Nature Immunology
- 7, 1299 - 1308 (2006)
Published online: 5 November 2006; Corrected online: 10 November 2006 | doi:10.1038/ni1406
Fever-range thermal stress promotes lymphocyte trafficking across high endothelial venules via an interleukin 6 trans-signaling mechanismQing Chen1, Daniel T Fisher1, Kristen A Clancy1, Jean-Marc M Gauguet2, Wan-Chao Wang1, Emily Unger1, Stefan Rose-John3, Ulrich H von Andrian2, Heinz Baumann4 & Sharon S Evans11
Departments of Immunology, Roswell Park Cancer Institute, Buffalo, New York 14263, USA. 2
The CBR Institute for Biomedical Research and Department of Pathology, Harvard Medical School, Boston, Massachusetts, 02115, USA. 3
Department of Biochemistry, Christian Albrechts University Kiel, D-24098 Kiel, Germany. 4
Molecular and Cellular Biology, Roswell Park Cancer Institute, Buffalo, New York 14263, USA.
Correspondence should be addressed to Sharon S Evans sharon.evans@roswellpark.org Fever is an evolutionarily conserved response during acute inflammation, although its physiological benefit is poorly understood. Here we show thermal stress in the range of fever temperatures increased the intravascular display of two 'gatekeeper' homing molecules, intercellular adhesion molecule 1 (ICAM-1) and CCL21 chemokine, exclusively in high endothelial venules (HEVs) that are chief portals for the entry of blood-borne lymphocytes into lymphoid organs. Enhanced endothelial expression of ICAM-1 and CCL21 was linked to increased lymphocyte trafficking across HEVs. A bifurcation in the mechanisms controlling HEV adhesion was demonstrated by evidence that the thermal induction of ICAM-1 but not of CCL21 involved an interleukin 6 trans-signaling pathway. Our findings identify the 'HEV axis' as a thermally sensitive alert system that heightens immune surveillance during inflammation by amplifying lymphocyte trafficking to lymphoid organs.
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