Biomedical subjects

M C Watkins

Publications and source records attributed to M C Watkins.

25 records · Page 2Linked to original sources

PubMed1979

Selective expression of antibody classes and contact sensitivity affected by genes in the major histocompatibility complex.

This report describes IgM, IgG and IgE antibody and contact sensitivity responses of strains of mice congenic at the major histocompatibility complex (MHC) to skin painting with picryl chloride or oxazolone. B10 had low responses of all classes to picryl chloride. This was also reflected by the DNA synthesis occurring in their draining lymph nodes after painting. B10BR were high responders to picryl chloride for all classes but B10A and B10D2 were high responders for all classes except IgE. This presents evidence that genes in the MHC can selectively control antibody classes. The contact sensitivity response of the congenics to oxazolone confirmed the low previously described responsiveness of B10 mice. Antibody responses to oxazolone (agglutinin and reagin) were low for all congenics with B10 backgrounds.

Agglutinins↗

PubMed1979

Suppression of antibody responses by cells from mice painted with picryl chloride.

T cells from mice painted with picryl chloride inhibit secondary IgG anti-TNP antibody responses of normal mice to the sensitizer. Like other suppressor T cells produced after painting which inhibit DNA synthesis and the generation of cytotoxic T cells, these cells could be produced in adult thymectomized mice but not by mice treated with high doses of cyclophosphamide (250 mg/kg). The cells had to be injected within 48 h of a primary painting to inhibit the response to challenge 2-3 weeks later. This associated with their ability to inhibit DNA synthesis in draining lymph nodes after a primary painting. Double transfer experiments using spleen and lymph node cells failed to show any further activation or induction of suppressor function after challenge with antigen. As judged by the ability of anti-theta treated cells from suppressed mice to function as anti TNP primed B cells in adoptive responses to TNP-KLH no defect in B-cell memory was found. When, however, the ability of painting with picryl chloride to prime for challenge with TNP-KLH was used as a measure of B-cell function in situ it was found that the cells could inhibit responses. Responses to primary and secondary injections of TNP-KLH were not inhibited.

Administration, Topical↗

PubMed1979

Suppressor cells for the afferent phase of contact sensitivity to picryl chloride: inhibition of DNA synthesis induced by T cells from mice injected with picryl sulfonic acid.

Previous reports have shown that picryl sulfonic acid (PSA) induces suppressor T cells that inhibit the effector phase of contact sensitivity, whereeas its DNP counterpart, dinitrobenzenesulfonate (DNBS) induces cells that inhibit the afferent phase of sensitization. Accordingly, cells from mice injected with DNBS, but not PSA, could be shown to inhibit the DNA synthesis in the lymph nodes that occurs during sensitization. It is now shown that PSA does induce T cells that suppress DNA synthesis but this can only be detected with enriched T cells or by using a regimen of PSA injection different frm previously used to induce suppressor cells for the effector phase. The T cells did not affect responses to oxazolone or dinitrofluorobenzene (DNFB) and were distinguishable from suppressors of the efferent phase in that they could be produced in adult thymectomized but not cyclophosphamide-treated mice. T cells from mice injected with DNBS that inhibited DNA synthesis to DNFB had the same properties.

Animals↗

PubMed1978

Antibody responses to contact sensitizing agents. Effect of sensitized cells.

Lymphocytes from mice immunized by painting with the contact sensitizing agent picryl chloride have been shown to produce regulatory effects on the DNA synthesis and contact sensitivity responses of normal mice painted with picryl chloride. This report describes the effect of these cells on antibody responses of normal mice to picryl chloride. Lymph node cells taken 5--7 days after painting increased early IgM antibody responses of normal mice to picryl chloride. Spleen cells were not effective. The increase was mediated by T cells as judged by anti-theta treatment and nylon wool filtration and could not be produced by killed, irradiated or allogeneic cells. A similar activity could be demonstrated in cells from mice painted with another contact sensitizing agent, oxazolone. The effect was strictly specific and cells from mice painted with picryl chloride or oxazolone would only increase responses to picryl chloride or oxazolone, respectively, even when presented with a mixture of the two antigens. The cel-s increasing antibody production were different from T cells previously shown to mediate contact sensitivity and T cells shown to regulate DNA synthesis in that they could not be generated in adult-thymectomized mice.

Animals↗

PubMed1978

Induction and modification of anti-TNP reaginic and IgG antibody responses by reactive trinitrophenyl derivatives.

The anti-TNP antibody response of mice exposed to picryl chloride is a response where IgE antibody can be preferentially produced. Skin-painting with picryl chloride induces IgM, IgG and IgE antibody. After repeated painting the titre and persistence of the IgE but not IgG antibody is increased. Feeding picryl chloride does not induce antibody but it does produce unresponsiveness for IgG without affecting responsiveness for IgE. Injection of picryl sulphonic acid produces unresponsiveness for both classes. The unresponsiveness (induced by feeding or injection) is found for responses to picryl chloride but responses to TNP-KLH are barely affected. Both the IgE and IgG responses to picryl chloride are initiated in the lymph nodes and then develop in the spleen. IgE and IgG antibody production are both T-cell dependent but not influenced by adult thymectomy.

Animals↗

PubMed1978

Reaginic antibody to contact sensitizing agents. Occurrence of cells which supress IgG and not reagin responses.

Mice painted with the contact sensitizing agent picryl chloride produce IgG and reaginic or IgE-type antibody. They concomitanly produce suppressor cells which can inhibit IgG responses of normal mice to picryl chloride. These cells were produced between 3 and 7 days after primary sensitization (skin painting) and were T cells, as evidenced by their sensitivity to anti-theta serum and by their passage through nylon wool columns. Although they inhibited IgG responses they did not significantly change IgE titres. This correlates with a previous observation that repeated painting with picryl chloride increased IgE and not IgG responses.

Animals↗

PubMed1976

Reaginic antibody produced in mice with contact sensitivity.

Mice produced reaginic antibody within 1 wk of painting with the contact sensitizing agent picryl chloride. The titers, measured by passive cutaneous anaphylaxis in rats, increased after repeated applications of picryl chloride. In contrast, serum agglutinins did not increase after two applications of picryl chloride. Reagin was also elicited by another contact sensitizing agent, oxazolone. Some strain variation of the response to picryl chloride was found, with CBA mice being good responders and BALB/c and C57BL/10 mice being poor responders.

Animals↗