Haldar J P, Ghose S, Saha K C, Ghose A C
Infect Immun. 1983 Nov;42(2):702-7. doi: 10.1128/iai.42.2.702-707.1983.
Cell-mediated immune (CMI) response in 16 Indian kala-azar (KA) and 12 post-kala-azar dermal leishmaniasis (PKADL) patients was studied in detail by in vitro lymphocyte transformation experiments and by in vivo skin testing. Peripheral blood lymphocytes of active KA patients failed to be stimulated by leishmania antigen. On the other hand, lymphocytes from a majority of the active KA patients could be stimulated by phytohemagglutinin. Active KA patients also failed to show delayed type hypersensitivity reaction to leishmanin, although 72% of them showed delayed type hypersensitivity to a purified protein derivative of tuberculin. Longitudinal studies indicated that antigen-specific CMI response usually appeared in treated KA patients after 12 to 20 weeks of antileishmanial drug therapy, although individual variations were noted. CMI response in PKADL patients was variable as about two-thirds of them showed positive sensitization to leishmania antigen in either in vivo or in vitro tests. Usually, patients with newly acquired PKADL exhibited better CMI response than those with chronic PKADL. However, lymphocytes from all of these patients could be stimulated normally by phytohemagglutinin. Results presented in this study show an impairment of CMI response in active KA which appears to be more specific to leishmania than generalized in nature. Moreover, restoration of specific T-cell responsiveness was aided by antileishmanial drug therapy which resulted in the reduction of antigenic load by parasite destruction and a concomitant decrease in circulating antibody levels, particularly that of the immunoglobulin G class. We suggest that the protection afforded by specific CMI response against Leishmania donovani infection may not be absolute and probably depends on other host-related factors leading to parasite destruction and patient recovery.
通过体外淋巴细胞转化实验和体内皮肤试验,对16例印度黑热病(KA)患者和12例黑热病后皮肤利什曼病(PKADL)患者的细胞介导免疫(CMI)反应进行了详细研究。活动性KA患者的外周血淋巴细胞未被利什曼原虫抗原刺激。另一方面,大多数活动性KA患者的淋巴细胞可被植物血凝素刺激。活动性KA患者对利什曼原虫素也未表现出迟发型超敏反应,尽管其中72%的患者对结核菌素纯蛋白衍生物表现出迟发型超敏反应。纵向研究表明,抗原特异性CMI反应通常在抗利什曼原虫药物治疗12至20周后出现在接受治疗的KA患者中,尽管存在个体差异。PKADL患者的CMI反应各不相同,约三分之二的患者在体内或体外试验中对利什曼原虫抗原有阳性致敏反应。通常,新感染PKADL的患者比慢性PKADL患者表现出更好的CMI反应。然而,所有这些患者的淋巴细胞都能被植物血凝素正常刺激。本研究结果显示,活动性KA患者的CMI反应受损,这似乎对利什曼原虫更具特异性,而非全身性受损。此外,抗利什曼原虫药物治疗有助于恢复特异性T细胞反应性,该治疗通过破坏寄生虫减少了抗原负荷,并同时降低了循环抗体水平,尤其是免疫球蛋白G类抗体水平。我们认为,特异性CMI反应对杜氏利什曼原虫感染提供的保护可能不是绝对的,可能取决于导致寄生虫破坏和患者康复的其他宿主相关因素。