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장상피세포에서 enteroinvasive E. coli에 의한 NF-k B와 NF-k B 목표유전자 활성화에 있어서 Nod1의 역할
김재규 ( Kim Jae Gyu ),( Martin F. Kagnoff ) 대한소화기학회 2003 대한소화기학회 추계학술대회 Vol.2003 No.-
선천면역 (innate immunity)은 숙주세포에는 없는 감염미생물이 공통으로 가지고 있는 구조물 (pathogen associated molecular pattern, PAMP)에 대한 반응으로 이루어지며 pattern-recognition receptor (PRR)에 의해 인식된다. Nod1 (CARD4)은 intracellular PRR의 하나이며 세포자멸사의 조절인자인 Apaf-1과 유사하고 caspase-9을 통해 세포자멸사를 촉진시키는 작
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.