Experimental hypersensitivity pneumonitis: effect of Thy1.2+ and CD8+ cell depletion.

We previously demonstrated that recipient CD4+ cells are necessary for expression of adoptive murine experimental hypersensitivity pneumonitis (EHP). In contrast, the acute inflammatory response to intratracheal (i.t.) administration of Micropolyspora faeni (direct EHP) is not CD4+ cell dependent (Am. J. Respir. Crit. Care Med. 1994;149:1286-1294). To further characterize the cells responsible for development of pulmonary inflammation in recipient animals, we depleted recipients of either Thy1.2+ or CD8+ cells before transfer of M. faeni-sensitized cultured C3H/HeJ spleen cells and i.t. challenge with M. faeni. We used the same depletion technique to determine the contribution of these cells to the pulmonary response to i.t. M. faeni in animals that did not receive cultured cells (direct EHP). The nature and extent of pulmonary inflammatory changes in these animals were assayed either 4 d after i.t. challenge with M. faeni in adoptive EHP or 2 d after i.t. challenge with M. faeni in direct EHP. We also tested the hypothesis that our previously demonstrated ablation of adoptive EHP caused by administration of anti-CD4 antibody was due to depletion of recipient CD4+ cells by allowing recovery of recipient CD4+ cells of anti-CD4-treated animals before i.t. challenge. In addition, we allowed Thy1.2+ cell recovery of anti-Thy1.2-treated animals before i.t. challenge. Cultured M. faeni-sensitized spleen cells could adoptively transfer EHP to animals treated with an irrelevant antibody or PBS. Depletion of Thy1.2+ but not CD8+ cells ablated the ability of recipient animals to express adoptive EHP. Direct EHP was not affected by depletion of Thy1.2+ or CD8+ cells.(ABSTRACT TRUNCATED AT 250 WORDS)