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Your search keyword '"Cowan, Peter J."' showing total 42 results
Start Over Author "Cowan, Peter J." Journal transplantation
42 results on '"Cowan, Peter J."'

10. Regulation of Clinical Xenotransplantation—Time for a Reappraisal

Author

Cooper, David K.C., primary, Pierson, Richard N., additional, Hering, Bernhard J., additional, Mohiuddin, Muhammad M., additional, Fishman, Jay A., additional, Denner, Joachim, additional, Ahn, Curie, additional, Azimzadeh, Agnes M., additional, Buhler, Leo H., additional, Cowan, Peter J., additional, Hawthorne, Wayne J., additional, Kobayashi, Takaaki, additional, and Sachs, David H., additional

Published
2017
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16. Antibody-Mediated Rejection in a Blood Group A-Transgenic Mouse Model of ABO-Incompatible Heart Transplantation

Author

Motyka, Bruce, primary, Fisicaro, Nella, additional, Wang, Szu-I, additional, Kratochvil, Annetta, additional, Labonte, Katrina, additional, Tao, Kesheng, additional, Pearcey, Jean, additional, Marshall, Thuraya, additional, Mengel, Michael, additional, Sis, Banu, additional, Fan, Xiaohu, additional, d'Apice, Anthony J. F., additional, Cowan, Peter J., additional, and West, Lori J., additional

Published
2016
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30. RENAL XENOGRAFTS FROM TRIPLE-TRANSGENIC PIGS ARE NOT HYPERACUTELY REJECTED BUT CAUSE COAGULOPATHY IN NON-IMMUNOSUPPRESSED BABOONS

Author

Cowan, Peter J., primary, Aminian, Atousa, additional, Barlow, Helen, additional, Brown, Ainslie A., additional, Chen, Chao-Guang, additional, Fisicaro, Nella, additional, Francis, David M. A., additional, Goodman, David J., additional, Han, Wenruo, additional, Kurek, Margarita, additional, Nottle, Mark B., additional, Pearse, Martin J., additional, Salvaris, Evelyn, additional, Shinkel, Trixie A., additional, Stainsby, Gerard V., additional, Stewart, Andrew B., additional, and d???Apice, Anthony J. F., additional

Published
2000
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31. DISSEMINATED INTRAVASCULAR COAGULATION COMPLICATES TRANSGENIC PIG RENAL XENOTRANSPLANTATION IN NON-IMMUNOSUPPRESSED BABOONS.

Author

Cowan, Peter J., primary, Goodman, David J., additional, Aminian, Atousa, additional, Brown, Ainslie, additional, Barlow, Helen, additional, Shinkel, Trixie A., additional, Kurek, Margarita, additional, Francis, David M., additional, Han, Wenruo, additional, Stewart, Alastair, additional, Nottle, Mark, additional, Chen, Ghao-Guang, additional, Salvaris, Evelyn, additional, Pearse, Martin J., additional, and dʼApice, Anthony J., additional

Published
2000
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33. KNOCK OUT OF ??1,3-GALACTOSYLTRANSFERASE OR EXPRESSION OF??1,2-FUCOSYLTRANSFERASE FURTHER PROTECTS CD55- AND CD59-EXPRESSING MOUSE HEARTS IN AN EX VIVO MODEL OF XENOGRAFT REJECTION

Author

Cowan, Peter J., primary, Chen, Chao-Guang, additional, Shinkel, Trixie A., additional, Fisicaro, Nella, additional, Salvaris, Evelyn, additional, Aminian, Atousa, additional, Romanella, Margarita, additional, Pearse, Martin J., additional, and d'Apice, Anthony J.F., additional

Published
1998
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38. KNOCK OUT OF α1,3GALACTOSYLTRANSFERASE OR EXPRESSION OFα1,2FUCOSYLTRANSFERASE FURTHER PROTECTS CD55 AND CD59EXPRESSING MOUSE HEARTS IN AN EX VIVO MODEL OF XENOGRAFT REJECTION

Author

Cowan, Peter J., Chen, ChaoGuang, Shinkel, Trixie A., Fisicaro, Nella, Salvaris, Evelyn, Aminian, Atousa, Romanella, Margarita, Pearse, Martin J., and d'Apice, Anthony J.F.

Abstract

Organs from transgenic animals with highlevel endothelial expression of the human complement regulatory factors CD55 and CD59 are significantly protected from human complementmediated injury. Elimination or reduction of the major xenoepitope αGal, achieved by knocking out theα1,3galactosyltransferase gene Gal KO or expressing humanα1,2fucosyltransferase H transferase or HTF, also affords protection, although to a lesser degree. In this study, we examined whether the protection provided by strong CD55 and CD59 expression can be augmented by the Gal KO or HTF modifications.

Published
1998

42. Sex, T Cells, and the Microbiome in Natural ABO Antibody Production in Mice.

Author

Adam I, Motyka B, Tao K, Jeyakanthan M, Alegre ML, Cowan PJ, and West LJ

Subjects
Male, Female, Mice, Animals, Humans, Mice, Inbred C57BL, Antibodies, CD4-Positive T-Lymphocytes, Mice, Knockout, Antibody Formation, Microbiota
Abstract

Background: "Natural" ABO antibodies (Abs) are produced without known exposure to A/B carbohydrate antigens, posing significant risks for hyperacute rejection during ABO-incompatible transplantation. We investigated anti-A "natural" ABO antibodies versus intentionally induced Abs with regard to the need for T-cell help, the impact of sex, and stimulation by the microbiome., Methods: Anti-A was measured by hemagglutination assay of sera from untreated C57BL/6 wild-type (WT) or T cell-deficient mice of both sexes. Human ABO-A reagent blood cell membranes were injected intraperitoneally to induce anti-A Abs. The gut microbiome was eliminated by maintenance of mice in germ-free housing., Results: Compared with WT mice, CD4 + T-cell knockout (KO), major histocompability complex-II KO, and αβ/γδ T-cell receptor KO mice produced much higher levels of anti-A nAbs; females produced dramatically more anti-A nAbs than males, rising substantially with puberty. Sensitization with human ABO-A reagent blood cell membranes did not induce additional anti-A in KO mice, unlike WT. Sex-matched CD4 + T-cell transfer significantly suppressed anti-A nAbs in KO mice and rendered mice responsive to A-sensitization. Even under germ-free conditions, WT mice of several strains produced anti-A nAbs, with significantly higher anti-A nAbs levels in females than males., Conclusions: Anti-A nAbs were produced without T-cell help, without microbiome stimulation, in a sex- and age-dependent manner, suggestive of a role for sex hormones in regulating anti-A nAbs. Although CD4 + T cells were not required for anti-A nAbs, our findings indicate that T cells regulate anti-A nAb production. In contrast to anti-A nAbs, induced anti-A production was T-cell dependent without a sex bias., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc.)

Published
2023
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