Sorrentino Richard Paul, Carton Yves, Govind Shubha
Department of Biology, City College of New York and Graduate School and University Center of the City University of New York, 138th Street and Convent Avenue, New York, New York 10031, USA.
Dev Biol. 2002 Mar 1;243(1):65-80. doi: 10.1006/dbio.2001.0542.
The mechanisms by which an organism becomes immune competent during its development are largely unknown. When infected by eggs of parasitic wasps, Drosophila larvae mount a complex cellular immune reaction in which specialized host blood cells, lamellocytes and crystal cells, are activated and recruited to build a capsule around the parasite egg to block its development. Here, we report that parasitization by the wasp Leptopilina boulardi leads to a dramatic increase in the number of both lamellocytes and crystal cells in the Drosophila larval lymph gland. Furthermore, a limited burst of mitosis follows shortly after infection, suggesting that both cell division and differentiation of lymph gland hemocytes are required for encapsulation. These changes, observed in the lymph glands of third-instar, but never of second-instar hosts, are almost always accompanied by dispersal of the anterior lobes themselves. To confirm a link between host development and immune competence, we infected mutant hosts in which development is blocked during larval or late larval stages. We found that, in genetic backgrounds where ecdysone levels are low (ecdysoneless) or ecdysone signaling is blocked (nonpupariating allele of the transcription factor broad), the encapsulation response is severely compromised. In the third-instar ecdysoneless hosts, postinfection mitotic amplification in the lymph glands is absent and there is a reduction in crystal cell maturation and postinfection circulating lamellocyte concentration. These results suggest that an ecdysone-activated pathway potentiates precursors of effector cell types to respond to parasitization by proliferation and differentiation. We propose that, by affecting a specific pool of hematopoietic precursors, this pathway thus confers immune capacity to third-instar larvae.
生物体在发育过程中获得免疫能力的机制在很大程度上尚不清楚。当被寄生黄蜂的卵感染时，果蝇幼虫会引发复杂的细胞免疫反应，其中专门的宿主血细胞，即扁平细胞和晶细胞，被激活并募集到寄生虫卵周围形成一个囊，以阻止其发育。在这里，我们报告说，黄蜂莱氏果蝇的寄生会导致果蝇幼虫淋巴腺中扁平细胞和晶细胞的数量急剧增加。此外，感染后不久会有有限的有丝分裂爆发，这表明淋巴腺血细胞的细胞分裂和分化对于形成包囊都是必需的。这些变化在三龄幼虫的淋巴腺中观察到，但在二龄宿主中从未观察到，几乎总是伴随着前叶自身的分散。为了证实宿主发育与免疫能力之间的联系，我们感染了在幼虫期或幼虫后期发育受阻的突变宿主。我们发现，在蜕皮激素水平较低（无蜕皮激素）或蜕皮激素信号传导受阻（转录因子broad的非化蛹等位基因）的遗传背景下，包囊反应严重受损。在三龄无蜕皮激素宿主中，感染后淋巴腺中的有丝分裂扩增不存在，晶细胞成熟度降低，感染后循环中的扁平细胞浓度降低。这些结果表明，蜕皮激素激活的途径增强了效应细胞类型的前体对寄生的增殖和分化反应能力。我们提出，通过影响特定的造血前体细胞群，该途径赋予三龄幼虫免疫能力。
