Schwarz M I, Dreisin R B, Pratt D S, Stanford R E
J Lab Clin Med. 1978 Jun;91(6):929-38.
Immunologic mechanisms have been implicated in the pathogenesis of the IIP's. Thirty five patients with IIP were divided into three groups: group I, seven subjects with DIP; group II, thirteen with UIP; and group III, fifteen with mural fibrosis. Lung biopsies were exposed to fluorescein-conjugated antisera to IgG, IgA, IgE, IgM, C3, fibrinogen, and albumin. In group I, all patients demonstrated IgG and C3 in a granular pattern lining alveolar walls. Similarly, in group II, all had IgG and 10 had C3 within alveolar walls. In contrast, only two group III subjects demonstrated IgG and none C3. Only one of 19 control subjects hav alveolar wall immunoglobulin and C3 deposition. The incidence of positive rheumatoid and antinuclear factors was similar in all three study groups. These data suggest that immune complex deposition may play a role in the pathogenesis of the cellular interstitial pneumonias and that once mural fibrosis supervenes, these complexes are no longer present.
免疫机制与特发性间质性肺炎（IIP）的发病机制有关。35例IIP患者被分为三组：第一组，7例脱屑性间质性肺炎（DIP）患者；第二组，13例寻常型间质性肺炎（UIP）患者；第三组，15例壁层纤维化患者。肺活检组织用异硫氰酸荧光素标记的抗IgG、IgA、IgE、IgM、C3、纤维蛋白原和白蛋白的抗血清进行检测。在第一组中，所有患者的肺泡壁均有颗粒状IgG和C3沉积。同样，在第二组中，所有患者肺泡壁均有IgG沉积，10例有C3沉积。相比之下，第三组中只有2例有IgG沉积，无一例有C3沉积。19例对照受试者中只有1例有肺泡壁免疫球蛋白和C3沉积。类风湿因子和抗核因子阳性率在三个研究组中相似。这些数据表明，免疫复合物沉积可能在细胞性间质性肺炎的发病机制中起作用，而一旦发生壁层纤维化，这些复合物就不再存在。
