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IgE Responses to Synthetic Polypeptide Antigens

I. Simultaneous Ir Gene and Isotype-Specific Regulation of IgE Responses to L-Glutamic Acid⁶⁰-L-Alanine³⁰-L-Tyrosine¹⁰ (GAT)¹

From the Department of Pathology, Harvard Medical School, 25 Shattuck Street, Boston, Massachusetts 02115

Abstract

The serum IgE response to the synthetic polypeptide antigen L-glutamic acid⁶⁰-L-alanine³⁰-L-tyrosine¹⁰ (GAT) was investigated. The present study details the experimental conditions required to elicit optimal IgE anti-GAT antibody titers, the genetics controlling this response, and the ability of anti-suppressor cell treatments to affect the magnitude and duration of IgE anti-GAT levels in responder and nonresponder strains of mice. Significant IgE anti-GAT titers were obtained in BALB/c (IgG responder) mice after administration of 1 to 100 µg of GAT in adjuvant (Maalox or Maalox-pertussis), with optimal secondary IgE titers after challenge with 1 or 10 µg doses. All IgE responses were transient in comparison to IgG antibody levels. IgE anti-GAT immunity was found to be regulated by a gene(s) in the I-A/I-B subregion of the H-2 complex, in agreement with earlier studies on serum IgG or cell-mediated immunity. Mice bearing the H-2^{ja, p, q, s} haplotypes were nonresponders, and treatment of SJL (H-2^s) or DBA/1 (H-2^q) mice with cyclophosphamide or low dose irradiation to remove suppressor cells failed to permit IgE anti-GAT responses, while markedly augmenting IgE anti-TNP responses in the same mice, and IgE anti-GAT responses in BALB/c mice. However, the presence of functional GAT-specific IgE B cells in nonresponder strains was established by demonstrating IgE anti-GAT responses to GAT complexed with methylated serum albumin in these mice. The implications of these data with respect to H-2 linked Ir gene function and class-specific regulation of antibody responses are discussed.

Footnotes

¹ This work was supported by Grant AI-14732 from the National Institutes of Health and by Grant PCM 75-22422 from the National Science Foundation.

² Supported by an Arthur Sachs grant from Harvard University and by the Pasteur Institute, Paris.