Prellner K, Braconier J H, Sjöholm A G
Acta Pathol Microbiol Immunol Scand C. 1985 Dec;93(6):257-63. doi: 10.1111/j.1699-0463.1985.tb02954.x.
The complement (C) profile was investigated in an adult patient with combined IgG2, IgG4 and IgA deficiency and recurrent pneumococcal infections. The analysis revealed no gross impairment of the classic and alternative pathways of C activation. However, the concentrations of circulating C1q were persistently decreased, and the sera contained an excess of C1r-C1s complexes, resembling the C1 aberrations previously found in children with recurrent acute otitis media. The concentrations of C4 in the patient were persistently low. This could be ascribed to partial C4 deficiency with lack of C4A variants. The patient's IgG and IgM antibody responses to pneumococcal capsular polysaccharides and to other bacterial carbohydrate antigens were very poor. Interestingly, pneumococcal C-polysaccharide (CPS) could be detected in serum obtained during infection-free periods. Since CPS has been shown to bind C1q without causing C1 activation, the possibility was considered that the C1 aberrations in serum were due to circulating CPS. After administration of intramuscular gammaglobulin to the patient, the serum C1q levels were observed to return to normal.
对一名患有IgG2、IgG4和IgA联合缺陷及复发性肺炎球菌感染的成年患者的补体(C)谱进行了研究。分析显示C激活的经典途径和替代途径没有明显损害。然而,循环C1q的浓度持续降低,血清中含有过量的C1r-C1s复合物,类似于先前在复发性急性中耳炎儿童中发现的C1异常。该患者的C4浓度持续较低。这可能归因于缺乏C4A变体的部分C4缺陷。该患者对肺炎球菌荚膜多糖和其他细菌碳水化合物抗原的IgG和IgM抗体反应非常差。有趣的是,在无感染期采集的血清中可检测到肺炎球菌C多糖(CPS)。由于已证明CPS可结合C1q而不引起C1激活,因此认为血清中的C1异常是由于循环CPS所致。给该患者肌肉注射丙种球蛋白后,观察到血清C1q水平恢复正常。