자가면역성 폐질환에 대한 실험적 연구 = Immunopathologic Studies of An Experimental Model Resembling Goodpasture`s Syndrome자가면역성 폐질환에 대한 실험적 연구

다국어 초록 (Multilingual Abstract)

Goodpasture`s syndrome has been used as the prototype for autoimmunity to the basement membrane. To induce autoimmune lung disease, we immunized Sprague-Dawley rats with type IU collagen, laminin or CFA (complete Freund`s adjuvant), and boosted twice biweekly. One half of the rats were exposed to 1009 09 for 48 hours or 60 hours and then sacrificed two weeks after the last immunization. The results were as follows: 1) The immunized rats of both groups showed a high antibody titer against each antigen and high lymphocyte proliferative response to concanavalin A and immunizing antigens. 2) Histopathologically; O2 exposed and immunized rats showed neutrophil and plasma rell infiltration into edematous stroma and exudate in alveoli without hemorrhage. There was no IgG depostition in lung tissue by immunofluorescence study. In conclusion, animals immunized with type IV collagen and laminin showed high antibody titer but no deposition of IgG in the alveolar basement membrane suggesting that: a) antibodies did not contact the alveolar basement membrane (ABM) b) antibodies produced are weak antibodies similar to the autologous phase of passive immunization, where the lesions produced are less severe than the heterologous and take longer to develop. Thus the 4H;md 60 hour of increased capillary permeablility may not have allowed enough contact time betwen the ABM and antibody to cause lesions. O2 injury and immune injury to ABM were additive in this rat model. Since there was no 1gCi deposition and thus no evidence for humoral injury, cell mediated immunity contributed to alveolar injury. Thus, in Goodpasture`s syndrome, cell mediated immunity as well as anitobdy and complement mediated injury may contribute to the pathologic changes seen.