dinitrobenzenes has been researched along with Hookworm-Infections* in 8 studies
1 review(s) available for dinitrobenzenes and Hookworm-Infections
Article | Year |
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Ontogeny and development of IgE-bearing B lymphocytes.
Topics: Animals; B-Lymphocytes; Bone Marrow; Cell Differentiation; Dinitrobenzenes; Hookworm Infections; Immunoglobulin E; Immunoglobulin G; Immunoglobulin M; Ovalbumin; Pokeweed Mitogens; Rats; Receptors, Antigen, B-Cell; Spleen | 1979 |
7 other study(ies) available for dinitrobenzenes and Hookworm-Infections
Article | Year |
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Possible approaches to turn off the IgE response.
Topics: Allergens; Animals; Antigens, Plant; B-Lymphocytes; Cell Differentiation; Dinitrobenzenes; Hookworm Infections; Humans; Immunoglobulin E; Mice; Nippostrongylus; Phytotherapy; Plant Proteins; Pollen; Polyglutamic Acid; Polylysine; Rats; Receptors, IgE; Receptors, Immunologic; Rhinitis, Allergic, Seasonal; T-Lymphocytes; T-Lymphocytes, Regulatory | 1982 |
Murine lymphocytes expressing Fc receptors for IgE (FcR epsilon). I. Conditions for inducing FcR epsilon + lymphocytes and inhibition of the inductive events by suppressive factor of allergy (SFA).
Topics: Animals; Antibodies; Antibodies, Monoclonal; B-Lymphocytes; Dinitrobenzenes; Epitopes; Female; Hookworm Infections; Immunoglobulin E; Immunosuppressive Agents; Lymphocyte Culture Test, Mixed; Lymphocytes; Male; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Organic Chemicals; Rats; Rats, Inbred BN; Rats, Inbred Lew; Receptors, Fc; Rosette Formation; T-Lymphocytes | 1981 |
Regulatory role of IgE-binding factors from rat T lymphocytes. I. Mechanism of enhancement of IgE response by IgE-potentiating factor.
T lymphocytes in the mesenteric lymph nodes of rats infected with Nippostrongylus brasiliensis spontaneously released a soluble factor that selectively potentiated the IgE-forming cell response of antigen-primed cells to homologous antigen. The factor could enhance the IgE response of DNP-OA-primed cells to DNP-HSA and T cell-replacing factor. In contrast, the treatment of OA-primed T cells with the factor failed to enhance either the IgE or IgG response of the mixture of DNP-KLH primed cells and OA-primed T cells to DNP-OA. The results collectively suggested that the target cells of the IgE-potentiating factor are B cells. Indeed, IgE potentiating factor was absorbed by B cells rather than T cells or thymocytes. Evidence was obtained that IgE-potentiating factor could be absorbed by IgE-bearing B cells or IgE-coupled Sepharose, indicating that the factor had affinity for IgE. It appeared that the potentiating factor bound to IgE-bearing B cells and selectively enhanced the differentiation of IgE-B cells to IgE-forming cells. It was also found that the major source of the factor was Fc epsilon R-bearing T cells. Topics: Absorption; Animals; Antibody-Producing Cells; B-Lymphocytes; Binding Sites, Antibody; Cell Differentiation; Cell-Free System; Dinitrobenzenes; Hookworm Infections; Humans; Immunoglobulin E; Ovalbumin; Rats; T-Lymphocytes | 1980 |
Regulatory role of IgE-binding factors from rat T lymphocytes. III. IgE-specific suppressive factor with IgE-binding activity.
Incubation with rat IgE of rat mesenteric lymph node cells obtained 8 days after infection with Nippostrongylus brasiliensis (Nb) resulted in the formation of soluble factors with affinity for IgE, i.e., IgE-binding factors(s). The factors were derived from T lymphocytes and were able to suppress an in vitro IgE response without affecting the IgG response. The minimum concentration of rat IgE for the induction of factor formation was 0.3 to 1.0 microgram/ml. Gel filtration of culture filtrates of the IgE-containing culture identified 2 components with IgE-binding activity; one component had a m.w. of between 10,000 and 20,000, and another component had a m.w. of between 25,000 and 50,000. Both factors could be purified by binding to IgE-Sepharose followed by elution at acid pH. Among the two IgE-binding factors, the lower m.w. component had the ability to suppress selectively the IgE response. In contrast to IgE-potentiating factor, which also had affinity for IgE, the IgE-suppressive factor failed to bind to lentil lectin Sepharose. Formation of IgE-specific suppressive factor was not limited to the lymphocytes obtained 8 days after Nb-infection. Incubation with IgE of lymphocytes obtained 4 wk after infection resulted in the formation of both IgE-specific suppressive factor and IgE-potentiating factor, and the activity of the suppressive factor was greater than that of the potentiating factor. Topics: Animals; Binding Sites, Antibody; Cells, Cultured; Chromatography, Gel; Dinitrobenzenes; Hookworm Infections; Immunoglobulin E; Lectins; Molecular Weight; Nippostrongylus; Ovalbumin; Rats; Rats, Inbred Lew; Rosette Formation; T-Lymphocytes | 1980 |
IgE levels in nude mice.
IgE levels in nude mice were estimated by the one-step single radial radiodiffusion method antisera prepared by immunization of guinea pigs with an IgE-rich fraction obtained from sera of normal mice infected with Nippostrongylus brasiliensis and immunized with DNP-ovalbumin in alum gel. 3 out of 8 nude mice had IgE levels significantly higher than those of normal mice. Topics: Animals; Dinitrobenzenes; Guinea Pigs; Hookworm Infections; Immunodiffusion; Immunoglobulin E; Immunoglobulin G; Mice; Mice, Inbred BALB C; Mice, Nude; Ovalbumin | 1979 |
Tolerizing effect of DNP-ficoll on IgE antibody production.
A/J and DBA/1 mice were infected with 750 third-stage larvae of Nippostrongylus brasiliensis and immunized with 1 mug dinitrophenylated N. brasiliensis extract (DNP-Nb) with 1 mg Al(OH)3 to produce high titers of anti-hapten IgG1 and IgE antibody. Partial tolerance to the production of anti-hapten IgG1 and IgE antibody could be induced by DNP-Ficoll from 5 weeks before to 1 week after the DNP-Nb immunization. The tolerized state persisted through the duration of the experiments. However, no tolerizing effect could be demonstrated on secondary antihapten IgE antibody production induced by DNP-Nb. Moreover, DNP-Ficoll failed to evoke anti-hapten IgG1 or IgE antibody production. Topics: Animals; B-Lymphocytes; Dinitrobenzenes; Female; Ficoll; Hookworm Infections; Immune Tolerance; Immunization Schedule; Immunoglobulin E; Immunoglobulin G; Immunologic Memory; Male; Mice; Mice, Inbred Strains; Nippostrongylus; Nitrobenzenes; Polysaccharides; Rats | 1977 |
Suppression of IgE antibody production in SJL mice. II. Expression of Ly-1 antigen on helper and nonspecific suppressor T cells.
Under appropriate conditions of immunization combined with irradiation, SJL/J mice show a high and persistent anti-DNP IgE antibody response. Spleen cells transferred from normal untreated SJL mice suppress this response. Elimination of Ly-1+ cells, but not of Ly-2+ cells, abolished the capacity of spleen cells to suppress the IgE response. Thus of the three T cell Ly subclasses presently identified, Ly-1, Ly-2,3, and Ly-1,2,3, the normal SJL spleen cell which suppresses the IgE response of irradiated-immunized SJL mice belongs to the Ly-1 set. It is not known whether this Ly-1 cell suppresses the IgE response directly or by helping another cell in the recipient. The carrier-specific helper cell activity for IgE and probably IgG1 antibody response belongs to Ly-1 subclass in the SJL strain also. Topics: Animals; Antibodies; Antibody-Producing Cells; Antigens; Dinitrobenzenes; Female; Hookworm Infections; Immunoglobulin E; Immunosuppression Therapy; Male; Mice; Mice, Inbred C57BL; Nippostrongylus; Rats; T-Lymphocytes | 1977 |