Abstract
(BALB/cxSJL)F1 mice, perinatally injected with peptide-N-glyconase F-treated, deglycosylated IgE heavy chain or recombinant IgE heavy chain (CHε2-CHε4), were profoundly inhibited in antigen-specific IgE production. There exist minimally two tolerogenic IgE peptides, residing in the CHε2 and CHε4 domains. Peptide I, generated by V8 protease, comprises 39 amino acids within CHε2, beginning at amino acid 103. Peptide E begins at amino acid 312 of the CHε 4 domain and extends through the CHε4 domain. The total lack of antigenspecific IgE responses in IgE peptide-treated mice was not due to overproduction of interferon-γ, nor lack of interleukin (IL)-4, as predicted by the Th2/IL-4 paradigm for IgE production. IgE-tolerant mice exhibited comparable levels of circulating anti-IgE antibodies to those of PBS-treated control mice. IgG obtained from sera of both sources failed to inhibit IgE responses in vitro. Moreover, IgE responses of spleen cells from IgE peptides-treated mice were restored by CD4+ T cells from PBS-treated control mice. We hypothesize that regulation of antigen-specific IgE responses is mediated by CD4+ T cells which normally recognize IgE peptides on IgE precursor B cells, and can be rendered tolerant by perinatal IgE peptide treatment.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1043-1049 |
| Number of pages | 7 |
| Journal | European Journal of Immunology |
| Volume | 26 |
| Issue number | 5 |
| DOIs | |
| State | Published - May 1996 |
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Keywords
- Cytokine
- IgE peptide
- Immunoregulation
- Tolerance
ASJC Scopus subject areas
- Immunology
Cite this
Peptides derived from IgE heavy chain constant region induce profound IgE isotype-specific tolerance. / Wang, Yanyu; Schmaltz, Robert; Liu, Fu-Tong; Robertson, Michael W.; Petro, Thomas M.; Chen, Swey Shen.
In: European Journal of Immunology, Vol. 26, No. 5, 05.1996, p. 1043-1049.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Peptides derived from IgE heavy chain constant region induce profound IgE isotype-specific tolerance
AU - Wang, Yanyu
AU - Schmaltz, Robert
AU - Liu, Fu-Tong
AU - Robertson, Michael W.
AU - Petro, Thomas M.
AU - Chen, Swey Shen
PY - 1996/5
Y1 - 1996/5
N2 - (BALB/cxSJL)F1 mice, perinatally injected with peptide-N-glyconase F-treated, deglycosylated IgE heavy chain or recombinant IgE heavy chain (CHε2-CHε4), were profoundly inhibited in antigen-specific IgE production. There exist minimally two tolerogenic IgE peptides, residing in the CHε2 and CHε4 domains. Peptide I, generated by V8 protease, comprises 39 amino acids within CHε2, beginning at amino acid 103. Peptide E begins at amino acid 312 of the CHε 4 domain and extends through the CHε4 domain. The total lack of antigenspecific IgE responses in IgE peptide-treated mice was not due to overproduction of interferon-γ, nor lack of interleukin (IL)-4, as predicted by the Th2/IL-4 paradigm for IgE production. IgE-tolerant mice exhibited comparable levels of circulating anti-IgE antibodies to those of PBS-treated control mice. IgG obtained from sera of both sources failed to inhibit IgE responses in vitro. Moreover, IgE responses of spleen cells from IgE peptides-treated mice were restored by CD4+ T cells from PBS-treated control mice. We hypothesize that regulation of antigen-specific IgE responses is mediated by CD4+ T cells which normally recognize IgE peptides on IgE precursor B cells, and can be rendered tolerant by perinatal IgE peptide treatment.
AB - (BALB/cxSJL)F1 mice, perinatally injected with peptide-N-glyconase F-treated, deglycosylated IgE heavy chain or recombinant IgE heavy chain (CHε2-CHε4), were profoundly inhibited in antigen-specific IgE production. There exist minimally two tolerogenic IgE peptides, residing in the CHε2 and CHε4 domains. Peptide I, generated by V8 protease, comprises 39 amino acids within CHε2, beginning at amino acid 103. Peptide E begins at amino acid 312 of the CHε 4 domain and extends through the CHε4 domain. The total lack of antigenspecific IgE responses in IgE peptide-treated mice was not due to overproduction of interferon-γ, nor lack of interleukin (IL)-4, as predicted by the Th2/IL-4 paradigm for IgE production. IgE-tolerant mice exhibited comparable levels of circulating anti-IgE antibodies to those of PBS-treated control mice. IgG obtained from sera of both sources failed to inhibit IgE responses in vitro. Moreover, IgE responses of spleen cells from IgE peptides-treated mice were restored by CD4+ T cells from PBS-treated control mice. We hypothesize that regulation of antigen-specific IgE responses is mediated by CD4+ T cells which normally recognize IgE peptides on IgE precursor B cells, and can be rendered tolerant by perinatal IgE peptide treatment.
KW - Cytokine
KW - IgE peptide
KW - Immunoregulation
KW - Tolerance
UR - http://www.scopus.com/inward/record.url?scp=0029979937&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0029979937&partnerID=8YFLogxK
U2 - 10.1002/eji.1830260513
DO - 10.1002/eji.1830260513
M3 - Article
C2 - 8647165
AN - SCOPUS:0029979937
VL - 26
SP - 1043
EP - 1049
JO - European Journal of Immunology
JF - European Journal of Immunology
SN - 0014-2980
IS - 5
ER -