Cargando…

ALLOANTISERUM-INDUCED INHIBITION OF MIGRATION INHIBITION FACTOR PRODUCTION IN IMMUNE RESPONSE GENE-CONTROLLED IMMUNE SYSTEMS

We have previously demonstrated that alloantisera prepared by reciprocal immunization of strain 2 and strain 13 guinea pigs specifically block stimulation of in vitro DNA synthesis in genetically controlled systems. In order to determine whether this blockade extends to other T-lymphocyte functions,...

Descripción completa

Detalles Bibliográficos
Autores principales: Ben-Sasson, Shlomo Z., Shevach, Ethan, Green, Ira, Paul, William E.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1974
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2139581/
https://www.ncbi.nlm.nih.gov/pubmed/4603011
_version_ 1782143829731704832
author Ben-Sasson, Shlomo Z.
Shevach, Ethan
Green, Ira
Paul, William E.
author_facet Ben-Sasson, Shlomo Z.
Shevach, Ethan
Green, Ira
Paul, William E.
author_sort Ben-Sasson, Shlomo Z.
collection PubMed
description We have previously demonstrated that alloantisera prepared by reciprocal immunization of strain 2 and strain 13 guinea pigs specifically block stimulation of in vitro DNA synthesis in genetically controlled systems. In order to determine whether this blockade extends to other T-lymphocyte functions, we examined the effect of alloantisera on the production of migration inhibition factor (MIF). (2 x 13)F(1) guinea pigs were immunized with a DNP derivative of the copolymer of L-glutamic acid and L-lysine (DNP-GL) and with DNP guinea pig albumin (GPA). The response to the former is controlled by a 2-linked Ir gene while that to the latter is mainly controlled by a 13-linked Ir gene. MIF production was assayed by an indirect procedure in which the migrating cell population lacked the histocompatibility antigen against which the alloantiserum was directed. Our results showed that anti-2 serum blocked MIF production by F(1) cells in response to DNP-GL but not DNP-GPA while anti-13 serum had the opposite effect. These experiments show that expression of a second major T-cell function is specifically blocked by alloantisera and suggest that Ir-gene products may act as antigen recognition substances on more than one type of T cell.
format Text
id pubmed-2139581
institution National Center for Biotechnology Information
language English
publishDate 1974
publisher The Rockefeller University Press
record_format MEDLINE/PubMed
spelling pubmed-21395812008-04-17 ALLOANTISERUM-INDUCED INHIBITION OF MIGRATION INHIBITION FACTOR PRODUCTION IN IMMUNE RESPONSE GENE-CONTROLLED IMMUNE SYSTEMS Ben-Sasson, Shlomo Z. Shevach, Ethan Green, Ira Paul, William E. J Exp Med Article We have previously demonstrated that alloantisera prepared by reciprocal immunization of strain 2 and strain 13 guinea pigs specifically block stimulation of in vitro DNA synthesis in genetically controlled systems. In order to determine whether this blockade extends to other T-lymphocyte functions, we examined the effect of alloantisera on the production of migration inhibition factor (MIF). (2 x 13)F(1) guinea pigs were immunized with a DNP derivative of the copolymer of L-glutamic acid and L-lysine (DNP-GL) and with DNP guinea pig albumin (GPA). The response to the former is controlled by a 2-linked Ir gene while that to the latter is mainly controlled by a 13-linked Ir gene. MIF production was assayed by an indirect procedure in which the migrating cell population lacked the histocompatibility antigen against which the alloantiserum was directed. Our results showed that anti-2 serum blocked MIF production by F(1) cells in response to DNP-GL but not DNP-GPA while anti-13 serum had the opposite effect. These experiments show that expression of a second major T-cell function is specifically blocked by alloantisera and suggest that Ir-gene products may act as antigen recognition substances on more than one type of T cell. The Rockefeller University Press 1974-08-01 /pmc/articles/PMC2139581/ /pubmed/4603011 Text en Copyright © 1974 by The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Article
Ben-Sasson, Shlomo Z.
Shevach, Ethan
Green, Ira
Paul, William E.
ALLOANTISERUM-INDUCED INHIBITION OF MIGRATION INHIBITION FACTOR PRODUCTION IN IMMUNE RESPONSE GENE-CONTROLLED IMMUNE SYSTEMS
title ALLOANTISERUM-INDUCED INHIBITION OF MIGRATION INHIBITION FACTOR PRODUCTION IN IMMUNE RESPONSE GENE-CONTROLLED IMMUNE SYSTEMS
title_full ALLOANTISERUM-INDUCED INHIBITION OF MIGRATION INHIBITION FACTOR PRODUCTION IN IMMUNE RESPONSE GENE-CONTROLLED IMMUNE SYSTEMS
title_fullStr ALLOANTISERUM-INDUCED INHIBITION OF MIGRATION INHIBITION FACTOR PRODUCTION IN IMMUNE RESPONSE GENE-CONTROLLED IMMUNE SYSTEMS
title_full_unstemmed ALLOANTISERUM-INDUCED INHIBITION OF MIGRATION INHIBITION FACTOR PRODUCTION IN IMMUNE RESPONSE GENE-CONTROLLED IMMUNE SYSTEMS
title_short ALLOANTISERUM-INDUCED INHIBITION OF MIGRATION INHIBITION FACTOR PRODUCTION IN IMMUNE RESPONSE GENE-CONTROLLED IMMUNE SYSTEMS
title_sort alloantiserum-induced inhibition of migration inhibition factor production in immune response gene-controlled immune systems
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2139581/
https://www.ncbi.nlm.nih.gov/pubmed/4603011
work_keys_str_mv AT bensassonshlomoz alloantiseruminducedinhibitionofmigrationinhibitionfactorproductioninimmuneresponsegenecontrolledimmunesystems
AT shevachethan alloantiseruminducedinhibitionofmigrationinhibitionfactorproductioninimmuneresponsegenecontrolledimmunesystems
AT greenira alloantiseruminducedinhibitionofmigrationinhibitionfactorproductioninimmuneresponsegenecontrolledimmunesystems
AT paulwilliame alloantiseruminducedinhibitionofmigrationinhibitionfactorproductioninimmuneresponsegenecontrolledimmunesystems