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.