The current hypothesis on the development of IPF conceptualizes ongoing, multiple, small focal episodes of epithelial lung injury followed by a pathologic fibrotic repair mechanism and an imbalance in the expression of T-helper type 1 (Th1) and Th2 cytokines [5,26] CD8+ TLs are known to produce type 2 cytokines such as interleukin-4 and interleukin-5 [27]. This evidence concerns the gene CD8A and idiopathic pulmonary fibrosis.