Rajan T V, Nelson F K, Shultz L D, Koller B H, Greiner D L
Department of Pathology, University of Connecticut Health Center, Farmington 06030.
J Parasitol. 1992 Aug;78(4):744-6.
Mice are resistant to the establishment of infection with the nematode parasite Brugia malayi, an etiologic agent of human lymphatic filariasis. We have recently shown that T and B lymphocyte-deficient C.B.-17 scid/scid mice are permissive for infection with this parasite, whereas coisogenic C.B.-17+/+ mice are resistant. This observation suggests that T and B lymphocytes that comprise the antigen-specific immune system orchestrate murine resistance to B. malayi. In order to define the component of the antigen-specific immune response that is responsible for this resistance, we have tested the susceptibility of beta 2M-/- mice to infection with B. malayi L3 larvae. These mice are homozygous for insertional disruption of their B2m genes, which encode beta 2-microglobulin, the small subunit of the major histocompatibility (MHC) antigens. They do not express beta 2-microglobulin and, as a consequence, fail to express the class I major histocompatibility antigens, and they do not develop the CD8+ class I MHC-restricted cytotoxic T cell subset. We find that these mice are completely resistant to B. malayi, indicating that the CD8+ T lymphocyte subset is not an obligate requirement for murine resistance to human filarial parasites.
小鼠对感染线虫寄生虫马来布鲁线虫具有抵抗力,马来布鲁线虫是人类淋巴丝虫病的病原体。我们最近发现,T和B淋巴细胞缺陷的C.B.-17 scid/scid小鼠对这种寄生虫感染具有易感性,而同基因的C.B.-17+/+小鼠则具有抵抗力。这一观察结果表明,构成抗原特异性免疫系统的T和B淋巴细胞协调了小鼠对马来布鲁线虫的抵抗力。为了确定负责这种抵抗力的抗原特异性免疫反应的组成部分,我们测试了β2M-/-小鼠对马来布鲁线虫L3幼虫感染的易感性。这些小鼠的B2m基因发生插入性破坏,该基因编码β2-微球蛋白,即主要组织相容性(MHC)抗原的小亚基,它们是纯合子。它们不表达β2-微球蛋白,因此无法表达I类主要组织相容性抗原,也不会发育出CD8+ I类MHC限制性细胞毒性T细胞亚群。我们发现这些小鼠对马来布鲁线虫完全具有抵抗力,这表明CD8+ T淋巴细胞亚群不是小鼠抵抗人类丝虫寄生虫的必要条件。