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Biomedical subjects

I Green

Publications and source records attributed to I Green.

At least 109 records · Page 6Linked to original sources

Identification of a tumor-associated antigen of the guinea pig L2C leukemia by using syngeneic antisera.

Inbred strain 2 guinea pigs immunized with L2C leukemia cells produced antibodies to L2C cells detected by 125I-protein A assay. L2C-associated tumor antigens were reacted with syngeneic antisera and analyzed by immunoprecipitation and SDS-polyacrylamide gel electrophoresis. These sera recognized idiotypic determinants on surface IgM molecules of L2C cells but did not recognize any determinants on normal strain 2 spleen cells. Thus, determinants on IgM molecular act as tumor-associated antigens in the L2C system and can be detected by syngeneic sera.

Animals↗

Solubilization and partial characterization of a tumor-associated transplantation antigen of the guinea pig L2C leukemia.

A tumor-associated transplantation antigen (TATA) from guinea pig L2C leukemia cells was solubilized by different methods. It was found that the 3 M KCl extraction yielded the most immunogenic TATA of L2C cells. Immunization of normal strain 2 guinea pigs with this extract in complete Freund's adjuvant gave complete protection against a subsequent challenge with tumor cells. Further fractionation of the KCl extract of L2C cells by Sephadex G-200 chromatography suggested that the immunogenic activity was present in the fraction containing materials with estimated m.w. of less than 20,000 daltons.

Ammonium Sulfate↗

The role of the macrophage as the stimulator cell in contact sensitivity.

In this study we examined the requirement for the type of stimulator cell for thymus-derived (T) lymphocyte activation to simple chemical haptens. T cells from picryl chloride-immune guinea pigs were challenged in vitro with various trinitrophenyl (TNP)-conjugated syngeneic stimulator cells and the extent of activation was determined by an increase in DNA synthesis. Hapten-specific T cell activation occurred with TNP-conjugated peritoneal exudate cells (PEC) and purified macrophages but not with TNP-conjugated erythrocytes, thymocytes, or nonadherent lymph node cells or PEC. In addition, T cell activation also occurred with TNP-conjugated guinea pig leukemia cells, but only in the presence of macrophages. Furthermore, it was shown that macrophages were required to process and/or present TNP-conjugated leukemia cell antigens rather than simply providing a growth-promoting function. These results suggest that a macrophage-like stimulator cell is required for hapten-specific T cell activation and that this particular stimulator cell may be important in contact sensitivity.

Animals↗

Human suppressor T cells induced by concanavalin A: suppressor T cells belong to distinctive T cell subclasses.

Human peripheral blood lymphocytes were stimulated by concanavalin A (Con A) and then evaluated by their suppressive activity for thymus-derived (T) cell- and bone marrow-derived (B) cell-proliferative responses to mitogen and allogeneic cells. Con A-activated T cells markedly suppressed these responses, but Con A-activated B cells failed to demonstrate suppressor activity. Discontinuous bovine serum albumin (BSA) density gradient separation of T cells which had been activated by Con A demonstrated that a fraction containing blast cells as well as fractions containing unproliferated cells manifest the same degree of suppressor capabilities. However, when density gradient separation of T cells followed by subsequent incubation with Con A was performed, fractions of proliferating cells of low density exhibited no suppression; a fraction containing high density T cells produced marked suppression, but this fraction incorporated only little thymidine in response to Con A. Thus, these studies indicate that Con A-induced suppressor T cells belong to a distinctive subpopulation which has already been programmed to express this function before exposure to Con A and that cell proliferation may not be a prerequisite for the development of such suppressor T cells.

B-Lymphocytes↗

Localization of receptors for activated complement on visceral epithelial cells of the human renal glomerulus.

Receptors for activated C3 have recently been demonstrated to be present in glomeruli of normal human kidneys. In the present communication, the precise location of these receptors within the renal corpuscle was studied with scanning electron microscopy. By this technique, the glomerular complement receptor (GCR) was found to be located on the visceral epithelial cell of the renal corpusle. This epithelial cell location was confirmed by comparison of in vitro GCR activity with the location of immunoglobulin and C3 deposited in vivo. Renal tissues in which Ig and C3 had been deposited in vivo diffusely in subepithelial loci had no in vitro GCR activity. Renal biopsies not showing Ig or C3 deposition or biopsies with Ig and C3 in the mesangium retained GCR activity. These results further confirm an important role for GCR in the trapping and deposition of C3 in some forms of immunologically mediated renal disease.

Binding Sites↗

The glomerular complement receptor in immunologically mediated renal glomerular injury.

We examined 25 renal-biopsy specimens to determine whether there is a relation between immunologically mediated renal diseases and the activity of complement receptors that selectively bind antigen-antibody complexes containing activated third component of complement (C3b). These receptors have been termed glomerular complement receptors. Renal lesions associated with in vivo deposition were associated with a loss of receptor sites as demonstrated by reduced or absent in vitro binding of C3b-coated test reagents by glomerular complement receptor. These findings suggest that binding of complement containing immune complexes to glomerular complement receptors in human subjects may participate in the immunopathologic processes of certain immune-complex-mediated renal diseases.

Antibody Specificity↗

Mutant lines of guinea pig L2C leukemia. I. Deletion of Ia alloantigens is associated with a loss in immunogenicity of tumor-associated transplantation antigens.

Five different lines of a strain 2 guinea pig leukemia (L2C) which had been carried in different laboratories share certain chromosomal markers and have a common surface immunoglobulin idiotypic determinant indicating that they have a common origin. All these leukemic lines have on their surface of the B alloantigen (equivalent of the murine H-2K and H-2D antigens) and four of these five lines have on their surface the Ia alloantigens normally present on the strain 2 lymphocytes. The result of a study of the growth and rejection patterns of these leukemias in inbred and random-bred guinea pigs of selected histocompatibility type indicates that both the B and Ia antigens can act as transplantation antigens in guinea pigs. Immunization protection tests in syngeneic animals demonstrated that the four Ia-positive leukemias possessed a tumor-associated transplantation antigen (TATA), while the one Ia-positive leukemias possessed a tumor-associated transplantation antigen (TATA), while the one Ia-negative leukemia by this criteria did not appear to have TATA. However, crisscross immunization protection tests demonstrated that preimmunization of syngeneic animals with an Ia-positive L2C line lead to a subsequent protection against challenge with the Ia-negative leukemia. Immunization with the Ia-negative line never protected against a subsequent challenge with any of the leukemic cells of L2C lines. These results strongly suggest that the Ia-negative leukemia possessed a TATA that can be recognized but is not itself immunogenic, and also indicate that Ia antigens on L2C cells are functionally associated with TATA and can act as immunological carries for tumor transplantation determinants.

Animals↗

Characterization of virus-free guinea pig tumors induced by Kirsten sarcoma virus.

Tumors were induced by Kirsten sarcoma virus (KiSV) in an inbred guinea pig, strain 13. The tumor cells were established in culture and characterized. The KiSV-induced sarcoma cells were virus-free and nonproducing; however, they contained resuable sarcoma genome. A type B guinea pig retravirus was readily activated from the tumor cells after induction with 5-bromodeoxyuridine (BUDR). BUDR induction of guinea pig retravirus was further enhanced by treatment with dexamethasone, a synthetic glucocorticoid hormone.

Animals↗

Mutant lines of guinea pig L2C leukemia. II. Comparative cytogenetic studies and banding analyses of normal and leukemic karyotypes.

Chromosomes of normal guinea pig (strain 2) cells and of cell lines dervied from a spontaneously arising leukemia were analyzed in detail. All cell lines studied, LG-L2C, GH-L2-C, BZ-LC, and EN-L2C, contained one M1 marker and two X chromosomes, in addition to other chromosome abnormalities specific for each cell line. The presence of the M1 marker and the two X chromosomes confirmed that all of these leukemic cell lines are derived from one ancestral line. Comparison of the chromosome markers and immunologic characteristics of these lines revealed that possibly the gene involved in the determination of C3 receptor sites is located on the terminal portion of the long arm of chromosome No. 2, but no other correlations could be made.

Animals↗

Heterologous sera: a target for in vitro cell-mediated cytotoxicity.

During the course of studies in inbred Strain 2 Guinea pigs on in vitro cell-mediated cytotoxicity to viral induced fibrosarcomas, it was observed that fetal calf serum in the medium in which the target cells were grown was responsible in some instances for much of the cytotoxicity observed. This fetal calf serum-specific cytotoxicity seemed mainly mediated by T cells and appeared to be independent on histocompatibility between target and killer cells.

Animals↗

Mutant lines of guinea pig L2C leukemia. III. The reaction of an alloantiserum detecting idiotypic determinants on a clonally derived guinea pig B cell leukemia with IgM and Ia molecules.

An alloantiserum was prepared in a strain 13 guinea pig against the GH line of the strain 2 guinea pig L2C leukemia. This serum contained antibodies to both IgM and Ia molecules. After absorption with normal spleen cells from a strain 2 guinea pig, this antiserum no longer reacted with strain 2 cells, but detected idiotypes on the IgM molecules of the L2C leukemia. These idiotypes were on the same IgM molecules detected by a xenogeneic sheep anti-L2C Fab mu antiserum. As assayed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the idiotype-bearing IgM molecules were synthesized by the cell, composed of normal sized mu and light chains, appeared on the cell surface as monomeric IgM, and were the only immunoglobulin molecules present on the cell. Although the alloantiserum potentially contained antibodies to unique Ia idiotypic determinants, none were found. Furthermore, the anti-IgM idiotype antisera did not react with any Ia-like molecules.

Animals↗