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Biomedical subjects

F C Grumet

Publications and source records attributed to F C Grumet.

At least 109 records · Page 6Linked to original sources
PubMed1979

Platelet transfusion tolerization by liver membrane treatment.

A nontoxic murine model has been developed in which sensitization to allogeneic platelet transfusions in adults can be prevented. This model is based upon allogeneic liver membrane (LM) induction of specific humoral tolerance to major histocompatibility alloantigens. In normal mice of the C3H background, syngeneic and H-2-incompatible congeneic platelets had a t1/2 = 15 +/- 3 hr; for mice of the C57BL background, the comparable t1/2 was 33 +/- 6 hr. Platelets of C3H background transfused into C57BL background recipients, and vice versa, had t1/22 midway between, 24 +/- 3 and 24 +/- 2 hr, respectively. These data suggest genetically determined variation in normal platelet survival. In passively immunized C3H background mice, the t1/2 was decreased to 10 +/- 2 hr. In C57BL background mice actively immunized i.p. with allogeneic lymphoid cells, t1/2 was decreased to 18 +/- 4 hr. When allogeneic LM was given concomitantly with the allogeneic cells, however, sensitization to foreign H-2 antigens was blocked, and survival of both C3H and C57BL background allogeneic platelets remained normal. These data demonstrate that in this free cell allograft system LM treatment is a safe and effective method for preventing adult sensitization to allogeneic platelets.

Animals↗
PubMed1979

A new low incidence red blood cell antigen, Pe.

A new low incidence red cell antigen (Pe), and its identifying IgG antibody are described. The antigen is destroyed by enzymes and is absent from serum, urine, saliva, and platelets. The Pe gene frequency is estimated to be less than 0.0003, and the Pe locus does not appear to be linked to Rh or Fy, nor carried by the X or Y chromosomes. The clinical significance of this antibody remains to be determined.

Aged↗
PubMed1978

Bw21 partition and crossreactivity of the components.

Available lymphocytotoxic antisera permitted the clear partition of the Bw21 antigen into two distinct components, Bw21.1 and Bw21.2. Bw21.1 is associated with W4 and is approximately twofold more frequent than the W6-associated Bw21.2. Cells of either Bw21 subtype were capable of absorbing specific anti-Bw21.1, anti-Bw21.2, and anti Bw21 (21.1 + 21.2) antibodies. Further, an F(ab')2 fragment prepared from an anti-Bw21.1 serum blocked cytotoxicity of anti-Bw21.1, anti-Bw21.2 and anti-Bw21 (21.1 + 21.2) sera. Based on the crossreactivity (by absorption) and blocking data, a model is proposed relating the Bw21 subtypes and the W4 and W6 antigens.

Cross Reactions↗
PubMed1978

Genetic control of murine resistance to Toxoplasma gondii.

The genetics of murine susceptibility to Toxoplasma gondii was investigated in inbred mice and their F1 and F2 offspring. Among four strains of congenic mice of the B10 background, those with H-2a/a and H-2b/b genotypes were more susceptible than were those with H-2d/d and H-2k/k genotypes. Breeding studies utilizing three of these strains demonstrated linkage between the H-2a allele and greater susceptibility. These data suggest the existence of an H-2-linked gene affecting susceptibility to T. gondii. In challenge of recombinant inbred mice derived from C57Bl/6J (high susceptibility) and BALB/c (low susceptibility) strains, lines BE, BJ, and BK were more susceptible than lines BD, BG, BH, and BI. These data are consistent with the existence of a second disease susceptibility gene linked to the H-13 locus. F1 offspring of the C57B1/6J X B10.D2 mice were significantly less susceptible than either parent. This phenotypic complementary suggests the presence of more than one genetic mechanism of resistance to T. gondii. From these combined data, we conclude that (i) susceptibility to T. gondii in mice is affected by at least two genes, (ii) one of the genes is linked to the H-2 and one to the H-13 locus, and (iii) more than a single mechanism of resistance must be considered to explain the observed genetic controls of susceptibility.

Animals↗
PubMed1977

HLA antigens in Addisonian pernicious anaemia: absence of a HLA and disease association.

An examination of HLA antigens in 72 unrelated Caucasian subjects with pernicious anaemia (PA) has revealed no significant association of any HLA-A or B genes with the disease. These data do not confirm the previous reports in the literature which had suggested an increased frequency of the B7 and/or A3 antigen among patients. In addition, the study of four families, each with two or more PA patients, does not support close linkage between disease susceptibility or autoantibody formation and the HLA locus. These data suggest that genes in or near the HLA region may not significantly affect susceptibility to PA.

Anemia, Pernicious↗
PubMed1976

T cell requirements for the expression of the lipopolysaccharide adjuvant effect in vivo: evidence for a T cell-dependent and a T cell-independent mode of action.

The in vivo adjuvant effect of lipopolysaccharide (LPS) in mice was investigated with the soluble synthetic polypeptide antigen (T, G)-A--L, the antibody response to which is determined by the Ir-1A gene. With this specific antigen it can be demonstrated that the LPS adjuvant effect has the following modes of action: a) a T cell-dependent enhancement of primary and secondary IgM antibody response; b) a T cell-dependent enhancement of IgG secondary andibody response; and c) a T cell-dependent induction of switchover from IgM to IgG andibody in some strains of Ir-1A low responders. Although T cells are necessary for some aspects of the adjuvant effect, these data do not distinguish between a mechanism involving a direct interaction between LPS and T cells or a direct interaction of LPS and B cells with a general requirement for T cells for expression of IgG antibody.

Adjuvants, Immunologic↗
PubMed1976

Strain-dependent differences in murine susceptibility to toxoplasma.

Susceptibility of seven inbred and outbred strains of mice to infection with trophozoites of Toxoplasma gondii at two different doses was determined. Stroking strain differences in susceptibility and changes of susceptibility with dosage change were seen. The data are consistent with the hypothesis that this may be due to genetic factors.

Animals↗
PubMed1976

IgM-mediated, T cell-independent suppression of humoral immunity.

The immunological unreactive state occurring in (T,G)-A-L nonresponder mice after secondary antigen challenge was investigated. Syngeneic IgM anti-(T,G)-A-L antibody-containing plasma, transferred at the time of the time of primary challenge, induced persistent suppression of autologous specific antibody production. Removal of plasma IgM with goat anti-mu antisera removed the ability of the plasma to supress. The induction and maintenance of the suppressed state were not different in thymectomized or sham-thymectomized animals. Primed animals subjected to graft-vs-host reaction (GVHR) at the time of secondary challenge switched over to IgG production. Animals suppressed by passive antibody transfer reacted to GVHR, at the time of secondary challenge, with specific IgM but not IgG antibody production. Transfused normal spleen cells partially abrogated suppression only when (suppressed) hosts had been lethally irradiated. Spleen cells from antigen-plus-antibody suppressed donors, upon transfer to previously normal, syngeneic hosts, were less immunocompetent than spleen cells from untreated donors. These data are consistent with a model of IgM mediated, T cell-independent persistent suppression of humoral immunity.

Animals↗