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R W Finberg

Publications and source records attributed to R W Finberg.

104 records · Page 6Linked to original sources
PubMed1984

Sendai virus-specific T cell clones. V. Induction of a virus-specific response by antiidiotypic antibodies directed against a T helper cell clone.

We used an antiidiotypic antibody directed against a Sendai virus-specific T helper cell clone to stimulate an immune response in vivo. In addition, the antiidiotypic antibody induced T cells that mediated a delayed-type hypersensitivity (DTH) response in several different mouse strains. Induction of the DTH response by the antiidiotypic antibody, in contrast to the DTH responses induced by virus, demonstrated a remarkable lack of H-2 restriction.

Animals↗
PubMed1984

Sendai virus-specific T-cell clones: induction of cytolytic T cells by an anti-idiotypic antibody directed against a helper T-cell clone.

We used a monoclonal anti-idiotypic antibody that is directed against a Sendai virus-specific helper T-cell clone to induce an anti-viral immune response in vivo. Splenocytes primed with the anti-idiotypic antibody mediated an antigen-specific cytolytic response. Preimmunization of mice with the anti-idiotypic antibody resulted in protection against a subsequent lethal infection with Sendai virus.

Animals↗
PubMed1984

Characteristics and functions of Sendai virus-specific T-cell clones.

Several murine Sendai virus-specific T-cell clones were characterized in vitro and in vivo. All T-cell clones were phenotypically Thy-1.2+, and most clones were Lyt-1+,2-; one T-cell clone was Lyt-1-,2-. Some of the clones proliferated in response to antigen presented on I region-compatible stimulator cells. Proliferation could be inhibited by monoclonal antibodies directed against class II antigens. Clones which proliferated in response to antigen secreted lymphokines which could be identified as Interleukin 2 and Interleukin 3. All of the clones tested in vivo induced a delayed-type hypersensitivity response in syngeneic mice challenged with antigens. Depending on the experimental conditions chosen, Interleukin 2-producing clones as well as non-Interleukin 2-producing clones mediated help for stimulation of cytolytic T lymphocytes.

Animals↗
PubMed1982

Cellular immunity to Bacteroides fragilis capsular polysaccharide.

The polysaccharide capsule of Bacteroides fragilis has been shown to be important in the virulence of the organism. The capsular polysaccharide (CP) of B. fragilis has been extensively purified. Using a murine model of intraabdominal abscess formation, we have been able to demonstrate cellular immunity to the capsular polysaccharide of B. fragilis. Immunization of C57BL/10J mice with the CP over 5 wk prevents abscess formation when the mice are challenged with B. fragilis intraperitoneally. This immunity can be transferred to naive mice with spleen cells from immune animals. The immune cells bear Thy-1.2 and Ly-2.2 antigens. The immune response has been shown to be antigen specific, but not H-2 restricted. The possibility that these immune cells are suppressor T cells is discussed. The experimental system presented provides a model for the examination of the cellular interactions responsible for abscess formation and the cellular response to bacterial pathogens.

Abdomen↗
PubMed1982

Sendai virus-specific T cell clones II. Induction of interferon production by Sendai virus-specific T helper cell clones.

Interferon (IFN) was detected upon co-culture of cloned Sendai virus (SV)-specific T lymphocyte with SV-presenting syngeneic stimulator cells. The antiviral activity was defined as IFN-alpha, beta. The T cell clones, upon contact with antigen-presenting stimulator cells, stimulated adherent cells present in the stimulator cell population to secrete IFN. Induction of IFN production was independent from interleukin 2 production by the T cell clones.

Animals↗
PubMed1982

Identification of idiotypic receptors on reovirus-specific cytolytic T cells.

Cytolytic T lymphocytes (Tc) specific for cells infected with reovirus type 3 were shown to lyse an uninfected B-cell hybridoma line (designated 87.92.6). This hybridoma expresses and secretes an anti-idiotypic antibody that reacts with a monoclonal antibody (termed G-5). G-5 recognizes a domain on the hemagglutinin of the reovirus that is relevant to virus tropism. The Tc cell response was H-2 restricted and could be inhibited by G-5. As shown by limiting dilution analysis, identical clones lysed reovirus-infected and anti-idiotype-bearing target cells. Tc cells induced by a variant of wild-type reovirus type 3 (immunologically selected by resistance to neutralization by G-5) were unable to recognize the anti-idiotype-bearing cells although they lysed reovirus type 3-infected tumor cells. We conclude that Tc cells must bear determinants that bind anti-idiotype molecules and, furthermore, that B cells and cytolytic T cells can share these idiotypic determinants.

Animals↗
PubMed1982

Antigen-specific suppression of cytotoxic T cell responses: an idiotype-bearing factor regulates the cytotoxic T cell response to azobenzenearsonate-coupled cells.

When A/J mice are injected subcutaneously with azobenzenearsonate- (ABA) coupled spleen cells, their splenocytes contain primed ABA-specific cytotoxic T lymphocyte (CTL) precursors. Animals that are not primed in vivo do not develop vigorous CTL activity when assessed after in vitro culture with ABA-coupled stimulators. Suppressor molecules derived from ligand-induced first-order ABA-specific suppressor T cells were evaluated for their ability to limit cytolytic T cell development. We have shown that an idiotype-bearing, hapten-specific suppressor factor suppresses priming for CTL in an H-2-unrestricted but allotype-restricted manner. The implication of these studies to regulatory networks is discussed.

Animals↗
PubMed1981

Ir gene control of the cytotoxic T lymphocyte response to Sendai virus: H-2k mice are low responders to Sendai.

H-2k mice generate a secondary in vitro cytotoxic T lymphocyte response to Sendai virus 20- to 100-fold weaker than those of other haplotypes tested (H-2b,d,q,s). This immune response defect maps to both H-2K and H-2D. H-2k x H-2d F1 mice (responder x nonresponder) only lyse targets that have the d allele at H-2K and/or H-2D. H-2k targets are equally lysable with anti-Sendai antibody. Furthermore, H-2k mice demonstrate normal antibody and T cell proliferation responses to Sendai virus. The Ir gene defect therefore appears to be limited to the generation of the cytotoxic T lymphocytes.

Animals↗
PubMedDate not supplied

Use of a model of intraabdominal sepsis for studies of the pathogenicity of Bacteroides fragilis.

Over the past eight years, a Wistar rat model for intraabdominal sepsis has been developed and used to document the role of obligate anaerobes in this infections. The ability of Bacteroides fragilis alone to provoke abscesses in this model system is due to a species-specific capsular polysaccharide. It has been shown that active immunization of rats with capsular polysaccharide of B. fragilis protects these animals against the development of abscesses after intraperitoneal challenge with this species. Passive transfer of hyperimmune globulin provided protection against B. fragilis bacteremia in nonimmune, challenged animals but did not confer protection against abscess development. Adoptive transfer of spleen cells from immunized to nonimmunized animals resulted in protection against abscess following challenge with B. fragilis, a finding suggesting that a T cell-dependent immune response was involved in protection. It has also been shown that inbred, congenitally athymic OLA/Rnu rats that were actively immunized developed abscesses despite the presence of capsular antibody, as did 100% of unimmunized athymic control rats. However, no phenotypically normal, littermate control rats that were actively immunized developed abscesses. These data suggest that a T cell-dependent immune response is an important part of immunity to B. fragilis. Additional experiments are being performed to better define the immunologic and chemical basis for the protection afforded by immunization.

Abscess↗