['Bronchiolitis obliterans syndrome (BOS) after lung transplantation (LTx) results from bronchial epithelial cell (BECs) damages, thought to be orchestrated by T cells primed by antigen-presenting cell (APC) presenting allo-antigens. In this cell cross-talk, BECs are also suspected to play a pivotal immunosuppressive role in T cell alloreactivity. We studied the immunomodulating role of BECs in a human ex-vivo model of allogeneic T cell response, both in healthy subjects and LTx recipients.', 'BECs from 35 LTx recipients (n=22 stable, n=13 BOS]) and healthy controls (n=25) were cultured as primary cell cultures. Their inhibitory capacities through the involvement of tolerogenic molecules (human leukocyte antigen [HLA]-G, transforming-growth factor [TGF-β], and interleukin [IL]-10) were tested on a mixed lymphocyte reaction between APCs and recipient T cells.', 'Control BECs inhibited T cell alloproliferation by a mean of 53±7%. This inhibitory effect of BECs was significantly reduced in the stable LTx group (24±8%, p=0.009), but not in the BOS TxP group (53±10%, p=0.97). Neutralization of HLA-G, TGF-β, and IL-10 partially restored T cell alloproliferation, arguing for their involvement in the immunosuppressive effect of BECs. BECs culture supernatant from stable LTx patients with impaired BEC properties showed a skewed Th2-type secretion profile (high IL-4/IFN-γ ratio).'] Is inhibition of T Cell Alloreactivity by Bronchial Epithelium Impaired in Lung Transplant Recipients , Through Pathways Involving TGF-β , IL-10 and HLA-G?