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


     
 


The Journal of Immunology, 1976, 117: 1145-1151.
Copyright © 1976 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 Remacle-Bonnet, M. M.
Right arrow Articles by Depieds, R. C.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Remacle-Bonnet, M. M.
Right arrow Articles by Depieds, R. C.

Inhibition of Normal Allogenic Lymphocyte Mitogenesis by a Soluble Inhibitor Extracted from Human Colonic Carcinoma1

Maryse M. Remacle-Bonnet, Gilbert J. Pommier, Solange Kaplanski, Roselyne J. Rance and Raymond C. Depieds

U.E.R. de Médecine, Laboratoire d'Immunologie, 27, Boulevard Jean Moulin, 13385, Marseille, Cedex 4, France

Abstract

Soluble extracts from human colonic tumors (STE) and from their hepatic metastases (SHME) were found to be unable to induce a proliferative response among normal allogenic lymphocytes. However, addition of these tissue extracts to cultures stimulated with various mitogens resulted in an almost complete inhibition of lymphocyte DNA synthesis. Nevertheless, they did not reduce the unstimulated lymphocyte spontaneous proliferation. Control experiments have shown that normal or nonmalignant tissues do not affect the lymphocyte reactivity to mitogens. The nonspecific immunosuppressive effect was found to be irreversible and to block lymphocyte activation at an early stage. The inhibitor was soluble (not sedimented at 220,000 x G for 2 hr) and not nonspecifically cytotoxic. STE was also found to induce morphologic alterations resulting in blastlike cell production. However, no mitotic figures were seen, even after colchicin treatment. It is suggested that STE might contain molecular component(s) which would exert a double effect: 1) trigger metabolic alterations responsible for the blast-like cell induction, and 2) inhibit the lymphoproliferative response. The significance of such a mechanism is discussed in connection with the nonspecific immunosuppression caused by a tumor and the immune unresponsiveness against the tumor itself. A preliminary characterization of this tumor material has shown that its molecular weight was about 70,000 and that it is not related to carcinoembryonic antigen or {alpha}-fetoprotein.

Footnotes

1 This work was supported by a grant from La Fondation pour la Recherche Médicale Francaise.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1976 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1976 by The American Association of Immunologists, Inc. All rights reserved.