migration of leucocytes obtained from clean animals, raised under tick-free conditions. The carrier animals exhibited typical skin sensitivity reaction on intradermal inocluation of the piroplasmal antigen. The known negative animals failed to evince a similar reaction.
Supernatants from human mononuclear cells cultured with PHA inhibited the migration of both human polymorphonuclear leucocytes and guinea-pig peritoneal exudate cells, but not human mononuclear cells. Using ultrafiltration it was shown that these supernatants contained two inhibiting factors, the one with a molecular weight of 15,000-50,000 inhibited only guinea-pig peritoneal exudate cells (MIF), whereas the fraction containing molecules of a size between 50,000 and 75,000 specifically inhibited the migration of polymorphonuclear leucocytes (LIF). The polymorphonuclear leucocyte inhibiting activity was heat labile. It is suggested that the leucocyte migration inhibition test is dependent upon the production of a lymphokine (LIF) which acts specifically on polymorphonuclear leucocytes causing their inhibition of migration.
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Four groups of rabbits injected with cardiac tissue and complete Freund's adjuvant or aluminum hydroxide gel adjuvant and two groups only injected with aluminum hydroxide gel adjuvant or complete Freud's adjuvant were studied. The humoral and cellular immunity in immunized animals was studied using heart soluble and insoluble extracts. The tests results from hemagglutination, immunoelectrophoresis and immunofluorescence have presented cross-reactions among sera and hearts of the several species. Similar cross-reactions were not revealed by immunodiffusion. The immunoelectrophoresis and hemagglutination reactions were related to heart soluble extract and the immunofluorescence reactions were related to insoluble extract located in sarcolemal, subsarcolemal and intermyofibrilar sites. By hemagglutination, it was verified the presence of antibodies to heart and skeletal muscle in the antisera. Is was not possible to negative completely the reactivity of these antibodies to heart by absorptions with skeletal muscle. Inhibition tests to leucocytes migration revealed that leucocytes from immunized animals present migration inhibition when faced to antigens sedimented at.....56.500 g.
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Cell-mediated immunity and antibody production to cartilage antigens were studied in rabbits. From day 3 of immunization an inhibition of leucocyte migration was observed in animals immunized with collagen-free fractions of bovine nasal or human rib cartilage. Delayed cutaneous hypersensitivity was elicited between 5 and 6 days and the circulating antibodies were demonstrated by passive haemagglutination on day 9. No significant correlation was observed between the antibody production and the cell-mediated immunity. Cell-mediated immune responses to cartilage antigens and to purified protein derivative were distinctly different, but the two antigens influenced one another when they were administered together. The 'species common' antigen of connective tissues may be primarily responsible for the early immune reactions.