Extract

Since the failure of the PANTHER trial in 2012 [1] and the demonstration that immunosuppressants could be harmful for idiopathic pulmonary fibrosis (IPF) patients, the role of immunity in lung fibrosis has been somehow neglected. Later, the negative results of clinical trials that evaluated the effect of a targeted inhibition of tumour necrosis factor-α [2], CCL2 [3], or interleukin (IL)-13 and/or IL-4 [4, 5], have reinforced the opinion that immune-related cytokines were not a target of choice in IPF. However, recent data have emerged suggesting that immune cells present within fibrotic areas of the lung might either accelerate or slow down the fibrotic process, through their interplay with alveolar epithelial cells and fibroblasts [6]. Ever since, the potential role of lymphoid cells in IPF is under serious consideration, supported by the identification of lymphoid populations essential for the reparative process after organ injury [7].