The JI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     
 


The Journal of Immunology, 1974, 113: 94-102.
Copyright © 1974 by The American Association of Immunologists, Inc.

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Brandchaft, P. B.
Right arrow Articles by Boone, C. W.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Brandchaft, P. B.
Right arrow Articles by Boone, C. W.

Increase in Gross (G) Antigen Sites on the Surface of AKR Virus-Induced Rat Lymphoma Cells after Treatment with Trypsin1

Phyllis B. Brandchaft2 and Charles W. Boone

From The Cell Biology Section, Viral Biology Branch, National Cancer Institute, Bethesda, Maryland 20014

Abstract

G (Gross) leukemia virus-associated surface antigens (G antigens) on AKR virus-induced Fischer rat lymphoma cells were measured with radioiodine-labeled syngeneic antiserum. Treatment of the lymphoma cells with trypsin resulted in a 3-fold increase in the number of surface antigen sites as compared to EDTA-treated cells. An increase in sites was seen after treatment with as low as 0.025 mg/ml trypsin. Prolonged treatment with trypsin did not decrease the number of G surface antigens, although all of the sites could be removed from the cells by treatment with papain. No increase in the number of antigen sites was observed after neuraminidase treatment of the cells. Blocking experiments with C57BL/6 anti-K36 (G-typing) mouse serum confirmed that the majority of the sites remaining on the cells after trypsin treatment were G cell surface antigens (GCSA). G antigens were also released from the cells by treatment with either trypsin or papain. Released G antigens were sensitive to degradation by trypsin.

Footnotes

1 This work was taken from a dissertation submitted by the first author to the Graduate School, Temple University, Philadelphia, Pennsylvania, in partial fulfillment of the requirements for the Ph.D. degree.

2 Present address: Immunology Section, Viral Leukemia and Lymphoma Branch, National Cancer Institute, Bethesda, Maryland 20014.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1974 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1974 by The American Association of Immunologists, Inc. All rights reserved.