Babu S, Shultz L D, Rajan T V
Department of Pathology, University of Connecticut Health Center, Connecticut, Farmington 06030, USA.
Exp Parasitol. 1999 Sep;93(1):55-7. doi: 10.1006/expr.1999.4438.
The host-parasite interactions of Brugia malayi in mice are complex and multifactorial. In order to study the role of T cells in early B. malayi development, we infected TCRalpha(null) mice, which retain a population of CD4+ TCRbeta+ cells and TCRbeta(null) mice, which lack all TCRalphabeta(+) T cells. TCRalpha(null) mice were permissive to L4 larval and adult worm development but TCRbeta(null) mice were not. Depletion of the CD4(+) T cells in the former abrogated the permissive phenotype. It appears that the CD4(+) TCRbeta(+) T cells that have been described in TCRalpha(null) mice may facilitate early B. malayi development. These data are similar to our earlier demonstration of the role of NK cells in facilitating worm growth in SCID mice.
马来布鲁线虫在小鼠体内的宿主-寄生虫相互作用是复杂且多因素的。为了研究T细胞在马来布鲁线虫早期发育中的作用，我们感染了TCRα基因敲除小鼠（其保留了一群CD4⁺ TCRβ⁺细胞）和TCRβ基因敲除小鼠（其缺乏所有TCRαβ⁺ T细胞）。TCRα基因敲除小鼠允许L4幼虫和成虫发育，但TCRβ基因敲除小鼠则不允许。前者中CD4⁺ T细胞的耗竭消除了这种允许性表型。看来，在TCRα基因敲除小鼠中所描述的CD4⁺ TCRβ⁺ T细胞可能促进马来布鲁线虫的早期发育。这些数据与我们早期关于NK细胞在促进SCID小鼠体内蠕虫生长中的作用的证明相似。
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