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Pathogenic T-Cell Recruitment into the Airway in Human Disease
aCenter for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts, 02129 USA bPulmonary and Critical Care Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, 02114 USA cDivision of Thoracic Surgery, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, 02114 USA dBiostatistics Center, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, 02114 USA ePulmonary Division, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA
Address for correspondence: Andrew D. Luster, M.D., Ph.D., Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Bldg. 149-8301, 13th St., Charlestown, MA 02129. Voice: 617-726-5710; fax: 617-726-5651. luster.andrew{at}mgh.harvard.edu
Effector T cells significantly contribute to inflammatory diseases. These cells are recruited into tissue, where they orchestrate an inflammatory response that can either protect against infection or sometimes stimulate human disease. The recruitment of T cells into tissue from the blood and lymphoid compartments is an active process controlled by chemokines and the chemokine receptors expressed on distinct effector T-cell subsets. Thus, the chemokines secreted in the tissue will determine the specific types of T lymphocyte recruited into that tissue based on the chemokine receptors expressed on these cells. It follows that the chemokine receptor profile on T cells isolated from the lungs of patients with inflammatory pulmonary disease will define the subtype of pathogenic T lymphocytes mediating the disease process and will identify the mechanisms that recruit these cells into the lung. This article reviews data from both human and animal studies that define the chemokine receptors involved in the recruitment of T lymphocytes into the lung in various inflammatory pulmonary diseases, including asthma, obliterative bronchiolitis, sarcoidosis, and chronic eosinophilic pneumonia. We then speculate on the potential role of these chemokine receptors in the pathogenesis of these disorders and potential novel therapeutic approaches suggested by these data.
Key Words: T cells • lung inflammation • sarcoidosis • asthma • lung transplantation • chemokines • chemokine receptors This article has been cited by other articles:
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