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C B Carpenter

Publications and source records attributed to C B Carpenter.

At least 199 records · Page 11Linked to original sources

The role of nonclassical Fc receptor-associated, Ag-B antigens (Ia) in rat allograft enhancement.

The ability of a hyperimmune Lew anti-BN serum (HIS) to induce enhancement of (Lew/BN)F1 kidneys transplanted into Lew recipients was compared to that of the same antiserum that had been depleted of hemagglutinating anti-Ag-B antibodies by absorption with Brown-Norway (BN) RBC-absorbed sera (RAS) or platelet-absorbed sera (PAS). The RAS and PAS were as effective as the unabsorbed HIS in abrogating early rejection as assessed by renal function and promotion of long-term survival. The absorbed sera retained the capacity to block the mixed lymphocyte culture (MLC) between Lew and BN lymphocytes and to a lesser degree the MLC between Lew and BUF, WF, AUG, and ACI lymphocytes; however, strain specificity was clearly evident at high antiserum dilutions. Similarly, these absorbed sera retained the capacity to block the Fc receptor of BN lymphocytes, and this effect was completely strain specific. In contrast, hemagglutinating and cytotoxic antibodies eluted from platelets used for antiserum absorption did not react with Fc receptors as assessed by rabbit antisheep (IgG)-coated SRBC (EA) rosette formation. F(Ab')2 fragments of PAS also blocked EA rosettes. On the other hand, complement rosettes (EAC) were not inhibited by the HIS. The antibodies were therefore directed against the Fc receptor itself or a structure spatially or functionally closely related to it. Both the Fc receptors and the enhancing capacity of the antisera were strictly specific for the BN genotype. It is suggested that the anti-"Fc receptor" antibody could play an important role in the induction of enhancement by impairing host T-B collaboration as a result of its binding to graft allogeneic "Fc receptors" which appear to be analogous to the major histocompatibility complex (MHC)-coded Ia antigens of the mouse.

Animals↗

Antibody-dependent lymphocyte-mediated cytotoxicity (Ab-LMC), definition of the "K cell" in the rat.

The nature and membrane characteristics of the "K cell" of antibody-dependent lymphocyte-mediated cytotoxicity (Ab-LMC) were investigated in a widely used rat model of transplantation. Treatment of sensitized effector cell populations with anti-immunoglobulin and complement eliminated K cell cytotoxicity without diminishing the component of T cell-mediated injury. EA and EAC depletion experiments, although demonstrating no loss of K cell cytotoxicity after removal of complement receptor-bearing lymphocytes, produced a marked abrogation of cytotoxicity following the removal of the Fc receptor-bearing lymphocyte pool. Studies on phagocytic properties showed K cell activity to be shared by an adherent as well as a nonadherent cell population. Thus, the Fc receptor emerged as the only constant surface marker of the rat K cell in Ab-LMC.

Animals↗

The chromosomal order of genes controlling the major histocompatibility complex, properdin factor B, and deficiency of the second component of complement.

The relationship of the genes coding for HLA to those coding for properdin Factor B allotypes and for deficiency of the second component of complement (C2) was studied in families of patients with connective tissue disorders. Patients were selected because they were heterozygous or homozygous for C2 deficiency. 12 families with 15 matings informative for C2 deficiency were found. Of 57 informative meioses, two crossovers were noted between the C2 deficiency gene and the HLA-B gene, with a recombinant fraction of 0.035. A lod score of 13 was calculated for linkage between C2 deficiency and HLA-B at a maximum likelihood value of the recombinant fraction of 0.04. 18 families with 21 informative matings for both properdin Factor B allotype and HLA-B were found. Of 72 informative meioses, three recombinants were found, giving a recombinant fraction of 0.042. A lod score of 16 between HLA-B and Factor B allotypes was calculated at a maximum likelihood value of the recombinant fraction of 0.04. A crossover was shown to have occurred between genes for Factor B and HLA-D, in which HLA-D segregared with HLA-A and B. These studies suggest that the genes for Factor B and C2 deficiency are located outside those for HLA, that the order of genese is HLA-A, -B, -D, Factor B allotype, C2 deficiency, that the genes coding for C2 deficiency and Factor B allotypes are approximately 3--5 centimorgans from the HLA-A and HLA-B loci, and that the apparent lack of recombinants between the Factor B gene and C2 deficiency gene suggests that these two genes lie in close proximity to one another.

Chromosome Mapping↗

Hereditary C2 deficiency: diagnosis and HLA gene complex associations.

Nine families with genetically controlled C2 deficiency have been described where the propositii and family members are heterozygous C2 deficient. The diagnosis of hereditary C2 heterozygous deficiency was suspected on the basis of analysis for CH50, C2 protein, and C2 function, and then confirmed by family studies. Analysis of HLA antigens in these families supported the close association of C2 defiency and HLA-A10 and/or B18, particularly the latter. Analysis by MLC studies revealed recombination in one family between the HLA and B and D loci and in another family probable recombination between the D and C2 complement loci. Therefore, the order of the loci on the sixth chromosome is likely to be C2 complement, HLA-D, HLA-B, HLA-A.

Chromosome Mapping↗

Studies on infiltrating host cells harvested from acutely rejecting rat cardiac allografts.

Although the cellular events of rejection of organ allografts have been fully described histologically, little information exists regarding actual mechanisms of graft destruction. Available concepts are based primarily upon assays performed in vitro. This study describes a model designed to correlate such in vitro information with events occurring in vivo within acutely rejecting organ allografts. Infiltrating host cells had been harvested by two techniques from heterotopic cardiac allografts in rats. The various cell classes have been noted and their differential rates of accumulation compared to serial histological observations. Subpopulations of cells have been identified by surface markers, and specific cytotoxicity against donor alloantigen has been determined as a T lymphocyte function. These techniques may be of aid in unraveling the complexities of graft rejection.

Animals↗

T and B cell patterns in irreversibly rejected human renal allografts. Correlation of morphology with surface markers and cytotoxic capacity of the isolated lymphoid infiltrates.

To define the composition and proliferative and functional activity of the rejection formed sheep erythrocyte rosettes (T cells), expressed surface Ig (B cells) or Fc receptors and specific lymphocyte-mediated cytotoxic activity. Small clumped lymphocytes (48.8 +/- 18.9 per cent) and plasma cells (18.8 +/- 10.9 per cent) were most common and correlated negatively (p less than 0.01). Percentages of surface Ig-bearing and small clumped lymphocytes correlated directly (p less than 0.05) as did the percentages of E rosette-forming and plasma cells (p less than 0.05). The percentages of surface Ig-bearing B cells correlated negatively with E rosette-forming T cells (p less than 0.05). Within this spectrum of rejection, three patterns could be identified. In the first pattern, humoral rejection (by immunofluorescence) was intense and cellular infiltration was primarily by surface Ig and Fc receptor-positive small clumped B lymphocytes. The second and most common pattern consisted of a mixed T and B cell infiltrate with intermediate to high lymphocyte-mediated cytotoxic activity and variable humoral rejection. In the third pattern, invitro studies showed primarily E rosette-forming T cells with paradoxically low lymphocyte-mediated cytotoxic activity. However, morphologic studies also revealed the highest percentages of plasma cells but only mild humoral rejection. Thus, combined morphologic and in vitro studies identified three patterns of protracted renal allograft rejection. Thus, combined morphologic and in vitro studies identified three patterns of protracted renal allograft rejection for which the percentages of plasma cells may provide a distinguishing morphologic marker. Furthermore, the degree of lymphocytic invasion of renal tubules and blood vessels may provide an estimate of lymphocyte-mediated cytotoxic activity.

Antibody Formation↗

Identity and cytotoxic capacity of cells infiltrating renal allografts.

To determine the identity and cytotoxic capacity of lymphoid cells involved in allograft rejection, we studied viable, monodispersed cells recovered from 10 rejected human renal allografts. A heterogeneous population of cells including macrophages and both bone-marrow (B) and thymus-derived (T) lymphocytes accumulate in rejected grafts. Infiltrating lymphocytes exerted a specific cytolytic effect on 51Cr-labeled peripheral blood lymphocytes bearing donor antigens, ranging from 7 to 44 per cent specific lysis in nine of 10 cases. Cytolysis was closely correlated (r equal 0.91, p less than 0.05) with the histologica grade of cellular rejection but not with humoral rejection, suggesting that cytotoxic lymphocytes are an important element in cellular rejection. Limited fractionation studies showed that both T cells (in early rejection) and non-T cells (in late rejection) may produce cytotoxicity. Since as many as 50 per cent of cells recovered bore Fc receptors, the rejection process may also involve antibody-dependent target-cell lysis.

Animals↗

Insulin-induced augmentation of lymphocyte-mediated cytotoxicity.

Physiologic concentrations of insulin enhance the ability of cytotoxic lymphocytes to injure target cells. The effect of insulin closely resembles the action of cholinomimetics and guanosine 3',5'-monophosphate upon this system. Since both insulin and cholinomimetics elevate intracellular concentrations of guanosine 3',5'-monophosphate, a common mode of action is suggested.

Animals↗

Immunosuppressive alpha globulin from bovine thymus and serum: mode of action upon afferent and efferent arcs of the mouse immune response.

Immunosuppressive bovine alpha globulins of both serum and thymus origin were analyzed for in vitro effects upon the afferent and efferent arcs of the immune system. Although considerable variation in potency occurs between preparations, the functional identity of thymus and serum fractions is apparent. Antigenic recognition and effector capability are not altered whereas the proliferative lymphocyte response is either augmented or suppressed, depending upon the concentration of alpha globulin. A rather selective effect is noted on DNA synthesis and is followed by parallel changes in the development of effector capability, as measured by the development of alloimmune cytotoxic lymphocytes.

Alpha-Globulins↗