Journal
NATURE IMMUNOLOGY
Volume 7, Issue 12, Pages 1299-1308Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1406
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Funding
- NCI NIH HHS [CA094045, CA85580, CA79765, CA16056] Funding Source: Medline
- NIAID NIH HHS [AI061663, AI069259] Funding Source: Medline
- NIAMS NIH HHS [P30 AR 42689] Funding Source: Medline
- NIDDK NIH HHS [DK33886] Funding Source: Medline
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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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