Antibodies to Toxoplasma gondii major surface protein (SAG-1, P30) inhibit infection of host cells and are produced in murine intestine after peroral infection.
Antibodies to Toxoplasma gondii major surface protein (SAG-1, P30) inhibit infection of host cells and are produced in murine intestine after peroral infection.
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DOI：
10.4049/jimmunol.150.9.3951
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发表时间：
1993-05
影响因子：
4.4
通讯作者：
J. Mineo;R. McLeod;D. Mack;J. Smith;I. Khan;K. Ely;L. Kasper
中科院分区：
文献类型：
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作者：
J. Mineo;R. McLeod;D. Mack;J. Smith;I. Khan;K. Ely;L. Kasper
弓形虫主要表面抗原（SAG-1，P30）的单克隆和多克隆单特异性抗体抑制人成纤维细胞和小鼠肠上皮细胞的感染。从抗P30的多克隆单特异性抗体制备的Fab也具有这种对侵袭的抑制作用，这表明该抗体直接阻断寄生虫对宿主细胞的感染，而不是凝集寄生虫。另一种表面蛋白（P22）的抗体并没有改变体外感染。如果抗体对P30的抑制作用是由于空间位阻或与P30邻接的表面表位的复合，则针对其他表面表位的抗体也将是抑制性的，而它们不是。抗体的尿素处理（其允许区分高和低亲合力抗体）不改变抗P30抗体的作用。这一观察结果表明，抗体对P30的影响不是抗体对P22和P30的亲合力差异的人为结果。来自感染RH或PTg菌株T的小鼠的热灭活抗血清。当用自体野生型寄生虫攻击时，弓形虫（P30+）分别抑制成纤维细胞的感染87%和40%。相反，这些抗血清对P30缺陷突变体（PTgB）感染人成纤维细胞的抑制作用很小（分别为13%和19%）。抗血清提出的P30缺陷型突变体没有显着的影响，感染细胞的野生型菌株具有表面P30。新糖蛋白，BSA-葡糖酰胺，竞争性阻断感染人成纤维细胞的P30+速殖子与表面P30在更高的水平比那些没有表面P30。这一观察结果表明，可能存在糖基化的宿主细胞受体，T。弓形虫主要表面抗原SAG-1（P30）结合。经口感染的小鼠产生针对T.刚地。因此，T.弓形虫SAG-1（P30）在弓形虫感染宿主细胞中具有重要的功能作用。经口感染后弓形虫和伊莱克斯肠抗体反应。
Monoclonal and polyclonal, monospecific antibodies to the major surface antigen of Toxoplasma gondii (SAG-1, P30) inhibit infection of human fibroblasts and murine enterocytes. Fab prepared from polyclonal, monospecific antibody to P30 also have this inhibitory effect on invasion, which indicates that this antibody directly blocks parasite infection of host cells rather agglutinating the parasite. Antibodies to another surface protein (P22) did not alter in vitro infection. If the inhibitory effect of antibody to P30 was due to steric hindrance or complexing of surface epitopes contiguous to P30, antibodies to other surface epitopes would also be inhibitory and they are not. Urea treatment of antibody (which permits discrimination of high and low avidity antibody) did not alter the effect of anti-P30 antibody. This observation indicates that the effect of the antibody to P30 was not an artifact of differences in the avidity of the antibody to P22 and P30. Heat inactivated antisera from mice infected with either RH or PTg strain T. gondii (P30+) inhibit infection of fibroblasts when challenged with autologous wild-type parasites by 87 and 40%, respectively. In contrast, these antisera have little inhibitory effect (13 and 19%, respectively) against infection of human fibroblasts by a P30-deficient mutant (PTgB). Antisera raised to the P30-deficient mutant had no significant effect on infection of cells by wild-type strains that have surface P30. The neoglycoprotein, BSA-glucosamide, competitively blocks infection of human fibroblasts by P30+ tachyzoites with surface P30 in higher level than those without surface P30. This observation indicates that there is likely to be a glycosylated host cell receptor to which T. gondii's major surface Ag SAG-1 (P30) binds. Mice infected perorally develop intestinal IgA antibody to the major 30-kDa epitope of T. gondii. Thus, the major surface epitope of T. gondii, SAG-1 (P30), has an important, functional role in infection of host cells by T. gondii and elicits an intestinal antibody response after peroral infection.