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Brief Definitive Report

Eric J. Kunkel^a,g, James J. Campbell^a,g, Guttorm Haraldsen^f, Junliang Pan^a,g, Judie Boisvert^b, Arthur I. Roberts^h, Ellen C. Ebert^h, Mark A. Vierra^c, Stuart B. Goodman^d, Mark C. Genovese^e, Andy J. Wardlawⁱ, Harry B. Greenberg^b, Christina M. Parker^j, Eugene C. Butcher^a,g, David P. Andrew^k, and William W. Agace^l

^a Laboratory of Immunology and Vascular Biology, Department of Pathology, the
^b Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305
^c Department of Surgery, Stanford University School of Medicine, Stanford, California 94305
^d Department of Functional Restoration, Stanford University School of Medicine, Stanford, California 94305
^e Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, California 94305
^f Laboratory of Immunohistochemistry and Immunopathology, Institute for Pathology, University of Oslo and Rikshospitalet, N-0027 Oslo, Norway
^g Center for Molecular Biology and Medicine, Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304
^h Department of Medicine, University of Medicine and Dentistry of New Jersey–Robert Wood Johnson Medical School, New Brunswick, New Jersey 08903
ⁱ Division of Respiratory Medicine, Institute for Lung Health, Leicester University Medical School, Leicester LEI 9QP, United Kingdom
^j Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115
^k Millennium Pharmaceuticals, Incorporated, Cambridge, Massachusetts 02142
^l Immunology Section, Department of Cell and Molecular Biology, Lund University, S-22100 Lund, Sweden
Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305-5324.650-858-3986650-852-3369

ebutcher{at}stanford.edu

The immune system has evolved specialized cellular and molecular mechanisms for targeting and regulating immune responses at epithelial surfaces. Here we show that small intestinal intraepithelial lymphocytes and lamina propria lymphocytes migrate to thymus-expressed chemokine (TECK). This attraction is mediated by CC chemokine receptor (CCR)9, a chemoattractant receptor expressed at high levels by essentially all CD4⁺ and CD8⁺ T lymphocytes in the small intestine. Only a small subset of lymphocytes in the colon are CCR9⁺, and lymphocytes from other tissues including tonsils, lung, inflamed liver, normal or inflamed skin, inflamed synovium and synovial fluid, breast milk, and seminal fluid are universally CCR9^–. TECK expression is also restricted to the small intestine: immunohistochemistry reveals that intense anti-TECK reactivity characterizes crypt epithelium in the jejunum and ileum, but not in other epithelia of the digestive tract (including stomach and colon), skin, lung, or salivary gland. These results imply a restricted role for lymphocyte CCR9 and its ligand TECK in the small intestine, and provide the first evidence for distinctive mechanisms of lymphocyte recruitment that may permit functional specialization of immune responses in different segments of the gastrointestinal tract. Selective expression of chemokines by differentiated epithelium may represent an important mechanism for targeting and specialization of immune responses.

Key Words: leukocyte • gastrointestinal tract • trafficking • epithelium • lamina propria lymphocytes

© 2000 The Rockefeller University Press

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