Although IL-17A was predominantly expressed by Vγ6+/Vδ1+ γδ T cells, a compensatory increase in IL-17A expression by CD4+ T cells was seen in the absence of γδ T cells that resulted in similar levels of IL-17A in the lungs of TCRδ(−/−) and wild-type C57BL/6 mice, suggesting an important role for IL-17A-expressing γδ or αβ T lymphocytes in eliminating the micro-organism and preventing excessive inflammation and eventual lung fibrosis.35 Likewise, in another study of this mouse model, γδ T cells expanded in the lung and inhibited collagen deposition. This evidence concerns the gene CD4 and pulmonary fibrosis.