In summary, the more severe fibrosis response of Tlr2,4−/− mice, compared to wildtype C57BL/6J mice, occurred with earlier onset neutrophilia, a reduced frequency of pulmonary Th1 cells in the presence of increased Th17 cell frequency, and greater amounts of Il6 and Il17; whereas the sparing of lung disease which occurred in the absence of Il17, featured a prominent pulmonary Th1 lymphocytic response. This evidence concerns the gene TLR2 and lung disorder.