Genetic control of T-cell proliferative responses to poly(glu40ala60) and poly(glu51lys34tyr15): Subregion-specific inhibition of the responses with monoclonal Ia antibodies

Constantin N. Baxevanis, Dorothee Wernet, Zoltan A. Nagy, Paul H. Maurer, Jan Klein

Research output: Contribution to journalArticle

60 Citations (Scopus)

Abstract

The relationship between Ir genes and Ia antigens was studied in the T-cell proliferative responses to two synthetic polypeptides poly(glu40ala60) (GA) and poly(glu51lys34tyr15) (GLT15). The response to GA was found to be controlled by an Ir gene in the I-A subregion, whereas the anti-GLT15 response was shown to be under dual control, one Ir gene mapping probably in the I-A subregion, and the other in the I-E subregion. We obtained two different lines of evidence suggesting identity of Ir and Ia genes. First, the presence of certain serologically identified allelic forms of the I-A-encoded A molecule correlated with the responder status to GA both in inbred strains and in B10.W lines, the latter carrying wild-derived H-2 haplotypes. Thus the Ir and Ia phenotypes were not separable in strains of independent origin. Second, the anti-GA response was completely inhibited by monoclonal antibodies against determinants on the A molecule (Ia.8, 15, and 19), but not by a monoclonal antibody against a determinant on the E molecule (Ia.7). In contrast, the anti-GLT15 response was only inhibited by a monoclonal antibody against the E molecule, but not by antibodies against the A molecule. Our data support the hypothesis that Ia antigens, as restriction elements for T-cell recognition, may in fact be the phenotypic manifestation of Ir genes.

Original languageEnglish (US)
Pages (from-to)617-628
Number of pages12
JournalImmunogenetics
Volume11
Issue number1
DOIs
StatePublished - Dec 1980

Fingerprint

Monoclonal Antibodies
T-Lymphocytes
Histocompatibility Antigens Class II
Genes
Chromosome Mapping
Haplotypes
Phenotype
Peptides
Antibodies

All Science Journal Classification (ASJC) codes

  • Immunology
  • Genetics

Cite this

Baxevanis, Constantin N. ; Wernet, Dorothee ; Nagy, Zoltan A. ; Maurer, Paul H. ; Klein, Jan. / Genetic control of T-cell proliferative responses to poly(glu40ala60) and poly(glu51lys34tyr15) : Subregion-specific inhibition of the responses with monoclonal Ia antibodies. In: Immunogenetics. 1980 ; Vol. 11, No. 1. pp. 617-628.
@article{2a7aab196c2c48cb998c58baf2187e3f,
title = "Genetic control of T-cell proliferative responses to poly(glu40ala60) and poly(glu51lys34tyr15): Subregion-specific inhibition of the responses with monoclonal Ia antibodies",
abstract = "The relationship between Ir genes and Ia antigens was studied in the T-cell proliferative responses to two synthetic polypeptides poly(glu40ala60) (GA) and poly(glu51lys34tyr15) (GLT15). The response to GA was found to be controlled by an Ir gene in the I-A subregion, whereas the anti-GLT15 response was shown to be under dual control, one Ir gene mapping probably in the I-A subregion, and the other in the I-E subregion. We obtained two different lines of evidence suggesting identity of Ir and Ia genes. First, the presence of certain serologically identified allelic forms of the I-A-encoded A molecule correlated with the responder status to GA both in inbred strains and in B10.W lines, the latter carrying wild-derived H-2 haplotypes. Thus the Ir and Ia phenotypes were not separable in strains of independent origin. Second, the anti-GA response was completely inhibited by monoclonal antibodies against determinants on the A molecule (Ia.8, 15, and 19), but not by a monoclonal antibody against a determinant on the E molecule (Ia.7). In contrast, the anti-GLT15 response was only inhibited by a monoclonal antibody against the E molecule, but not by antibodies against the A molecule. Our data support the hypothesis that Ia antigens, as restriction elements for T-cell recognition, may in fact be the phenotypic manifestation of Ir genes.",
author = "Baxevanis, {Constantin N.} and Dorothee Wernet and Nagy, {Zoltan A.} and Maurer, {Paul H.} and Jan Klein",
year = "1980",
month = "12",
doi = "10.1007/BF01567830",
language = "English (US)",
volume = "11",
pages = "617--628",
journal = "Immunogenetics",
issn = "0093-7711",
publisher = "Springer Verlag",
number = "1",

}

Genetic control of T-cell proliferative responses to poly(glu40ala60) and poly(glu51lys34tyr15) : Subregion-specific inhibition of the responses with monoclonal Ia antibodies. / Baxevanis, Constantin N.; Wernet, Dorothee; Nagy, Zoltan A.; Maurer, Paul H.; Klein, Jan.

In: Immunogenetics, Vol. 11, No. 1, 12.1980, p. 617-628.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Genetic control of T-cell proliferative responses to poly(glu40ala60) and poly(glu51lys34tyr15)

T2 - Subregion-specific inhibition of the responses with monoclonal Ia antibodies

AU - Baxevanis, Constantin N.

AU - Wernet, Dorothee

AU - Nagy, Zoltan A.

AU - Maurer, Paul H.

AU - Klein, Jan

PY - 1980/12

Y1 - 1980/12

N2 - The relationship between Ir genes and Ia antigens was studied in the T-cell proliferative responses to two synthetic polypeptides poly(glu40ala60) (GA) and poly(glu51lys34tyr15) (GLT15). The response to GA was found to be controlled by an Ir gene in the I-A subregion, whereas the anti-GLT15 response was shown to be under dual control, one Ir gene mapping probably in the I-A subregion, and the other in the I-E subregion. We obtained two different lines of evidence suggesting identity of Ir and Ia genes. First, the presence of certain serologically identified allelic forms of the I-A-encoded A molecule correlated with the responder status to GA both in inbred strains and in B10.W lines, the latter carrying wild-derived H-2 haplotypes. Thus the Ir and Ia phenotypes were not separable in strains of independent origin. Second, the anti-GA response was completely inhibited by monoclonal antibodies against determinants on the A molecule (Ia.8, 15, and 19), but not by a monoclonal antibody against a determinant on the E molecule (Ia.7). In contrast, the anti-GLT15 response was only inhibited by a monoclonal antibody against the E molecule, but not by antibodies against the A molecule. Our data support the hypothesis that Ia antigens, as restriction elements for T-cell recognition, may in fact be the phenotypic manifestation of Ir genes.

AB - The relationship between Ir genes and Ia antigens was studied in the T-cell proliferative responses to two synthetic polypeptides poly(glu40ala60) (GA) and poly(glu51lys34tyr15) (GLT15). The response to GA was found to be controlled by an Ir gene in the I-A subregion, whereas the anti-GLT15 response was shown to be under dual control, one Ir gene mapping probably in the I-A subregion, and the other in the I-E subregion. We obtained two different lines of evidence suggesting identity of Ir and Ia genes. First, the presence of certain serologically identified allelic forms of the I-A-encoded A molecule correlated with the responder status to GA both in inbred strains and in B10.W lines, the latter carrying wild-derived H-2 haplotypes. Thus the Ir and Ia phenotypes were not separable in strains of independent origin. Second, the anti-GA response was completely inhibited by monoclonal antibodies against determinants on the A molecule (Ia.8, 15, and 19), but not by a monoclonal antibody against a determinant on the E molecule (Ia.7). In contrast, the anti-GLT15 response was only inhibited by a monoclonal antibody against the E molecule, but not by antibodies against the A molecule. Our data support the hypothesis that Ia antigens, as restriction elements for T-cell recognition, may in fact be the phenotypic manifestation of Ir genes.

UR - http://www.scopus.com/inward/record.url?scp=0019301531&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0019301531&partnerID=8YFLogxK

U2 - 10.1007/BF01567830

DO - 10.1007/BF01567830

M3 - Article

C2 - 6086092

AN - SCOPUS:0019301531

VL - 11

SP - 617

EP - 628

JO - Immunogenetics

JF - Immunogenetics

SN - 0093-7711

IS - 1

ER -