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


     
 


The Journal of Immunology, 1973, 110: 791-800.
Copyright © 1973 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 Lotzová, E.
Right arrow Articles by Cudkowicz, G.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Lotzová, E.
Right arrow Articles by Cudkowicz, G.

Resistance of Irradiated F1 Hybrid and Allogeneic Mice to Bone Marrow Grafts of NZB Donors1

Eva Lotzová and Gustavo Cudkowicz

Department of Pathology, School of Medicine, State University of New York at Buffalo, Buffalo, New York 14214

Abstract

Heavily irradiated mice of several inbred and F1 hybrid strains were classified as resistant or susceptible to allogeneic or parental grafts of 106 NZB bone marrow cells depending on the 5-day hemopoietic repopulation of host spleens. Several strains did not support the growth of donor cells despite the total-body irradiation. NZW x NZB F1 mice resisted the growth of as many as 4 x 107 parental cells, the strongest barrier ever observed in mice for marrow transplants. The failures of growth were due to host-anti-graft reactions depressible by pretreatment of recipients with cyclophosphamide or horse anti-mouse thymocyte serum. Analysis of the progeny of two separate backcrosses of F1 mice to NZB indicated that two non-linked autosomal genes controlled resistance. One of these genes was in linkage group IX, 31.42 crossing-over units away from the D end of H-2, specifying or controlling the expression of alloantigen-like components of hemopoietic cells (Hh-gene). The second gene had an epistatic effect, probably by regulating the recognition of, or the reactivity to, Hh-gene products.

Footnotes

1 Supported in part by United States Public Health Service Research Grants AM-13,969 and CA-12,844 from the National Institutes of Health, and by American Cancer Society Grant IC-35B.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1973 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1973 by The American Association of Immunologists, Inc. All rights reserved.