Investigation of anti-WI-l adhesin antibody-mediated protection in experimental pulmonary blastomycosis
Investigation of anti-WI-l adhesin antibody-mediated protection in experimental pulmonary blastomycosis
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DOI：
10.1086/315473
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发表时间：
2000-05-01
影响因子：
6.4
通讯作者：
Klein, BS
中科院分区：
文献类型：
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作者：
Wüthrich, M;Klein, BS
皮肤芽生菌感染后，对WI-1产生强烈的抗体反应，该抗体主要针对粘附结构域，一个25个氨基酸的重复序列，串联重复序列特异性单克隆抗体（mAbs）研究了它们的体外调理活性和它们在小鼠实验性芽生菌病中过继转移保护的能力，针对WI-1的mAbs增强了B的结合和进入。16细胞，但不增强酵母的杀伤或生长抑制。被动转移的8个单克隆抗体WI-1到3个不同的近交系小鼠也没有改善实验感染的过程中，有时恶化。mu缺陷小鼠更耐实验芽生菌病比完整的同窝出生，和被动转移的单克隆抗体到这些小鼠没有保护他们免受实验感染。因此，WI-1的抗体似乎不能改善鼠芽生菌病的结果，并可能增强感染。
Infection with Blastomyces dermatitidis elicits strong antibody responses to the surface adhesin WI-1, The antibodies are directed chiefly against the adhesive domain, a 25-amino-acid repeat, Tandem-repeat-specific monoclonal antibodies (mAbs) were studied for their opsonic activity in vitro and their capacity to adoptively transfer protection in murine experimental blastomycosis, mAbs to WI-1 enhanced binding and entry of B. dermatitidis yeasts into J774.16 cells but did not enhance killing or growth inhibition of the yeast. Passive transfer of 8 mAbs to WI-1 into 3 different inbred strains of mice also did not improve the course of experimental infection and sometimes worsened it. mu-deficient mice were more resistant to experimental blastomycosis than were intact littermates, and passive transfer of the mAbs into these mice did not protect them against experimental infection. Thus, antibody to WI-1 does not appear to improve the outcome of murine blastomycosis and may enhance the infection.