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


     
 


The Journal of Immunology, 1973, 110: 1238-1244.
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 Zaleski, M.
Right arrow Articles by Milgrom, F.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Zaleski, M.
Right arrow Articles by Milgrom, F.

Complementary Genes Controlling Immune Response to {vartheta}-AKR Antigen in Mice1

Marek Zaleski2 and Felix Milgrom

From the Department of Microbiology, School of Medicine, State University of New York at Buffalo, Buffalo, New York 14214

Abstract

The primary response of mice to {vartheta}-AKR antigen was measured by means of plaque assay detecting cells producing antibodies lytic for AKR thymocytes (PFC). It was found that 3 of 12 different F1 hybrids produced significantly more PFC than either parental strain. In segregating populations of C57BL/6J and DBA/2J mice, H-2 homozygotes responded like parental mice, whereas most but not all H-2 heterozygotes responded like F1 hybrids. In the F2 population 7% and in the backcross population to C57BL/6J parent 20% of H-2 heterozygotes responded like parental mice. On the basis of experimental data, a hypothesis was advanced that thre eloci in the IXth linkage group are involved in genetic control of the response to {vartheta}-AKR antigen. Each locus has at least two alleles, one dominant and one recessive. Dominant alleles complement each other which explains why the response to certain F1 hybrids is higher than the response of their parents. Two of three hypothetical loci are closely linked to each other as well as to the H-2 complex and might be considered components of the Ir-1 system.

Footnotes

1 This work was supported by United States Public Health Service Research Grant AI-06754 from the National Institute of Allergy and Infectious Diseases.

2 Recipient of a Henry C. and Bertha H. Buswell fellowship.







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.