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Immunomodulatory Effect of Interleukin-16 on Allergic Airway Inflammation*

Frederic F. Little, MD; Joris de Bie, PhD; Anton van Oosterhout, PhD; Hardy Kornfeld, MD; David M. Center, MD; William W. Cruikshank, PhD
Author and Funding Information

*From the Pulmonary Center (Drs. Little, Kornfeld, Center, and Cruikshank), Boston University School of Medicine, Boston, MA; and Department of Pharmacology (Drs. de Bie and van Oosterhout), Utrecht University, Utrecht, The Netherlands.

Correspondence to: Frederic F. Little, MD, Pulmonary Center R-304, BUSM, 715 Albany St, Boston, MA 02118; e-mail: flittle@lung.bumc.bu.edu



Chest. 2003;123(3_suppl):431S-432S. doi:10.1378/chest.123.3_suppl.431S
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Extract

Atopy is characterized by dysregulated T-helper type 2 (Th2) lymphocyte activation and cytokine synthesis. This aberrant immune response, when present in the lung, leads to the cardinal pathologic and physiologic features of asthma. Interleukin (IL)-16 is a pleiotropic cytokine that uses CD4 as its receptor and has been identified in the airway epithelium and BAL in human and murine allergic airway inflammation. While its effector function is incompletely understood, our preliminary experiments lead us to propose that IL-16 is a naturally occurring modulator of Th2 cell-mediated airway inflammation.

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