THE IMMUNOAUGMENTING PROPERTIES OF MURINE IGD RESIDE IN ITS C(DELTA)1 AND C(DELTA)3 REGIONS - POTENTIAL ROLE FOR IGD-ASSOCIATED GLYCANS
THE IMMUNOAUGMENTING PROPERTIES OF MURINE IGD RESIDE IN ITS C(DELTA)1 AND C(DELTA)3 REGIONS - POTENTIAL ROLE FOR IGD-ASSOCIATED GLYCANS
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DOI：
10.1093/intimm/5.6.607
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发表时间：
1993-06-01
影响因子：
4.4
通讯作者：
COICO, RF
中科院分区：
文献类型：
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作者：
AMIN, AR;TAMMA, SML;COICO, RF
单次注射二聚体或聚集的IgD后24小时内，小鼠体内具有免疫增强特性的携带CD4+ T细胞的IgD受体（IgD- r）被诱导。在本研究中，我们试图确定IgD中负责IgD- r上调和IgD免疫增强作用的区域。体外和体内CD4+ T细胞上的IgD- r可通过戊二醛聚集的突变体IgD或酶切IgD分子片段(具有C(delta)1结构域（Fd(delta)）或C(delta)3结构域（Fc(delta)）上调。新糖蛋白（d -半乳糖- BSA和n -乙酰- d -氨基葡萄糖- BSA）可以竞争性地阻断体外IgD对IgD- r的上调。此外，当在抗原前1天注射时，聚集的IgD衍生分子KWD1（缺乏C(δ)1）， KWD6(缺乏C（δ)1 + C(δ)-hinge）和Fab（δ）都可以引起抗原特异性一抗和二抗反应的增强，与完整聚集的IgD相比。此外，通过同时注射单体形式的KWD6和Fab(delta)，一抗反应中完整寡聚IgD分子的免疫增强作用被竞争性地阻断。这些结果表明，IgD与IgD- r的结合，之前被证明依赖于存在于Fd（δ）和Fc（δ）区域的n聚糖，也有助于IgD- r的上调和免疫增强。
IgD receptor (IgD-R) bearing CD4+ T cells with immunoaugmenting properties in vivo are induced in mice within 24 h after a single injection of dimeric or aggregated IgD. In the present study, we sought to identify the region(s) of IgD responsible for upregulation of IgD-R and for the immunoaugmenting effect of IgD. IgD-R can be upregulated on CD4+ T cells in vitro and in vivo by glutaraldehyde-aggregated mutant IgD or by fragments of enzymatically digested IgD molecules possessing either the C(delta)1 domain (Fd(delta)) or the C(delta)3 domain (Fc(delta)). Neoglycoproteins (D-galactose - BSA and N-acetyl-D-glucosamine - BSA), can competitively block upregulation of IgD-R by IgD in vitro. Furthermore, when injected 1 day before antigen, the aggregated IgD derived molecules, KWD1 (which lacks C(delta)1), KWD6 (which lacks C(delta)1 plus C(delta)-hinge), and Fab(delta) can all cause augmentation of antigen-specific primary and secondary antibody responses comparable to that achieved with intact aggregated IgD. Moreover, the immunoaugmenting effect of intact oligomeric IgD molecules in primary antibody responses is competitively blocked by simultaneous injection of monomeric forms of KWD6 and Fab(delta). These results suggest that the binding of IgD to IgD-R, previously shown to be dependent on N-glycans present on Fd(delta) and Fc(delta) regions, also contributes to the upregulation of IgD-R and immunoaugmentation.