Search PubMed⌕ Search

Biomedical subjects

R Riblet

Publications and source records attributed to R Riblet.

61 records · Page 4Linked to original sources
PubMed1975

Induction of antiphosphorylcholine antibody formation by anti-idiotypic antibodies.

Anti-idiotypic antibodies have been used to mimic antigen in the mouse antiphosphorylcholine response in order to investigate the induction of precursors of antibody-forming cells. We have shown that interaction of anti-idiotype antibody with receptor antibody molecules induces the formation of antibodies that are specific for phosphorylcholine and carry the idiotypic determinants. This induction is dependent on the recognition of carrier determinants on the anti-idiotype antibody by helper T cells. We conclude that receptor antibody molecules on the surface of the precursors of antibody-forming cells deliver the antigenic signal for the induction of these cells.

Animals↗
PubMed1975

Genetics of mouse antibodies. II. Recombination between VH genes and allotype.

The BAB/14 (BALB/c. C57BL/Ka-Ig-1b/HZ) congenic mouse strain was found to respond to (4-hydroxy-3-nitrophenyl)acetyl (NP)-chicken globulin immunization with nonheteroclitic anti-NP antibodies as does the BALB/c inbred partner strain. This is in contrast to the heteroclitic anti-NP response of the C57BL/Ka allotype donor strain and indicates that the allotype linked VH-NP gene was inherited with the VH-DEX gene from BALB/C rather than with the allotype genes from C57BL/Ka. This verifies the interpretation of BAB/14 as an immunoglobulin gene recombinant. Two recombinants between VH-DEX and Ig-1 allogype genes have been found among 554 chromosomes tested yielding a recombination frequency of 0.4%. Analysis of the BAB/14 recombinant showed that this crossover occurred between VH genes implying that VH genes and CH genes are not organized in separate clusters separated by a larger spacer region but are contiguous. Analysis of the recombination frequencies indicates that the total number of VH genes must be at least 50.

Animals↗
PubMed1975

Genetic control of responses to bacterial lipopolysaccharides in mice. II. A gene that influences a membrane component involved in the activation of bone marrow-derived lymphocytes by lipipolysaccharides.

C3H/HeJ mice contain a defect in a single autosomal locus which is not linked to the H-2 histocompatibility or the heavy chain allotype loci that restrict immune, mitogenic, and polyclonal responses to bacterial lipopolysaccharides (LPS). Adult thymectomized C3H/HeJ mice that have been irradiated and reconstituted with C3HeB/FeJ bone marrow cells respond well to LPS. Cell-mixing experiments using C3H/HEJ-C3HeB/FeJ spleen cultures show that the failure of C3H/HeJ spleen cells to support responses to LPS is not due to nonspecific or LPS-induced suppressive events, or the lack of accessory cell types. C3H/HeJ and C3HeB/FeJ spleen cells bind LPS and respond to other B cell mitogens equally well. We suggest that the B lymphocytes of C3H/HeJ mice have a defect in a membrane component that is activated via interaction with LPS, and initiates the intracellular events that lead to cell proliferation.

Animals↗
PubMed1974

Genetic control of responses to bacterial lipopolysaccharides in mice. I. Evidence for a single gene that influences mitogenic and immunogenic respones to lipopolysaccharides.

In vivo immune responses and in vitro mitogenic responses to bacterial lipopolysaccharides (LPS) have been compared in strains of C3H mice. C3H/HeJ spleen cultures did not support mitogenic responses to LPS and in vivo these mice produce low IgM responses to LPS. On the basis of these two responses, C3H/HeJ mice have been termed low LPS responders. All other strains of C3H mice tested (C3HeB/FeJ, C3H/DiSn, C3H/Str, CWB, CSW, and C3H/Sf and its H-2 congenics) are high LPS responders supporting large in vitro mitogenic and in vivo immune responses to LPS. The immune response difference between low and high LPS responders is a quantitative one. IgM responses are observed in C3H/HeJ mice in the range of 1.0-10 microg LPS. At lower and higher LPS concentrations, immune responses are not observed. In contrast, high LPS responders elicit LPS immune responses over a much wider dose range (0.1-200 microg). The ability to respond well to LPS is dominant as shown by the response of F(1) hybrid mice of low responder and high responder strains. The linkage relationships of mitogenic and immune responsiveness to LPS have been investigated in backcross (C3H/HeJ x CWB)F(1) x CWB mice. All mice that gave in vivo immune responses to LPS also supported mitogenic responses to LPS. The defect in C3H/HeJ mice that limits mitogenic and immune responsiveness to be due to a single autosomal gene which is not linked to the H-2 histocompatibility or heavy-chain allotype loci.

Animals↗
PubMed1972

Active suppression of immunoglobulin allotype synthesis. II. Transfer of suppressing factor with spleen cells.

The mechanism of chronic allotype suppression in (SJL x BALB/c)F(1) mice has been investigated by means of cell transfer studies. These mice are phenotypically negative for serum Ig-1b, the paternal allotype determinant on gammaG(2a) immunoglubulin, as a result of perinatal exposure to maternal anti-Ig-1b. When spleen or bone marrow (B) cells from suppressed mice were injected into irradiated BALB/c "indicator" hosts, detectable levels of Ig-1b were demonstrated in the sera of a majority of the recipients early after transfer. These results indicate that Ig-1b-producing cells or their precursors are present in the lymphoid tissues of suppressed mice, even though they are not expressed. Within 5-7 wk, it was no longer possible to detect Ig-1b in the sera of these hosts, although cells producing another paternal allotype (Ig-4b) were shown to persist. Control BALB/c mice, injected with spleen and B cells from normal mice, continued to produce high levels of immunoglobulin carrying this allotype. The disappearance of serum, Ig-1b occurred most frequently in the recipients of suppressed spleen cells. Similar results were obtained using a mixture of spleen cells from normal and suppressed mice. Ig-1b production in the recipient mice ceased within a few weeks, even though the majority of cells in the mixture were obtained from normal (nonsuppressed) donors. The data are interpreted as evidence that chronic allotype suppression in mice is actively maintained by cells which are resident in the lymphoid tissues, splenic cells being the most effective. These cells are capable of proliferating in a new host and exerting their suppressive influence on Ig-1b-producing cells and/or their precursors.

Animals↗