Dr. Aritra Bhattacharyya is an Assistant Professor at the Indian Statistical Institute, Kolkata, India, specializing in human genetics, pulmonary immunology, and translational research. He earned his Ph.D. in Microbiology from Humboldt University of Berlin, Germany, in 2018. His research focuses on lung fibrosis, immune regulation, macrophage biology, and host–pathogen interactions. Previously, he served as a Scientist-I at Deciduous Therapeutics Inc., USA, and conducted postdoctoral research at the University of California, San Francisco. Dr. Bhattacharyya has published extensively in peer-reviewed journals and has presented his work at international conferences, including the American Thoracic Society and Keystone Symposia.

Immune Cells in Pulmonary Fibrotic Niche: Friend or Foe?Lung fibrosis is a disease characterized by progressive scarring of the lung parenchyma with mean survival rate of 3-5 years. Even though there are currently three FDA approved drugs for the treatment of lung fibrosis, these drugs only reduce the progress of the diseases and not its reversal. Macrophages have recently been identified as key players in the fibrotic niche. In this current study1, we show that the anti-inflammatory cytokine IL10 through its receptor, IL10RA leads to profibrotic polarization of macrophages. Once polarized, these macrophages release pro-fibrotic factor platelet-derived growth factor A (pdgfa) which in turn promotes fibroblast activation. Not only pdgfa, our study2 has also shown that these macrophages secrete ATP via connexin hemi-channel, Cx43. The secreted ATP in turns binds to purinergic receptor, P2rx4 and promotes fibroblast proliferation and myofibroblast activation. Finally, to counteract this myofibroblast activation by macrophages, our study3 demonstrated that treatment of mice post lung injury with AAV9 mediated sphingolipids (AAV-SGPL1) leads to better outcome of pulmonary fibrosis. Thus, taken together, macrophage-fibroblast cross talk is crucial for the development of lung fibrosis and targeting this interaction will help us develop novel therapeutics against lung fibrosis.