Antigen-specific inhibition of ongoing murine IgE responses. II. Inhibition of IgE responses induced by treatment with glutaraldehyde-modified allergens is paralleled by reciprocal increases in IgG2a synthesis.
Antigen-specific inhibition of ongoing murine IgE responses. II. Inhibition of IgE responses induced by treatment with glutaraldehyde-modified allergens is paralleled by reciprocal increases in IgG2a synthesis.
复制标题
抗原特异性抑制正在进行的小鼠 IgE 反应。
DOI：
10.4049/jimmunol.147.8.2455
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发表时间：
1991
影响因子：
4.4
通讯作者：
W. Stefura
中科院分区：
文献类型：
--
作者：
K. HayGlass;W. Stefura
高分子量给药在C57 BL/6小鼠的OVA-[Al（OH）3]免疫之前，用戊二醛解聚的OVA（称为OVA-POL）显著地损害它们产生OVA特异性IgE应答的能力，同时导致Ag特异性IgG 2a应答的显著增强。我们在这里证明，这类化学修饰的过敏原的治疗也导致在体内进行的IgE反应的显着抑制。在用OVA-POL处理后引起的良好建立的鼠IgE应答的消除（i）是有效的（97%），（ii）是长寿命的，并且（iii）反映了体内Ag特异性IgE和IgG 2a应答的相互调节。此外，OVA-POL处理的小鼠产生二次IgE应答的能力在至少260天和随后的6次天然过敏原免疫中仍然强烈降低，尽管没有用修饰的过敏原进一步处理。IgE和IgG 2a反应性的这些变化是Ag特异性和T细胞依赖性的。
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.