Total lung gene expression data of Pneumocystis-infected wildtype and IFN-gamma knockout mice.

Pulmonary hypertension (PH) is a disease of diverse etiology. While primary PH can develop in the absence of prior disease, PH more commonly develops in conjunction with other pulmonary pathologies. We previously reported a mouse model in which PH occurs as a sequelae of Pneumocystis infection in the context of transient CD4 depletion. Here, we demonstrate that instead of the expected Th2 pathways, the Th1 cytokine IFN- was essential for the development of PH, as wild type mice developed PH, but not IFN- knockout mice.

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