Idiopathic pulmonary fibrosis (IPF) entails complex pathophysiological processes and complicated mechanisms. It is a type of lung disease that has no known cure. The disease's chronic inflammatory response is triggered by the abnormal activation of alveolar cells that create mediators that promote the development of myofibroblast and fibroblast foci. Usually, there is an excessive level of collagens and extracellular matrix deposition that lead to the destruction of the lung's architecture. The cause and pathogenesis of IPF are relatively complicated and unknown. The role of inflammation in the pathogenesis of IPF is still controversial. If only inflammation was the only crucial element to the disease events, lung fibrosis pathology would mean an influx of inflammatory cells, and the disease would act in response to immunosuppression. However, neither of these is true. Recent studies indicate that the pathophysiology of the disease is more a consequence of fibroblast dysfunction than poorly modulated inflammation. A broad range of factors has been recognized as crucial mediators in fibrosis. This article does not intend to deliver a comprehensive review of the molecular mechanisms in IPF but will concentrate on specific topics relating to IPF pathogenesis with relevance to immune modulation. In addition, we focus on the key mediators driving the pathogenesis of pulmonary fibrosis irrespective of their etiology, in conjunction with an overview of how these studies can be translated into appropriate or future diagnostic/therapeutic applications.