HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Richman, A. V. Articles by Defendi, V. Search for Related Content PubMed Articles by Richman, A. V. Articles by Defendi, V.

Induction of Marked Hypergammaglobulinemia with Xenogeneic Tumors in Hamsters: Immunopathologic Studies¹

Wistar Institute of Anatomy and Biology, 36th Street at Spruce, Philadelphia, Pennsylvania 19104 and the Department of Pathology, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19174

Abstract

Human heteroploid cells derived from a benign prostatic adenoma, MA160, can grow progressively in the subcutaneous tissues of 2-day-old nonimmunosuppressed hamsters. The growth of these xenografts is associated with certain immunopathologic features. These features are:

1. A marked increase in the serum of electrophoretically restricted IgG which parallels tumor growth.

2. The appearance of noncytotoxic antibody against membrane antigens of the transplanted cells which is related to the IgG elevation but which constitutes only a very minor part of this elevation; and the fixation of antibody to the tumor cell membrane in situ.

3. The extensive plasma cell proliferation, and the presence of circulating immune complexes (as indicated by the granular deposition of IgG and complement (C3) in the renal glomeruli).

4. The lack of demonstrable biologic activity of the serum (enhancement or cytotoxicity).

This transplantation system has analogies with certain chronic viral infections in animals; and our inability to detect antibody specificity for much of the IgG may be related to the presence of circulating immune complexes. Finally we suggest that this system may provide a model from which to study the evolution and pathogenesis of plasma cell dyscrasias.

Footnotes

¹ Supported in part by American Cancer Society Grants VC-73 and PRP-45 and United States Public Health Service Research Grants CA-10815 from the National Cancer Institute and RR-05540 from the Division of Research Resources.