Antigen-specificity of continuous T cell lines.
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Animals↗
Biomedical subjects
W R Thomas
Publications and source records attributed to W R Thomas.
Anti-T-cell idiotype activity in serum of mice injected with syngeneic hapten-specific T-cell lines.
T cells able to mediate specific delayed type hypersensitivity (DH) in mice in response to the haptens azobenzenearsonate (ABA), oxazolone (OX), and picryl chloride have been grown in continuous cultures. They were tested for their ability to react with the hapten in vitro and to induce anti-idiotype antibody in syngeneic mice. Incubation in vitro with OX-glycine blocked the ability of an anti-OX cell line to produce DH in vivo but had no effect on an anti-ABA cell line. However, this was inhibited by ABA conjugated to bovine serum albumin (ABA-alb) but not by irrelevant haptens such as OX-glycine or trinitrophenyl-alb. Antisera prepared by immunizing syngeneic mice with the anti-OX line blocked the inhibitory effect of OX-glycine on that line but did not reverse the effect of ABA-alb on the anti-ABA line. Neither normal mouse serum nor inappropriate anti-line antisera could influence the effect of OX-glycine on the anti-OX line. When given alone to naive mice, a specific anti-line antiserum induced DH specific for the antigen to which the line was responsive. Thus, for example, antiserum directed to an anti-OX line produced OX-specific DH. The results suggest that anti-T-cell idiotype antibodies can be induced by immunizing mice with syngeneic antigen-specific T-cell lines and that these antibodies can block the specific in vitro interaction of antigen with the corresponding antigen-specific T cells and induce specific DH in vivo.
Animals↗
Contact sensitivity to azobenzenearsonate and its inhibition after interaction of sensitized cells with antigen-conjugated cells.
Painting mice on the skin with the diazonium salt of p-arsanilic acid elicited two types of T cell activity. One was restricted by the I region of the major histocompatibility complex and was responsible for the transfer of azobenzenearsonate (ABA) sensitivity to naive mice. The other was H-2K restricted and could be demonstrated by its ability to interact specifically with ABA-coupled cells in vitro and to inhibit nonspecifically the transfer of sensitivity by cells sensitized either to ABA or to another antigen. Free antigen, or antibody directed against the cross-reactive idiotype on the anti-ABA antibodies of A/J mice, could inhibit the H-2K-restricted suppressive activity induced in the ABA immune A/J cells.
Animals↗
Induction of delayed-type hypersensitivity to azobenzenearsonate by a monoclonal anti-idiotype antibody.
Azobenzenearsonate (ABA)-specific sensitivity was induced in A/J mice by injecting a monoclonal anti-idiotype reagent, 14A, directed against a determinant present on a minor subpopulation of immunoglobulin molecules within the anti-ABA antibodies of A/J mice. Sensitivity was transferrable by purified T cells and this was abrogated by treating the cells with 14A, rabbit anti-mouse immunoglobulin and complement, not by treatment with only the last two reagents. The transfer was restricted by the K-end of the major histocompatibility complex.
Animals↗
Suppression of antibody responses by cells from mice treated with picryl sulfonic acid: T cells that suppress IgG antibody without inhibiting concomitant IgE responses.
T cells from mice injected with picryl sulfonic acid (PSA) can inhibit the anti-trinitrophenyl (TNP) antibody responses of mice produced after skin painting with picryl chloride (PCl). This had unusual specificity because the cells could inhibit IgG PFC responses in draining lymph nodes by 90% without affecting anti-TNP IgE responses as measured by heterologous adoptive cutaneous anaphylaxis. Although showing specificity for the class of antibody, the suppressors did inhibit IgG antibody responses to another sensitizer, oxazolone, although to a lesser degree. Responses to TNP-KLH, however, were unaffected.
Anaphylaxis↗
Differences in the ability of T cells to suppress the induction and expression of contact sensitivity.
T cells from mice injected with picryl sulphonic acid (PSA) inhibit the expression of contact sensitivity to picryl chloride. Adult thymectomy (aTx) prevents the production of cells which inhibit the effector stage but cells from aTx mice are, however, still able to suppress the induction of contact sensitivity. These cells are antigen-specific T cells but unlike suppressor cells for the effector phase, they cannot be produced in cyclophosphamide (Cy)-treated mice. Similar properties have been reported for cells inhibiting the DNA synthesis in lymph nodes of mice painted with picryl chloride. It was also shown that cells from Cy-treated but non-thymectomized mice could not inhibit sensitivity when injected at the time of sensitization, i.e. suppressors of the effector phase, which are induced in Cy-treated mice cannot inhibit sensitivity when injected at the induction phase. These results show there are distinct mechanisms and probably distinct cells which inhibit the induction and expression of contact sensitivity.
Animals↗
Suppressor cells and the handling of antigen.
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Animals↗
Antigen-specific mast cell degranulation in contact sensitivity to picryl chloride. An early event.
Mast cells from the peritoneum of mice painted with the contact sensitizing agent picryl chloride degranulate when exposed to antigen (TNP) in vitro. Degranulation was consistently demonstrated 4 days after painting which associated with the ability of mice to produce contact sensitivity reactions as measured by ear swelling and radiometric assays. Serum reagin or reagin-producing cells could not be detected until 6 days after painting but TNP-phage neutralizing activity was detected after 2 days. Mast cell degranulation could be elicited by TNP or DNP derivatives indicating the involvement of antibody.
Animals↗
Experimental erythrocyte autoimmunity. I. Mice congenic for immunoglobulin allotypes vary in production of autoantibodies but produce suppressor cells not restricted by allotypes.
Erythrocyte autoantibodies can be elicited in mnce by injections of rat RBC which are cross-reactive with mouse RBC. This report shows that induction of autoantibodies is dependent, in part, on gene(s) outside the H-2 complex. Using CBA mice congenic for Ig allotype and the F1 and F2 hybrids, a higher incidence of autoantibody production was observed in mice bearing the Ig allotype 1b (1b/b or 1a/b) in contrast to mice homozygous for the allotype Ig-1a. Serum haemagglutination titres against rat RBC were not reduced in the groups of mice with the lower incidence of autoantibody production. A probable explanation for these observations is that the change in Ig allotype is associated with some change in the variable region determining autoimmune specificity that is governed by VH genes linked to allotype genes. The transfer of 30 x 10(6) spleen cells from Coombs' positive mice to syngeneic recipients before starting the immunization regime with rat RBC suppressed autoantibody production and enhanced antibody production against rat RBC. These suppressor cells were effective in congenic mice and in F1 hybrids, which suggest that the Ig allotype is not a crucial site for the effector stage of suppression of this autoimmune response.
Animals↗
Distribution of immunogenic cells after painting with the contact sensitizers fluorescein isothiocyanate and oxazolone. Different sensitizers form immunogenic complexes with different cell populations.
The distribution of fluorescent cells in the draining lymph nodes of mice painted with the contact sensitizing agent fluorescein isothiocyanate (FITC) was investigated using a fluorescence-activated cell sorter. Up to 30% of the cells were fluorescent after 18 h and this decreased thereafter becoming undetectable after 4-5 days. Most of the fluorescent cells were morphologically lymphocytes, theta - ve and adherent to nylon wool. Immunogenicity of these cells was tested by injecting them into the footpads of normal mice and measuring contact sensitivity after 6 days. This was restricted to large cells which represented less than 5% of the white cell population and nearly all of which became fluorescent after skin painting. The large fluorescent cells were a mixture of monocytes and lymphocytes. Most of the lymphocytes had surface immunoglobulin. The immunogenicity was reduced by nylon filtration but was not affected by silica and anti-theta. These results showed that the immunogenicity is not associated with T cells. In contrast, similar immunogenic activity in the draining lymph nodes of mice painted with oxazolone is associated with T cells. The results therefore showed that different sensitizers form immunogenic complexes with different cell populations, perhaps in this case becuase of the different water solubilities of FITC and oxazolone. They also suggested that this may cause important differences in antigen presentation, for example in their association with different MHC products.
Animals↗
The prevention of superficial infection in neonates.
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Chlorhexidine↗
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↗
Contact sensitivity and the DNA response in mice to high and low doses of oxazolone: low dose unresponsiveness following painting and feeding and its prevention by pretreatment with cyclophosphamide.
Cyclophosphamide was used to assess the role of suppressor cells in the contact sensitivity reaction. A single painting with 300 microgram and 30 microgram oxazolone produced poor contact sensitivity reactions (ear swelling). Cyclophosphamide (200 mg/kg) 2 days before painting increased the response to the lower doses but had less effect on the response to 3 mg oxazolone. A single feed with 10 mg oxazolone caused strong contact sensitivity while lower doses (10-1000 microgram) caused poor responses. Cyclophosphamide increased the response to the lower doses but not to the highest dose of oxazolone. These results suggested that the poor response to painting and feeding lower doses of oxazolone was due to a suppressor system which was sensitive to cyclophosphamide. A different result was obtained when contact sensitivity was measured by arrival of radioactively labelled cells. Cyclophosphamide had the greatest effect on cell arrival when high doses were fed. This indicates that ear swelling and cell arrival measure separate aspects of the contact sensitivity response. The lower doses of oxazolone, which caused little contact sensitivity, reduced the response to a standard immunizing dose. This low dose unresponsiveness occurred after either painting or feeding (Chase-Sulzberger phenomenon). It did not occur in mice treated with cyclophosphamide before the first exposure to oxazolone. This suggested that the low dose unresponsiveness was due to suppressor cells. The response to oxazolone was also assessed by DNA synthesis in the regional lymph nodes. A small dose of oxazolone (30 microgram) caused a peak of DNA synthesis on day four while a high dose (3 mg) caused a peak on day three. Pretreatment with cyclophosphamide depressed the response to 30 microgram although it increased contact sensitivity. The secondary response was smaller than the primary on days 3, 4 and 5 after immunization but larger on day two. The depression but not the increase was prevented by cyclophosphamide and was probably due to a suppressor system.
Animals↗
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↗
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↗
Cigarette smoke and phagocyte function: effect of chronic exposure in vivo and acute exposure in vitro.
Phagocytic function was studied in mice chronically exposed to cigarette smoke, and the effects of in vitro exposure to cigarette smoke on macrophage activity were also assessed. Cultures of radiolabeled Pseudomonas aeruginosa were employed to investigate phagocyte activity in vivo and in vitro. Mice were exposed on weekdays to fresh cigarette smoke for periods up to 37 weeks and the bactericidal and clearance activity of their lungs was measured. Both pulmonary clearance and bactericidal activity was impaired. The clearance of intravenously injected bacteria from the blood of smoke-exposed mice occurred at the same rate as in control mice, but the accumulation of radiolabel by the liver was decreased. In addition, the rate of elimination of radiolabel from the liver was less than the controls. Macrophages exposed to cigarette smoke in vitro initially had a depressed phagocytic rate, but if phagocytosis over a prolonged period was measured it was eventually enhanced over the rate of control macrophages. The vapor phase of cigarette smoke could also transiently inhibit and then enhance the phagocytic activity.
Animals↗
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↗
Suppressor T cells which block the induction of cytotoxic T cells in vivo.
Mice pretreated with cyclophosphamide have an increased ability to produce anti-trinitrophenyl cytotoxic T cells after painting with the contact sensitizing agent picryl chloride. This could be abrogated by injecting normal cells or cells from mice exposed to trinitrophenyl derivatives at the time of painting. If the injection of cells was delayed until 1 day after painting specificity could be demonstrated. Normal cells and cells from mice injected with dinitrobenzene sulphonate were ineffective whereas cells from donors injected with picryl sulphonic acid were inhibitory. Inhibitory cells were also shown in mice painted with picryl chloride, particularly after adult thymectomy. Using this system it was found that cells from picryl chloride but not oxazolone painted mice were inhibitory when injected 1 day after painting the recipients. The suppressor cells from the mice injected with picryl sulphonic acid and from the mice painted with picryl chloride were shown to be cyclophosphamide sensitive T cells and were not affected by adult thymectomy. These properties have helped to classify the suppressor cells induced by trinitrophenyl derivatives.
Animals↗