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Your search keyword '"J Stafford-Hollis"' showing total 5 results
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5 results on '"J Stafford-Hollis"'

1. Antibody Expression and Engineering

Author

HENRY Y. WANG, TADAYUKI IMANAKA, D. K. Robinson, D. DiStefano, S. L. Gould, G. Cuca, T. C. Seamans, D. Benincasa, S. Munshi, C. P. Chan, J. Stafford-Hollis, G. F. Hollis, D. Jain, K. Ramasubramanyan, G. E. Mark, M. Siberklang, Hidekazu Sawada, Kazuaki Kitano, R. S. Barnett, K. L. Limoli, T. B. Huynh

Published
1995

2. Induction of peri-insulitis but not diabetes in islet transplants expressing a single foreign antigen. A multi-stage model of disease

Author

V M Holers, G F Hollis, B D Schwartz, R J Evans, J Strauss-Schoenberger, J C Carel, D L Barney, B Li, J Stafford-Hollis, and P E Lacy

Subjects
Immunology, Immunology and Allergy
Abstract

We have created a new transgenic model in which the human Epstein-Barr virus receptor, CR2 (CD21), has been expressed in pancreatic beta-cells. Mice derived from three transgenic founders bred into H-2b (C57BL/6) or H-2k (CBA) genetic backgrounds did not become spontaneously diabetic. After transplantation of CR2-expressing islets under the kidney capsule of genetically matched recipients, a histologic picture of peri-insulitis was found. However, animals did not manifest cellular invasion of the islets, destruction of the islets, or diabetes for at least 230 days. Significant numbers of both T and B lymphocytes were found in the cell population surrounding the islets. A pronounced serologic response to CR2 was also present and appeared to precede the onset of peri-insulitis. Thus, in this model, we have separated the process of diabetes induction into at least two phases. One is associated with peri-islet infiltration and an antibody response. However, at least one second signal is likely necessary for the process of islet destruction to follow.

Published
1993
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3. Production of Engineered Antibodies in Myeloma and Hybridoma Cells

Author

D. Benincasa, G. Cuca, M. Siberklang, T. C. Seamans, David K. Robinson, Daniel J. DiStefano, G. E. Mark, D. Jain, Sandra L. Gould, K. Ramasubramanyan, G. F. Hollis, Christine Chan, Sonal Munshi, and J. Stafford-Hollis

Subjects
biology, Chemistry, Gene expression, biology.protein, Process design, Antibody, Cell biology
Published
1995
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4. Optimization of a fed-batch process for production of a recombinant antibody

Author

Theodora A. Bibila, Sandra L. Gould, B. Daugherty, Konstantin Glazomitsky, T. C. Seamans, D. K. Lee, Melvin Silberklang, Christine Chan, Sonal Munshi, J. Stafford-Hollis, Daniel J. DiStefano, G. F. Hollis, L. O'neill Palladino, and David K. Robinson

Subjects
DNA, Complementary, Recombinant Fusion Proteins, Genetic Vectors, Cytomegalovirus, HIV Antibodies, HIV Envelope Protein gp120, General Biochemistry, Genetics and Molecular Biology, law.invention, Mice, History and Philosophy of Science, law, Genes, Reporter, Glutamate-Ammonia Ligase, Culture Techniques, Genes, Synthetic, Tumor Cells, Cultured, Production (economics), Animals, Humans, Amino Acids, Promoter Regions, Genetic, Chromatography, biology, Chemistry, General Neuroscience, Antibodies, Monoclonal, Gene Expression Regulation, biology.protein, Recombinant DNA, Batch processing, Immunoglobulin Light Chains, Antibody, Immunoglobulin Heavy Chains, Plasmacytoma
Published
1994

5. Induction of peri-insulitis but not diabetes in islet transplants expressing a single foreign antigen. A multi-stage model of disease.

Author

Holers VM, Hollis GF, Schwartz BD, Evans RJ, Strauss-Schoenberger J, Carel JC, Barney DL, Li B, Stafford-Hollis J, and Lacy PE

Subjects
Animals, Antibody Formation, Female, Humans, Male, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Mice, Transgenic, Receptors, Complement 3d genetics, Autoimmune Diseases etiology, Diabetes Mellitus, Experimental etiology, Disease Models, Animal, Islets of Langerhans pathology, Islets of Langerhans Transplantation, Receptors, Complement 3d immunology
Abstract

We have created a new transgenic model in which the human Epstein-Barr virus receptor, CR2 (CD21), has been expressed in pancreatic beta-cells. Mice derived from three transgenic founders bred into H-2b (C57BL/6) or H-2k (CBA) genetic backgrounds did not become spontaneously diabetic. After transplantation of CR2-expressing islets under the kidney capsule of genetically matched recipients, a histologic picture of peri-insulitis was found. However, animals did not manifest cellular invasion of the islets, destruction of the islets, or diabetes for at least 230 days. Significant numbers of both T and B lymphocytes were found in the cell population surrounding the islets. A pronounced serologic response to CR2 was also present and appeared to precede the onset of peri-insulitis. Thus, in this model, we have separated the process of diabetes induction into at least two phases. One is associated with peri-islet infiltration and an antibody response. However, at least one second signal is likely necessary for the process of islet destruction to follow.

Published
1993

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