Mesenchymal progenitor in adult lung: Translational work from my laboratory started the field of lung-resident
mesenchymal stromal cells (LR-MSCs) by demonstrating the presence of ling lived mesenchymal progenitors
in transplanted lungs (JCI 2007). We have since defined its role as biomodulators (JI 2008; AJRCMB 2011;
AJPath 2011) and biomarkers (AJRCCM 2011 & JSHLT 2021) and have recently identified its in vivo niche
along the bronchovascular bundles (JCI 2021).

Mechanism(s) of Fibrogenesis and pathogenesis of chronic lung allograft rejection (CLAD): Our work is
focused on understanding transcriptional and translation mechanisms of fibrotic differentiation and autocrine
activation of mesenchymal progenitors. We have defined novel mTORC2/mTORC1 /eIF4E/4EBP/Col1 (J Biol
Chem 2017 & 2018) and NFAT/autotaxin/LPA/beta-catenin signaling axis with role in CLAD pathogenesis
(Stem cells 2012; JCI 2017; Scientific reports 2021). Present R01 funded work is investigating eIF4E
phosphorylation at S209 in fibrotic transformation of LR-MSCs.

Improving lung allograft surveillance: My clinical research interest lie in advancing early detection,
prognostication, and phenotyping of chronic graft failure via use of combined physiologic, radiographic, and
biological markers (Am. J. Respir. Crit. 2005, 2007, 2011, 2015, 2017, 2021). We are presenting conducting a
multi-center study investigating a novel HRCT based quantitative analysis methodology in CLAD prediction.

Animal modelling of chronic graft rejection: We are very proud to have developed two new animal models to
study chronic lung allograft rejection. These orthotopic mouse lung transplant models mimic the two human
phenotypes of chronic rejection (BOS and RAS; AJPath 2015 & JCI insight 2021) and continue to provide us
with a unique resource to study their diverse pathogenesis. New work will harness these models to decipher
mesenchymal progenitors and humoral immune response skewing in RAS.