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Am. J. Respir. Crit. Care Med., Vol 149, No. 5, May 1994, 1286-1294.

Experimental hypersensitivity pneumonitis. Effect of CD4 cell depletion

M Schuyler, K Gott, B Edwards and KJ Nikula
Department of Medicine, Albuquerque Veterans Administration Medical Center, NM 87108.

We previously demonstrated that Thy1.2+, CD4+, Ia-T cells are responsible for transfer of adoptive murine experimental hypersensitivity pneumonitis (adoptive EHP). To characterize the cells responsible for development of pulmonary inflammation in the recipient animals, we depleted recipients of CD4+ cells using monoclonal antibody GK1.5 before administration of Micropolyspora faeni-sensitized cultured C3H/HeJ spleen cells (SC) and intratracheal (i.t.) challenge with M. faeni. We also 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 days after i.t. challenge with M. faeni in adoptive EHP or 2 days after i.t. challenge with M. faeni in direct EHP. Cultured M. faeni-sensitized SC could transfer EHP to naive animals or those treated with an irrelevant antibody. Depletion of CD4+ cells ablated the ability of recipient animals to express adoptive EHP. Two days after i.t. M. faeni (direct EHP), there was extensive neutrophilic infiltration of the lung that was not affected by depletion of CD4+ cells. We conclude that the ability to express adoptive EHP is dependent on the presence of CD4+ cells. In contrast, the acute inflammatory response to M. faeni is not CD4+ cell dependent.


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Copyright © 1994 American Thoracic Society