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Biomedical subjects

C B Carpenter

Publications and source records attributed to C B Carpenter.

At least 181 records · Page 10Linked to original sources
PubMed1977

Cellular components of allograft rejection: identity, specificity, and cytotoxic function of cells infiltrating acutely rejecting allografts.

Functioning mononuclear cells have been harvested from heterotopic rat cardiac allografts during maximal transplant cellular infiltration. T cells, identified by a T cell-specific absorbed rabbit anti-rat brain serum, constituted two-thirds of the total cells recovered. Approximately 20% of the infiltrating cells bear and synthesize surface immunoglobulin. Macrophages, identified by latex ingestion and morphologic and cytochemical techniques, comprise 9% of the graft infiltrate. Donor-specific cytotoxic T lymphocytes are concentrated within the graft. A separate population of Fc receptor-positive recovered cells mediate antibody-dependent LMC (Ab-LMC). Neither effector cell was adherent or phagocytic. These studies have conclusively established that cytotoxic T lymphocytes accumulate within rejecting allografts; however, the enriched presence of cytotoxic T cells within the grafts is not fully dependent upon antigen recognition per se, since Lew animals grafted with both BN and BUF hearts have Lew anti-BN and Lew anti-BUF killer cells in each graft.

Animals↗
PubMed1977

Pathways of complement activation in membranoproliferative glomerulonephritis and allograft rejection.

The complement system is comprised of at least 18 plasma proteins and consists of four functional divisions: two pathways for activation (classical and alternative), a common amplification mechanism for the activating pathways, and a final common effector pathway to which the activating and amplifying sequences are directed. The classical pathway is activated by certain antigen-antibody complexes, while the alternative pathway may be initiated non-immunologically by various microbial polysaccharides. Indeed, mixtures of purified C3, B, D, and P regulated to low-grade interaction by the presence of C3bINA and beta1 H respond to zymosan with amplified C3 and B inactivation. Both pathways form enzymes termed C3 convertases that cleave C3 to generate its major fragment, C3b. C3b interacts with each C3 convertase to permit C5 cleavage in activation of the effector complement sequence, and it interacts with alternative-pathway factors B and D to generate additional C3 convertase, C3bBb, in the amplification pathway. As C3 cleavage represents the most critical step in the elaboration of the biologic effects of the complement system, modulation of this reaction by generation, stabilization, and inactivation of the amplification convertase C3bBb may well determine whether initial activation of the complement sequence eventuates in beneficial or detrimental effects for the host. Initial generation of C3bBb is dependent on prior cleavage of C3, which may occur by the classical pathway or the alternative pathway. Stabilization of C3bBb is achieved with either P or C3NeF after their binding to C3b and C3bBb, respectively. Control of this amplifying step occurs at three levels: intrinsic decay of the inherently labile C3bBb complex, extrinsic decay-dissociation of Bb from the complex by beta1H, and inactivation of C3b by C3bINA. In the presence of stabilizing factors the control proteins must function in sequence, since C3bINA cannot act on C3bBb; beta1H-mediated decay of protective Bb must precede C3b inactivation by C3bINA. C3NeF, which is found in the sera of some patients with MPGN and persistent depressions of serum C3, circumvents all three controls because of its capacity to create a stabilized convertase that is relatively resistant to decay-dissociation by beta1H. The effector complement sequence is activated by cleavage of C3 and C5, which releases vasoactive and chemotactic peptides, C3a and C5a, and generates the major fragments C3b and C5b. C3b, in addition to its function in the amplifying reaction and the C5 convertases, mediates immune adherence to cells possessing membrane-associated receptors for C3b; this in turn promotes the phagocytic and secretory functions unique to each cell type. Cell-bound C5b serves to assemble the cytolytic complex C5b6789, while fluid-phase C5d generates the hemolytically inactive chemotactic complex C567d...

Complement C3↗
PubMed1977

Passive enhancement of rat renal allografts by antibodies to a non-SD (Ag-B) locus analogous to Ia and demonstration of linkage to the MHC.

The rat MHC contains a distinct locus for Ia-like antigens. The alleles of this locus are not always associated with like alleles of the MLR and Ag-B (SD) loci in inbred strains. This is demonstrated by the Fischer strain, which is MLR and tag-B (SD) 1 (H-11) but shares an Ia specificity with BN (Ag-B3, H-1n). The biologic significance of anti-Ia is distinctive, having in vivo graft-enhancing capability, even when it is cross-reacting (i.e., Lew anti-Fi enhances BN). In contrast, anti-AG-B (SD) does not enhance in the rat model.

Animals↗
PubMed1977

Pretransplant assays of alloimmunity in predicting renal graft outcome.

Forty-one renal allograft recipients were studied for evidence of specific antidonor alloimmunity prior to transplantation. Pretransplant evidence of antibody to the donor as detected by ADCC correlated with the occurrence of early graft loss. This suggests that the ADCC may serve as a useful pretransplant corssmatching procedure.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1976

Maternal-fetal relation. Absence of an immunologic blocking factor from the serum of women with chronic abortions.

We investigated an immunologic mechanism that might explain the apparent "tolerant" state of the mother during pregnancy. Cellular-immune reactivity in vitro to paternal alloantigens was demonstrated in multigravid women by production of lymphocyte migration inhibitory factor. Serum from normal multigravid women contained a factor that blocked production of migration inhibitory factor by maternal lymphocytes to paternal antigens in a specific manner. The blocking factor was an IgG antibody whose activity was removed by absorption with paternal lymphocytes but not with pooled human platelets. We tested the biologic importance of this blocking factor in women who have difficulty maintaining a normal term pregnancy. Our observations indicate that women who experience idiopathic spontaneous abortions produce lymphocyte migration inhibitory factor to paternal alloantigens, but their serums lack the blocking factor. The presence of the serum blocking factor during pregnancy may contribute to the success of the fetus as an allograft.

Abortion, Habitual↗