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Biomedical subjects

S B Salvin

Publications and source records attributed to S B Salvin.

13 recordsLinked to original sources

Adjuvants in the induction of suppressor cells.

The effect of different mycobacterial adjuvants on the parameters of delayed hypersensitivity was investigated in strain 13 guinea pigs. The composition of the tubercle bacilli and the type of vehicle in which the antigen was presented determined the presence and extent of suppressor cell activity. When antigen was introduced in complete Freund adjuvant, both adherent and nonadherent cells had suppressive properties, with the suppressive effect demonstrable in vitro from 1 to 5 weeks after sensitization. Suppressor activity was indicated in vivo by a reduction of delayed footpad hypersensitivity in animals presensitized with complete Freund adjuvant.

Adjuvants, Immunologic

Type I and II interferons and migration inhibitory factor: production in Mycobacterium bovis BCG-infected mice desensitized with old tuberculin or lipopolysaccharide.

Mice with delayed hypersensitivity induced by infection with Mycobacterium bovis strain BCG were desensitized by a single large dose of specific antigen (old tuberculin, OT) or a nonspecific interferon stimulus (bacterial lipopolysaccharide, LPS). Subsequent challenge of the desensitized animals revealed only a homologous hyporeactivity, that is, mice desensitized with OT showed decreased type II and migration inhibitory factor (MIF) responses to the specific antigen, which were unaffected by desensitization with LPS. Conversely, mice desensitized with LPS showed a decreased type I interferon and MIF response to LPS, which was unaffected by desensitization with OT. These results suggest that type I interferon and its accompanying low-titered MIF activity are produced by cell populations different from those that produce type II interferon and its accompanying high-titered MIF activity.

Animals

In vivo studies on the cellular source of migration inhibitory factor in mice with delayed hypersensitivity.

Mice sensitized intravenously with 300 microgram of BCG cell walls in Drakeol-Tween 80 and challenged intravenously 3 weeks later with 50 mg of old tuberculin released migration inhibitory factor (MIF) into the circulating blood in quantities that could be detected in serum dilutions of 1:64 to 1:128. When thymus-derived lymphocytes (T-cells) were absent at the time of sensitization, as in neonatally thymectomized mice or in athymic nude mice, detectable amounts of MIF were not formed. Sensitized mice treated with either anti-theta serum or anti-bone marrow-derived lymphocyte (B-cell) serum before intravenous challenge with old tuberculin released reduced amounts of MIF into the circulation. Mice lethally irradiated, reconstituted with B-cells, sensitized with BCG cell walls, and then challenged intravenously 3 weeks later with old tuberculin did not release MIF into the circulation. When T-cells were injected at least 10 days before challenge, however, MIF appeared.

Animals

Cellular source of interferons in the circulation of mice with delayed hypersensitivity.

The cellular origins of type I and type II interferons released into the circulation of mice with delayed hypersensitivity were investigated. We determined the effect of treatment with various immunosuppressive agents, including cyclophosphamide, cycloheximide, antithymocyte serum, and whole-body X-irradiation, on the release of interferons after intravenous injection of specific (old tuberculin) or nonspecific (lipopolysaccharide) stimuli. The results suggest that (i) a heterogeneous population of lymphocytes (T and B cells) produces type II interferon, (ii) type I interferon is produced by a different cell population, and (iii) type II interferon is produced de novo after challenge with old tuberculin of mice sensitized with Mycobacterium bovis BCG.

Antilymphocyte Serum

Production of migration inhibitory factor in inbred rats.

Strains of genetically inbred rats representative of the known Ag-B groups produced migration inhibitory factor in response to immunization with live bacillus Calmette-Guerin bacilli and intracardiac challenge with old tuberculin; the assays were performed by both in vitro and in vivo methods. None of the strains immunized in this fashion developed delayed hypersensitivity skin reactions to purified protein derivative.

Animals

T and B lymphocytes in the regulation of delayed hypersensitivity.

A correlation was demonstrated between the transient nature of a) delayed intradermal responses of guinea pigs sensitized to hen egg albumin in incomplete Freund's adjuvant and b) the proliferative response of sensitized lymphocytes to the specific antigen. Spleen cells from sensitized animals suppressed the proliferative response of lymph node cells to specific antigen. This suppression was dependent on the dose of spleen cells and the time of their removal after sensitization. Thymus cells were suppressive to a lesser extent, and their activity was not correlated with the time of removal after sensitization. Separation of spleen and thymus cells into T and B populations indicated that the B cell was the major suppressor cell in the spleen, while the T cell in the thymus had a similar but less pronounced action.

Animals

Migration inhibitory factor and type II interferon in the circulation of mice sensitized with mycobacterial components.

Migration inhibitory factor (MIF) and type II interferon were released into the circulation after mice had been sensitized i.v. with a bacillus of Calmette and Guerin (BCG) cell-wall-in-oil vaccine and then challenged four weeks later with 50 mg old tuberculin. At least two components of BCG, protein (PPD) and lipid (P-3), have been identified which are essential for the type of sensitization in which mediators are released after appropriate challenge. The route of sensitization had a marked effect on the development of delayed footpad reactions, release of lymphokines, and resistance to infection with virulent tubercle bacilli. Sensitization by the subcutaneous route tended to induce more pronounced delayed footpad reactions, whereas the i.v. route of sensitization was associated with maximum release of mediators. A close correlation existed between the conditions of sensitization that resulted in maximum production of lymphokines (MIF and Type II interferon) and those that caused protection against aerosol challenge with a virulent strain of Mycobacterium tuberculosis.

Animals