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K Kline

Publications and source records attributed to K Kline.

66 records · Page 4Linked to original sources
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MHC coded B-G homodimer and heterodimer heterogeneity among different chicken lines.

Chicken lines were classified into six distinct groups based on expression of B-G molecules by peripheral red blood cells (RBC). In addition to the previously reported 48 kD subunits of homodimeric B-G molecules, subunits of 60, 40, and possibly 20 kD were detected in certain of the chicken lines. Several of the chicken lines express the previously reported 40 and 44 kD subunits of heterodimeric B-G molecules; however, B21B21 chickens expressed 44 kD subunits only and B5B5 and B13B13 chickens did not express detectable levels of any heterodimeric-related molecules. These studies provide further evidence for the polymorphic nature of the B-G antigens.

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IgG immunoglobulin deficiency in muscular dystrophic chickens.

Plasma immunoglobulin profiles of New Hampshire strain muscular dystrophic chickens were determined by radial immunodiffusion, immunoelectrophoresis and polyacrylamide gel electrophoresis. Muscular dystrophic chickens have reduced levels of IgG but maintain normal levels of total serum proteins, IgA and IgM. The relationship and significance of the IgG deficiency to muscular dystrophy remains to be determined.

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Lymphocyte capping in hereditary muscular dystrophic chickens and mice: no evidence for a systemic membrane defect.

Splenic lymphocytes from both the Storrs and Davis strains of muscular dystrophic chickens and the C57BL/6J-2J strain of muscular dystrophic mice cap FITC-Con A and FITC-Ig in a manner similar to normal controls. In analyses of testcross progeny of Storrs muscular dystrophic chickens, no difference in the ability of lymphocytes to cap were observed among the segregating progeny. Neither were any significant differences observed in lymphocyte capping among F2 segregating progeny of C57BL/6J-2J mice. These studies do not support the systemic membrane defect hypothesis for muscular dystrophy.

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Erythrocyte alloantigens in the Storrs strain of hereditary muscular dystrophic chickens and segregating testcross progeny.

The Storrs strain of muscular dystrophic chickens were typed for erythrocyte alloalleles at 10 loci, including the B locus. Gene fixation is present at five loci and expression of the predominate alloantigen varied in frequency from 0.53 to 0.91 at the other five loci tested. The Storrs strain of muscular dystrophic chickens are not fixed at the B locus, expressing the B2/B2 allelic combination 81 percent of the time and B2/B23 the remaining percentage. Testcross progeny segregating for the muscular dystrophy trait did not show any alloantigen associations at the 10 loci examined. No association of the MD train with a particular B genotype could be ascertained. CPK levels as a measure of muscle destruction in the muscular dystrophic testcross progeny segregating at the B locus did not reveal an association with any B haplotype. Serum IgG levels and low Con A response in muscular dystrophic testcross progeny also were not associated with any specific B locus alloantigen combinations. The possibility remains that the establishment of a pathological index for muscular dystrophy in MD chickens may reveal an association with the B locus.

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PubMedDate not supplied

Analyses of muscular dystrophy and Con A deficiency traits in testcross progeny of chickens.

Hereditary muscular dystrophic chickens of the Storrs strain possess two genetic disorders, muscular dystrophy (MD) and a deficient concanavalin A (Con A), a T-cell mitogen, mediated splenic lymphocyte blastogenic response. A possible amelioration of the MD phenotype in MD chickens expressing normal Con A was postulated on the basis of progeny segregating for these two traits in F2 genetic analyses. To test this possibility, testcross progeny were examined for segregation of MD and Con A deficiency traits, and for the degree of muscle destruction and Con A deficiency. The data show both traits to be inherited independently as autosomal recessive traits, and do not support any phenotypic modifications occurring in chickens expressing MD with normal Con A. In the testcross progeny, the Con A deficiency disorder is equally deficient in normal and MD progeny, and the degree of muscle destruction as measured by serum creatine phosphokinase levels is equally great in MD chickens with or without the Con A deficiency trait. The reduced numbers of MD chickens in the testcross progeny can be accounted for by chance and probably reflect losses during in ovo development.

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Characterization of different B-F (MHC class I) molecules in the chicken.

B-F alloantisera recognized distinct 45-Kd molecules on peripheral red blood cells (RBC) from embryonic chickens and heterogeneous molecules of approximately 40 to 44 Kd on peripheral RBC from adult chickens, provisionally referred to as type 1 and type 2, respectively. Type 2 molecules migrated to the basic end of isoelectric focusing gels, exhibited multiple isomorphic variants, and were associated with a smaller polypeptide of approximately 11 to 12 Kd assumed to be beta-2-microglobulin. Type 1 molecules migrated to the acidic end of isoelectric focusing gels, exhibited limited heterogeneity, and were not associated with a smaller polypeptide. Type 1 and type 2 molecules were also shown to be distinct by peptide mapping and serological analyses. In addition, two distinct molecular-weight forms of the type 2 molecules were distinguished, provisionally referred to as 2A (45 Kd) and 2B (42 Kd). In vivo-derived avian erythroblastosis virus (AEV)-transformed erythroleukemia cells expressed type 2A molecules. In vitro-derived AEV-transformed erythroleukemia cells expressed very low levels of B-F molecules; however, they expressed type 2B molecules when induced to differentiate. Normal bursa-derived lymphoid cells expressed type 2A molecules, whereas normal thymus-derived lymphoid cells expressed type 2B molecules. Cloned reticuloendotheliosis virus (REV)-transformed immature lymphoid cells expressed either type 2A or type 2B molecules.

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PubMedDate not supplied

Characterization of two distinct disulfide-linked B-G molecules in the chicken.

Alloantisera specific for B-G antigens recognized a complex of molecules of apparent molecular weights of 90 and 98 Kd under nonreducing conditions and molecules of 40, 44, and 48 Kd under reducing conditions on both embryo- and adult-derived peripheral red blood cells (RBC). The chicken B-G molecules produced a unique two-dimensional "diagonal" pattern. Two antisera permitted the characterization of the complex B-G molecular profile as a homodimer composed of 48-Kd subunits and as a heterodimer composed of 40- and 44-Kd subunits. A rabbit antiserum produced against B-G molecules preferentially recognized the 48-Kd reduced molecules, suggesting that the 90-Kd molecule was a homodimer composed of two 48-Kd molecules. One B-G reagent was capable of recognizing only the 98-Kd nonreduced B-G molecule that gave rise to 40- and 44-Kd molecules under reducing conditions, suggesting that the 98-Kd molecule was a heterodimer composed of 44- and 40-Kd subunits. Adult chicken B-G2 molecules produced a variety of two-dimensional isoelectric focusing/sodium dodecyl sulfate-polyacrylamide gel electrophoresis (IEF/SDS-PAGE) patterns depending on the characteristics of the reagent employed in the immunoprecipitation. B-G molecules were immunoprecipitated from primitive and definitive chicken RBCs but not from any nonerythroid cells tested. B-G molecules were not expressed by avian erythroblastosis virus (AEV)-transformed erythroleukemia cells, nor were they induced to appear with butyric acid-induced erythroid differentiation.

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PubMedDate not supplied

Modulation of immune suppression and enhanced tumorigenesis in retrovirus tumor challenged chickens treated with vitamin E.

Vitamin E(dl-alpha-tocopherol) dissolved in ethanol with polyethylene glycol as the vehicle and administered by intraperitoneal injections of 0.1 mg/gm body weight at two day intervals, was demonstrated to be a potent immunomodulating reagent in young chickens challenged with avian reticuloendotheliosis virus-transformed tumor cells. Vitamin E treatment enhanced the mitogen-induced proliferative responses of spleen cells from age matched, unchallenged chickens; reduced the tumor cell-induced suppression of host splenic lymphocyte mitogen responses; and eliminated tumor cell-induced suppressor cell activity. However, inspite of an improved immune status the vitamin E treated-tumor cell challenged chickens exhibited enhanced tumorigenesis.

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