Nutman T B, Kumaraswami V, Pao L, Narayanan P R, Ottesen E A
J Immunol. 1987 Jun 1;138(11):3954-9.
The immunoregulatory mechanisms involved in B cell function in patients with varying clinical manifestations of bancroftian filariasis were examined by studying the ability of peripheral blood mononuclear cells (PBMC) or PBMC subpopulations from patients with elephantiasis, asymptomatic microfilaremia (MF), and acute tropical pulmonary eosinophilia (TPE) to produce polyclonal and parasite-specific antibody in vitro, both spontaneously and in response to a mitogen (PWM) and to parasite antigen. When the spontaneous or mitogen-driven polyclonal responses were examined, all groups produced significant amounts of IgM and IgG; those with TPE produced extremely high levels. However, when in vitro parasite antigen-specific responses were examined, those with MF were unable to produce filaria-specific antibody either spontaneously or in response to PWM or parasite antigen; in contrast, patients with chronic lymphatic obstruction or TPE produced large quantities. Removal of neither adherent cells nor T8+ T cells affected the parasite-specific B cell anergy seen in those with MF. This absent or severely diminished capacity to produce antibody on parasite antigenic stimulation in patients with MF is likely responsible for the low levels of parasite-specific antibody seen in this most common clinical manifestation of bancroftian filariasis. Its inability to be reversed by the removal of "suppressor elements" suggests a state of B cell unresponsiveness to the parasite.
通过研究来自象皮肿患者、无症状微丝蚴血症（MF）患者和急性热带肺嗜酸性粒细胞增多症（TPE）患者的外周血单个核细胞（PBMC）或PBMC亚群在体外自发以及对丝裂原（PWM）和寄生虫抗原产生多克隆抗体和寄生虫特异性抗体的能力，来检测班氏丝虫病不同临床表现患者中参与B细胞功能的免疫调节机制。当检测自发或丝裂原驱动的多克隆反应时，所有组均产生了大量的IgM和IgG；TPE患者产生的水平极高。然而，当检测体外寄生虫抗原特异性反应时，MF患者无论是自发还是对PWM或寄生虫抗原均无法产生丝虫特异性抗体；相比之下，慢性淋巴阻塞患者或TPE患者则产生大量抗体。去除贴壁细胞或T8 + T细胞均不影响MF患者中所见的寄生虫特异性B细胞无反应性。MF患者在寄生虫抗原刺激下产生抗体的能力缺失或严重减弱，可能是导致班氏丝虫病这种最常见临床表现中寄生虫特异性抗体水平低下的原因。其无法通过去除“抑制元件”而逆转，提示B细胞对寄生虫无反应状态。
