Miller S, Schreuer D, Hammerberg B
Department of Microbiology, Pathology and Parasitology, College of Veterinary Medicine, North Carolina State University, Raleigh 27606.
J Immunol. 1991 Aug 1;147(3):1007-13.
Long standing Brugia pahangi infections in seven dogs, restricted to one rear limb popliteal lymph node and its afferent ducts, were monitored with regard to proliferative responses and antibody production specific for a PBS extract of B. pahangi (BpA) by cells from infected and uninfected lymph nodes and by PBL. Five of 10 dogs were negative for proliferative responses to BpA in node cells from infected limbs, yet they had positive PBL responses, and another was negative in both node cells and PBL. Production of BpA-specific antibody was detected in cultures of node cells from infected limbs of 9 of 10 dogs, but only in two cultures of node cells from uninfected limbs and not at all in PBL cultures. Three dogs with responsive node cells produced the least amount of anti-BpA antibody in culture. Injections of B. pahangi adult worm excretory/secretory products (ES), totaling 1 mg over 48 h, into the limb of the original infections in seven dogs, resulted in inhibition of Ag-driven proliferation by cell populations previously responsive to BpA. There was a loss of PBL responsiveness by all but one infected dog and a loss of node cell response by the two dogs previously responsive in infected and uninfected nodes. This loss of responsiveness lasted at least 28 days in three dogs. There was no evidence of suppression of responses to mitogens either before or after ES injection. In contrast, BpA-specific antibody production was greatly increased in node cells from infected limbs injected with ES. Similar injections into the uninfected limbs of two infected dogs produced no change of proliferative responses or of antibody production in the uninfected node. These results indicate that ES can modulate immune cell, Ag-driven proliferation, and simultaneously enhance antibody production in previously infected nodes. This may promote parasite survival by inhibiting cellular attack based on delayed-type hypersensitivity while directing immune responses toward production of antibodies that are less damaging to the adult helminth.
对7只长期感染马来布鲁线虫的犬进行了监测，感染局限于一侧后肢腘淋巴结及其输入淋巴管，观察感染和未感染淋巴结的细胞以及外周血淋巴细胞（PBL）对马来布鲁线虫PBS提取物（BpA）的增殖反应和抗体产生情况。10只犬中有5只对感染肢体淋巴结细胞对BpA的增殖反应呈阴性，但它们的PBL反应呈阳性，另一只犬的淋巴结细胞和PBL反应均为阴性。在10只犬中，有9只感染肢体淋巴结细胞培养物中检测到了BpA特异性抗体，但未感染肢体的淋巴结细胞培养物中只有两份检测到该抗体，PBL培养物中则完全未检测到。3只淋巴结细胞有反应的犬在培养物中产生的抗BpA抗体量最少。向7只犬原感染肢体注射总共1mg马来布鲁线虫成虫排泄/分泌产物（ES），分48小时注射，导致先前对BpA有反应的细胞群体的抗原驱动增殖受到抑制。除一只感染犬外，所有感染犬的PBL反应性均丧失，先前在感染和未感染淋巴结中有反应的两只犬的淋巴结细胞反应性丧失。这种反应性丧失在3只犬中持续了至少28天。在注射ES之前或之后，均没有证据表明对丝裂原的反应受到抑制。相比之下，注射ES的感染肢体淋巴结细胞中BpA特异性抗体的产生大大增加。对两只感染犬的未感染肢体进行类似注射，未感染淋巴结的增殖反应或抗体产生没有变化。这些结果表明，ES可以调节免疫细胞的抗原驱动增殖，同时增强先前感染淋巴结中的抗体产生。这可能通过抑制基于迟发型超敏反应的细胞攻击来促进寄生虫存活，同时引导免疫反应产生对成虫危害较小的抗体。
