INTERLEUKIN-1-BETA PARTIALLY ALLEVIATES CYCLOSPORINE-A-INDUCED SUPPRESSION OF IGG1 ISOTYPE RESPONSE TO THYROGLOBULIN IN BALB C MICE IN-VIVO/

Citation
Sk. Dalai et al., INTERLEUKIN-1-BETA PARTIALLY ALLEVIATES CYCLOSPORINE-A-INDUCED SUPPRESSION OF IGG1 ISOTYPE RESPONSE TO THYROGLOBULIN IN BALB C MICE IN-VIVO/, Immunology, 95(1), 1998, pp. 83-89
Citations number
27
Categorie Soggetti
Immunology
Journal title
ISSN journal
00192805
Volume
95
Issue
1
Year of publication
1998
Pages
83 - 89
Database
ISI
SICI code
0019-2805(1998)95:1<83:IPACS>2.0.ZU;2-X
Abstract
Cyclosporin A (CsA) at 120 mg/kg body weight when injected subcutaneou sly into BALB/c mice along with thyroglobulin emulsified in incomplete Freund's adjuvant (IFA) was found to suppress antigen-specific IgG ti tre by 86%. Isotyping revealed that both IgG1 and IgG2a titres were su ppressed by 87% and 57%, respectively. But under identical conditions when complete Freund's adjuvant (CFA) was used, the suppression of ant igen-specific IgG, IgG1 and IgG2a titres was 50%, 51% and 55%, respect ively. Injection of anti-IL-1 beta-neutralizing hamster monoclonal ant ibodies along with thyroglobulin and CsA emulsified in CFA increased t he suppression of antigen-specific IgG titre. Under such conditions th e IgG1 titre was suppressed more than the IgG2a titre. Recombinant hum an interleukin-1 receptor antagonist (rhuIL-1ra) also enhanced the sup pression caused by CsA in the presence of CFA but control hamster immu noglobulin had no such effect. Recombinant human IL-1 beta, when admin istered along with thyroglobulin and CsA emulsified in IFA, alleviated the suppression of antigen-specific Ige titre and the IgG1 titre was alleviated more than the IgG2a titre. Under identical conditions, rhuI L-1ra did not alleviate CsA-induced suppression. Lymphocytes from the lymph nodes of thyroglobulin-sensitized BALB/c mice when stimulated in vitro by thyroglobulin in the presence of CsA, secreted very little i nterferon-gamma (IFN-gamma) and IL-4, but on addition of an optimal do se of rhuIL-1 beta, IFN-gamma and IL-4 secretion was partially restore d.