| First Author | Maeno T | Year | 2007 |
| Journal | J Immunol | Volume | 178 |
| Issue | 12 | Pages | 8090-6 |
| PubMed ID | 17548647 | Mgi Jnum | J:148578 |
| Mgi Id | MGI:3845726 | Doi | 10.4049/jimmunol.178.12.8090 |
| Citation | Maeno T, et al. (2007) CD8+ T Cells are required for inflammation and destruction in cigarette smoke-induced emphysema in mice. J Immunol 178(12):8090-6 |
| abstractText | Increased numbers of T lymphocytes are observed in the lungs of patients with chronic obstructive pulmonary disease, but their role in the disease process is not known. We investigated the role of CD8+ T cells in inflammatory cell recruitment and lung destruction in a cigarette smoke-induced murine model of emphysema. In contrast to wild-type C57BL/6J mice that displayed macrophage, lymphocyte, and neutrophil recruitment to the lung followed by emphysema in response to cigarette smoke, CD8+ T cell-deficient (CD8-/-) mice had a blunted inflammatory response and did not develop emphysema when exposed to long-term cigarette smoke. Further studies supported a pathogenetic pathway whereby the CD8+ T cell product, IFN-gamma-inducible protein-10, induces production of macrophage elastase (matrix metalloproteinase 12) that degrades elastin, both causing lung destruction directly and generating elastin fragments that serve as monocyte chemokines augmenting macrophage-mediated lung destruction. These studies demonstrate a requirement for CD8+ T cells for the development of cigarette smoke-induced emphysema and they provide a unifying pathway whereby CD8+ T cells are a central regulator of the inflammatory network in chronic obstructive pulmonary disease. |
