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Interleukin-13 and Interferon Modulators of Dendritic Cell Migration in the Lungs* FREE TO VIEW

Janice Hwang, BS; David Yen, BS; Thomas Tschernig, MD; Donna Rennick, PhD; Gabriele Grunig, DVM, PhD
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*From the Department of Pathology (Mrs. Hwang and Dr. Grunig), Columbia University, J. P. Mara Center for Respiratory Diseases, St. Luke's-Roosevelt Hospital, New York, NY; DNAX Research Institute for Molecular and Cellular Biology (Mr. Yen and Dr. Rennick), Palo Alto, CA; and Department of Anatomy (Dr. Tschernig), Medical University of Hannover, Germany.

Correspondence to: Gabriele Grunig, DVM, PhD, St. Luke's Roosevelt Hospital, 432 W 58th St, Lab 504, New York, NY 10019; e-mail: gg398@columbia.edu

Chest. 2003;123(3_suppl):439S. doi:10.1378/chest.123.3_suppl.439S
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Mixed T-cell responses characterized by the simultaneous presence of T-helper type 2 and T-helper type 1 cytokines (eg, interleukin [IL]-13 and interferon [IFN]-γ) critically contribute to chronic inflammatory diseases of the lungs, including asthma. We examined the effects of the simultaneous presence of IL-13 and IFN-γ by challenging mice with recombinant cytokines intranasally. Increased numbers of dendritic-like cells accumulated in the airways of mice challenged with IL-13 and IFN-γ. Because immune responses are induced most efficiently in the lymph nodes, we asked if dendritic cells also migrated at increased numbers from the airways to lymph nodes in mice challenged with IL-13 and IFN-γ. Dendritic cells were prepared from the bone marrow, labeled, and transferred into recipient mice by intranasal instillation. Increased numbers of labeled dendritic cells were found in the draining lymph nodes 36 h after transfer in mice challenged with IL-13 and IFN-γ as compared to mice given control protein. These data will be confirmed using dendritic cells made from mice that are transgenic for green fluorescent protein that is expressed in every cell type.

Because chemokines and their receptors are very likely to play a central role in this process, lungs were examined for the expression of transcripts of chemokines and their receptors. Relative to lungs challenged with IL-13 or IFN-γ alone, IL-13 and IFN-γ administered together induced to an equivalent or a higher extent the chemokine/chemokine receptor (CCR) pairs RANTES (regulated upon activation, normal T-cell expressed and secreted) and CCR-5, monocyte chemoattractant protein-1, monocyte chemoattractant protein-3 and CCR-2, and mammary epithelial cell (CC = chemokine ligand [CCL] = 28) and CCR-10. While markedly induced, CCL-28 and CCR-10 were transcribed at low levels. Future experiments are designed to determine critical roles of CCR-2, CCR-5, and CCR-10, as well as CCR-7 (this CCR has been shown to be critical for dendritic cell migration to the lymph nodes in organs other than the lungs) by using dendritic cells made from CCR-deficient mice and by using dendritic cells that are transduced with CCRs to induce high surface expression.

Abbreviations: CCL = CC chemokine ligand; CCR = chemokine receptor; IFN = interferon; IL = interleukin

Funded by American Lung Association, Speakers Grant from the New York Academy of Science, J. P. Mara Center for Diseases of the Lung, and American Heart Association.

DNAX Research Institute is supported by Schering Plough Corporation.




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