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경구면역을 통한 항원 특이적 IgA 항체 합성에 있어 Cholera Toxin과 Alginate-Microsphere의 효과
송민형,유진수,권명상,성승룡,김용희,권익찬,정서영,양재명,김평현 大韓免疫學會 1996 大韓免疫學會誌 Vol.18 No.3
Secretory (S-IgA) isotype antibody (Ab) is known to play an essential role in the primary defense against various infectious agents in mucosal tissue. However, it has been mostly unsuccessful in the induction of antigen (Ag)-specific IgA Ab response in this site by peroral vaccination. In the present study, we investigated the effect of cholera toxin (CI) as a mucosal adjuvant and alginates-microspheres as a carrier on BSA-specific IgA Ab response in gut-associated lymphoid tissue`(GALT). Peroral immunization of BSA plus CT conferred a great BSA-specific IgA response but IgG response on intestinal fluid (IF). In contrast, intraperitoneal immunization of BSA with Freund's adjuvant readily induced BSA-specific IgG response but IgA response in IF. Further, number of CT specific IgA-secreting cells was substantially increased in mesenteric lymph node when CT-encapsulated-VI alginates-microspheres was administered perorally. Taken together, these results indicate that peroral immunization of soluble antigen in combination of CT or microspheres significantly enhances antigen-specific IgA response in GALT.
Cholera Toxin and Cholera Toxin B Subunit Induce IgA Switching Through the Action of TGF-β1¹
Pyeung-Hyeun Kim,Lars Eckmann,Wha Jung Lee,Wonkyo Han,Martin F,Kagnoff 강원대학교 기초과학연구소 1998 기초과학연구 Vol.9 No.-
Cholera toxin (CT) and its B subunit (CTB) are potent immonogens and adjuvants that, either alone or linked to protein Ags, can stimulate mucosal immune responses, modulate the induction of oral tolerance, and stimulate IgA isotype switching. The present studies addressed the mechanisms by which CT and CTB promote IgA switching. CT and rCTB, in the presence of IL-2, significantly increased IgA isotype switching at the clonal level in populations of purified and LPS-activated murine surface IgA ̄spleen B cells, as determined by ELISA, enzyme linked immunospot assays, and limiting dilution analysis. The IgA stimulatory effects of CT and CTB were independent of the a subunit of CT.CTB and CT dld not increase the secretory rate of IgA-producing cells or the clonal burst size of IgA clones. and did inhibit B cell growth. Because TGF-β1 also Inhibits B cell growth and promotes IgA switching, further studies tested whether the activity of CTB and CT on IgA isotype switching was mediated through TGF-β1. Anti-TGFβ Ab and soluble TGF-β1 type ILR inhibited CTB-and CT-stimulated IgA isotype switching. Furthermore increased TGF-β1 mRNA levels and bioactive TGF-β1, within a range shown to induce IgA isotype switching, were detected in cultures of surface IgA ̄B cells stimulated with CT or CTB and IL-2. These data indicate that CTB-and CT-stimulated IgA isotype switching are mediated through TGF-β1. The finding that CTB up-regulates TGF-β1 activity has important implications for understanding the mechanisms by which CTB promotes both IgA mucosal immunity and oral tolerance.
Pyeung-Hyeun Kim,박석래,김현아,Sung-Ki Chun,Jae-Bong Park 한국분자세포생물학회 2005 Molecules and cells Vol.19 No.3
Activation-induced cytidine deaminase (AID) is needed for Ig class switch recombination (CSR). We explored the effect of LPS on the expression of AID during B cell differentiation, and the role of AID in IgA isotype expression. In normal spleen B cells, LPS increased AID transcription up to 48 h post-stimulation, i.e. around the time of Ig CSR. TGF-β1 and AID were requiredfor IgA expression, and LPS contributed toTGFβ1-induced IgA production largely by inducing AID. Interestingly, LPS repressed AID transcription in sIgA+ B cells but still stimulated IgA production mainly by increasing the rate of IgA secretion. Our data indicate that LPS contributes to TGFβ1-induced IgA isotype expression in at least two ways: by stimulating AID transcription before CSR and by enhancing the IgA secretion rate after CSR.