Abstract
The many experimental models of immunologically-induced pulmonary damage have proved that contact with inhaled antigen will induce acute and chronic inflammatory changes in lung, varying from acute, neutrophil-rich interstitial and intra-alveolar exudates, to granulomatous interstitial reactions and interstitial fibrosis. This knowledge is emphasized by the work presented in this Conference by Drs. Richerson and Moore and their colleagues. For most of the studies involving animal models, however, it has been difficult to be precise about the immunopathologic events involved, because of the likelihood that both cellular and humoral immunoreactivities are present.
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