The T Cell and the Airway's Fibrotic Response in Asthma

Stephen T. Holgate D.Sc.¹; Ratko Djukanovi M.D.¹; Peter H. Howarth M.D.¹; Stephen Montefort M.B.B.S.¹; and William Roche Ph.D.²

¹ The Immunopharmacology Group, Southampton General Hospital, Southampton, UK.
² The Pathology Department, Southampton General Hospital, Southampton, UK.

As T cells appear to play a pivotal role in initiating allergic airway inflammation involving mast cells and eosinophils, the epithelium appears to be a major target for the response. With epithelial disruption, myofibroblast proliferation provides a mechanism for the laying down interstitial collagens in an attempt to minimize the effects of losing selective permeability. However, like the epithelium in asthma, myoflbroblasts may take on another function—namely, to provide an additional source of cytokines with their capacity to maintain the inflammatory response. From a functional standpoint, subepithelial fibrosis could contribute to the mechanical disability of the airways in asthma as exemplified by steroid-resistant hyperresponsiveness, and if the process spreads deeper into the airway wall to bronchodilator-resistant airways obstruction, a sequel of poorly controlled and severe disease.