Regulation of antibody production by helper T cell clones in experimental autoimmune myasthenia gravis is mediated by IL-4 and antigen-specific T cell factors

D. Asthana, Y. Fujii, G. E. Huston, J. Lindstrom

Research output: Contribution to journalArticle

52 Citations (Scopus)

Abstract

Acetylcholine receptor (AChR)-specific rat T cell clones (CD4+, CD8-, and OX22-) were shown to secrete both Th1 and Th2 lymphokines, IL-2, IL-4, and IFN-γ following stimulation with AChR. These clones helped production of antibody to AChR by B cells which was found to be regulated primarily by IL- 4, not by IL-2, secreted by the T cells in response to AChR. Cell-free supernatants from some AChR-activated T cell clones led to production of low levels of antibody to AChR by B cell-enriched, AChR-primed lymph node cells. Supernatant-regulated help in antibody production by B cells was antigen specific, and antibodies to T cell receptors blocked the antigen-specific activity. Thus, supernatant-mediated help may not be due solely to IL-4, and other factors, possibly including some fragment of the T cell antigen receptor present in the supernatant, appear to contribute to helping antibody production by B cells.

Original languageEnglish
Pages (from-to)240-248
Number of pages9
JournalClinical Immunology and Immunopathology
Volume67
Issue number3 I
DOIs
StatePublished - Jan 1 1993
Externally publishedYes

Fingerprint

Autoimmune Experimental Myasthenia Gravis
Cholinergic Receptors
Helper-Inducer T-Lymphocytes
Interleukin-4
Antibody Formation
Clone Cells
B-Lymphocytes
T-Cell Antigen Receptor
T-Lymphocytes
Interleukin-2
Antibodies
Lymphokines
antigen-specific helper factors
Lymph Nodes
Antigens

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy
  • Pathology and Forensic Medicine

Cite this

Regulation of antibody production by helper T cell clones in experimental autoimmune myasthenia gravis is mediated by IL-4 and antigen-specific T cell factors. / Asthana, D.; Fujii, Y.; Huston, G. E.; Lindstrom, J.

In: Clinical Immunology and Immunopathology, Vol. 67, No. 3 I, 01.01.1993, p. 240-248.

Research output: Contribution to journalArticle

@article{c47c4b4464a54b82bb8a584a89cbf711,
title = "Regulation of antibody production by helper T cell clones in experimental autoimmune myasthenia gravis is mediated by IL-4 and antigen-specific T cell factors",
abstract = "Acetylcholine receptor (AChR)-specific rat T cell clones (CD4+, CD8-, and OX22-) were shown to secrete both Th1 and Th2 lymphokines, IL-2, IL-4, and IFN-γ following stimulation with AChR. These clones helped production of antibody to AChR by B cells which was found to be regulated primarily by IL- 4, not by IL-2, secreted by the T cells in response to AChR. Cell-free supernatants from some AChR-activated T cell clones led to production of low levels of antibody to AChR by B cell-enriched, AChR-primed lymph node cells. Supernatant-regulated help in antibody production by B cells was antigen specific, and antibodies to T cell receptors blocked the antigen-specific activity. Thus, supernatant-mediated help may not be due solely to IL-4, and other factors, possibly including some fragment of the T cell antigen receptor present in the supernatant, appear to contribute to helping antibody production by B cells.",
author = "D. Asthana and Y. Fujii and Huston, {G. E.} and J. Lindstrom",
year = "1993",
month = "1",
day = "1",
doi = "10.1006/clin.1993.1071",
language = "English",
volume = "67",
pages = "240--248",
journal = "Clinical Immunology",
issn = "1521-6616",
publisher = "Academic Press Inc.",
number = "3 I",

}

TY - JOUR

T1 - Regulation of antibody production by helper T cell clones in experimental autoimmune myasthenia gravis is mediated by IL-4 and antigen-specific T cell factors

AU - Asthana, D.

AU - Fujii, Y.

AU - Huston, G. E.

AU - Lindstrom, J.

PY - 1993/1/1

Y1 - 1993/1/1

N2 - Acetylcholine receptor (AChR)-specific rat T cell clones (CD4+, CD8-, and OX22-) were shown to secrete both Th1 and Th2 lymphokines, IL-2, IL-4, and IFN-γ following stimulation with AChR. These clones helped production of antibody to AChR by B cells which was found to be regulated primarily by IL- 4, not by IL-2, secreted by the T cells in response to AChR. Cell-free supernatants from some AChR-activated T cell clones led to production of low levels of antibody to AChR by B cell-enriched, AChR-primed lymph node cells. Supernatant-regulated help in antibody production by B cells was antigen specific, and antibodies to T cell receptors blocked the antigen-specific activity. Thus, supernatant-mediated help may not be due solely to IL-4, and other factors, possibly including some fragment of the T cell antigen receptor present in the supernatant, appear to contribute to helping antibody production by B cells.

AB - Acetylcholine receptor (AChR)-specific rat T cell clones (CD4+, CD8-, and OX22-) were shown to secrete both Th1 and Th2 lymphokines, IL-2, IL-4, and IFN-γ following stimulation with AChR. These clones helped production of antibody to AChR by B cells which was found to be regulated primarily by IL- 4, not by IL-2, secreted by the T cells in response to AChR. Cell-free supernatants from some AChR-activated T cell clones led to production of low levels of antibody to AChR by B cell-enriched, AChR-primed lymph node cells. Supernatant-regulated help in antibody production by B cells was antigen specific, and antibodies to T cell receptors blocked the antigen-specific activity. Thus, supernatant-mediated help may not be due solely to IL-4, and other factors, possibly including some fragment of the T cell antigen receptor present in the supernatant, appear to contribute to helping antibody production by B cells.

UR - http://www.scopus.com/inward/record.url?scp=0027190533&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027190533&partnerID=8YFLogxK

U2 - 10.1006/clin.1993.1071

DO - 10.1006/clin.1993.1071

M3 - Article

C2 - 7684661

AN - SCOPUS:0027190533

VL - 67

SP - 240

EP - 248

JO - Clinical Immunology

JF - Clinical Immunology

SN - 1521-6616

IS - 3 I

ER -