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 language | English |
|---|---|
| Pages (from-to) | 240-248 |
| Number of pages | 9 |
| Journal | Clinical Immunology and Immunopathology |
| Volume | 67 |
| Issue number | 3 I |
| DOIs | |
| State | Published - Jan 1 1993 |
| Externally published | Yes |
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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 journal › Article
}
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.
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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 -