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Biomedical subjects

G Haughton

Publications and source records attributed to G Haughton.

At least 73 records · Page 4Linked to original sources
PubMed1978

A simple method for the preparation of antisera specific for murine immunoglobulin heavy chains.

Rabbit antisera were prepared against mouse immunoglobulin mu and gamma chains by immunizing rabbits with their own erythrocytes coated with murine anti-rabbit erythrocyte immunoglobulin. In the preparation of these antisera, we exploited the observation that the primary immune response in C57BL/10ScSn (B10) mice is almost exclusively IgM, while hyperimmune antiserum of A/WySn (A) is mostly IgG. After appropriate absorption with thymocytes and rabbit erythrocytes (Rrbc) coated with B10 or A antiRrbc Ig, the sera were shown to be specific by immunoelectrophoresis, indirect immunofluorescent staining, and complement-mediated cytotoxicity. This technique is simple, requires almost no equipment, and a large quantity of specific antiserum can be prepared quite economically.

Animals↗
PubMed1978

Antigen-induced murine B cell lymphomas. I. Induction and characterization of CH1 and CH2.

Two unusual murine lymphomas, designated CH1 and CH2, were produced in the newly developed double congenic strain of mice, B10 H-2a H-4b p/Wts. Both tumors lack the T cell-specific antigen (thy-1), but express cell surface immunoglobulin and the H-2K, H-2D, and Ia specificities determined by the H-2a haplotype. Further studies have demonstrated that these tumors represent "early" B cells in that they express surface IgM (mu heavy and lambda light chains), but do not bear surface delta, gamma, or alpha heavy chains. CH1 and CH2 lack surface C3 receptors and results from assays for Fc receptors have proven variable. A competition radioimmunoassay directed against the gp71 group-specific antigen of Friend leukemia virus has shown that there is a murine leukemia virus associated with these tumors, however, we have been unable to establish a causal relationship between the virus and this malignancy. A comparison of the surface characteristics of these tumors with other mammalian B cell lymphomas is presented.

Animals↗
PubMed1978

Antigen-induced murine B cell lymphomas. II. Exploitation of the surface idiotype as tumor specific antigen.

In the accompanying report, we have described the characterization of two unusual murine B cell lymphomas, CH1 and CH2. A heterologous antiserum, which we refer to as "anti-idiotype" serum, has been raised to the detergent-solubilized surface immunoglobulin of CH1. The following criteria have established that this antiserum is specific for the CH1 tumor and that it reacts with V region determinants of the tumor surface IgM: 1) the antiserum reacts with CH1 tumor cells, but not normal mouse lymphoid cells or CH2 tumor cells, in indirect immunofluorescence and C-dependent cytotoxicity testing, 2) capping with the anti-idiotype serum removes all or most of the tumor surface Ig, 3) the antiserum forms a single band of precipitation against serum from CH1 tumor-bearing mice, when tested by double diffusion precipitin analysis, and 4) a single band of precipitation is formed in the electrophoretic migration position of IgM when the anti-idiotype antiserum is tested against serum from CH1 tumor-bearing mice in immunoelectrophoresis. Furthermore, we have demonstrated that this antiserum is useful in monitoring tumor growth and is a potent immunotherapeutic agent. Specifically, 50% of mice injected with a lethal tumor inoculum and given a small dose of anti-idiotype serum 2 days later remain tumor free, whereas all tumor-challenged control mice died within 30 days.

Absorption↗
PubMed1977

H-2 effects on cell-cell interactions in the response to single non-H-2 alloantigens. I. Donor H-2D region control of H-7.1-immunogenicity and lack of restriction in vivo.

Genes in the H-2 complex regulate the relative immunogenicity of the H-7.1 histocompatibility alloantigen, as measured by survival times of H-7.1-incompatible skin grafts in vivo. The gene controlling relative rejectability of H-7.1-incompatible grafts has been mapped to the H-2D region. H-7.1-incompatible skin grafts donated by H-2Db donors were rejected significantly more rapidly by H-2a/H-2b heterozygous recipients than similar H-7.1-incompatible grafts donated by H-2Dd donors. Further, there was absolutely no evidence of H-2 restriction in cytotoxic effector activity. In vivo cross-priming, as indicated by accelerated secondary graft rejection, was extensive. The efficiency of cross-priming was dependent upon the primary and secondary graft donor H-2 haplotypes.

Animals↗
PubMed1976

Antigenic cross-reactivity between adenocarcinoma of the breast and fibrocystic disease of the breast.

Peripheral lymphocytes obtained from 12 of 13 patients who had fibrocystic disease (FCD) of the breast were specifically cytotoxic to breast adenocarcinoma cells, as measured in vitro by the microcytotoxicity test. Sera from 6 women with active FCD or metastatic breast cancer could specifically block the cytotoxicity of lymphocytes from either population of patients against cancer cells. This implied extensive antigenic cross-reactivity between benign and malignant hyperplastic disease of the breast. Sera from 4 individuals clinically free of FCD or breast fibroadenoma (FAD) neutralized the blocking activity in the sera of patients with metastatic breast cancer. Patients "cured" of FCD or FAD represented a pool of potential plasma donors for immunotherapy of recurrent breast cancer.

Adenofibroma↗
PubMed1975

Antigenic cross reactivity between benign prostatic hyperplasia and adenocarcinoma of prostate.

Tissue cultures were established from biopsy specimens of adenocarcinoma of the prostate (ACP) and benign prostatic hyperplasia (BPH). Generally, peripheral blood lymphocytes from BPH and ACP patients were cytotoxic to both ACP and BPH cells, but not normal fibroblasts nor cells cultured from other types of malignant tissue. Peripheral blood lymphocytes from normal control patients or from patients with other types of cancer were not cytotoxic to ACP- or BPH-derived cells. These findings are consistent with a cross reactive autoimmune response in ACP and BPH patients, directed against a common antigen(s) present on both ACP and BPH cells.

Adenocarcinoma↗
PubMed1973

Suppression or augmentation of the antihapten response in mice by antibodies of different specificities.

We have measured the production by (C57 x CBA)F(1) mice of hapten-binding antibody in response to a standard dose of 50 microg of alum-precipitated NIP(12)-CG and the influence on this response of the prior administration of hyperimmune antisera raised against the homologous conjugate, the carrier globulin alone, the hapten conjugated to a non-cross-reactive carrier (NIP(4)-OA), or a related hapten (NP) coupled to CG. The homologous antiserum was strongly immunosuppressive; a dose capable of binding about 1% of the administered hapten caused significant suppression. High doses of anticarrier serum caused significant but modest suppression (about 50%); low doses had no effect. High doses of the serum prepared against NIP(4)-OA suppressed the 19 day response by more than 97%, while 100-1,000 times lower doses caused the response to be elevated to about double the control level. The antibodies responsible for immunosuppression could be removed from this serum, as could the NIP-binding antibodies, by absorption with NIP coupled through ethylenediamine to insoluble Sepharose. The ability of this serum to augment the response was not reduced by such absorption. Augmenting antibodies could be removed by absorption with HOP-BSA-Sepharose. Thus, immunosuppression and augmentation are functions of two different populations of antibody. The former are specific hapten-binding antibodies, the latter seem to be directed against new antigenic determinants created by coupling any of the family of haptens through lysine to protein carriers. In support of this contention, it was observed that rabbit antiserum to NP-CG, after absorption with CG-Sepharose, augmented the response of mice to standard immunization with NIP(12)-CG. Female mice produced significantly more NIP-binding antibody than did males.

Adsorption↗