Hayglass K T, Stefura W P
Department of Immunology, University of Manitoba, Winnipeg, Canada.
J Immunol. 1991 Oct 15;147(8):2455-60.
Administration of high m.w. glutaraldehyde-polymerized OVA (termed OVA-POL) before OVA-[A1(OH)3] immunization of C57BL/6 mice markedly impairs their capacity to generate OVA-specific IgE responses, while simultaneously resulting in striking enhancement of Ag-specific IgG2a responses. We demonstrate here that treatment with this class of chemically modified allergen also results in pronounced inhibition of ongoing IgE responses in vivo. The abrogation of well established murine IgE responses that is elicited after treatment with OVA-POL (i) is potent (97%), (ii) is long lived, and (iii) reflects reciprocal regulation of Ag-specific IgE and IgG2a responses in vivo. Moreover, the capacity of OVA-POL-treated mice to generate secondary IgE responses remains strongly decreased for at least 260 days and six subsequent immunizations with native allergen, despite there being no further treatment with modified allergen. These changes in IgE and IgG2a responsiveness are Ag specific and T cell dependent.
在C57BL/6小鼠接受OVA-[A1(OH)3]免疫之前,给予高分子量戊二醛聚合的OVA(称为OVA-POL)会显著损害其产生OVA特异性IgE反应的能力,同时导致Ag特异性IgG2a反应显著增强。我们在此证明,用这类化学修饰的变应原进行治疗还会在体内对正在进行的IgE反应产生明显抑制作用。用OVA-POL治疗后引发的已建立的小鼠IgE反应的消除:(i)效力强大(97%),(ii)持续时间长,并且(iii)反映了体内Ag特异性IgE和IgG2a反应的相互调节。此外,经OVA-POL处理的小鼠产生继发性IgE反应的能力在至少260天内以及随后用天然变应原进行的六次免疫中仍大幅降低,尽管没有再用修饰的变应原进行治疗。IgE和IgG2a反应性的这些变化具有Ag特异性且依赖于T细胞。