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Fibroblasts as Sentinel Cells*: Role of the CD40-CD40 Ligand System in Fibroblast Activation and Lung Inflammation and Fibrosis

Julia Kaufman, MS; Beth A. Graf, BS; Edmund C. Leung, PhD; Stephen J. Pollock, BS; Laura Koumas, MS; Sireesha Y. Reddy, MD; Timothy M. Blieden, DMD, PhD; Terry J. Smith, MD; Richard P. Phipps, PhD
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*From the University of Rochester School of Medicine and Dentistry, Cancer Center and Department of Microbiology and Immunology, Rochester, NY.

Correspondence to: Richard P. Phipps, PhD, University of Rochester Cancer Center, Box 704, 601 Elmwood Ave, Rochester, NY 14642; e-mail: Richard_Phipps@urmc.rochester.edu



Chest. 2001;120(1_suppl):S53-S55. doi:10.1378/chest.120.1_suppl.S53
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Lung injury may occur as a consequence of trauma, infection, occupational exposure to respiratory toxicants, or cancer therapy. No matter what the insult, lung injury must be resolved. Tissue repair begins with the coagulation cascade and the activation of platelets. This is followed by the release of inflammatory mediators important for chemotaxis of WBCs and activation of resident cells involved in the wound repair process, ie, endothelial cells, epithelial cells, and fibroblasts. The remodeling phase is primarily dependent on the ability of the fibroblast to synthesize and degrade extracellular matrix components. An adequate wound healing response results in minimal scarring and maintenance of normal lung architecture and function. Dysregulation at any point of this process can lead to extensive scarring and loss of function.

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