Abstract
Th17 cell trafficking in response to leukotriene signaling is poorly understood. Here we showed that Th17 cells express high levels of leukotriene B4 receptor 1 (LTB4R1) and cysteinyl leukotriene receptor 1 (CysLTR1). Th17 cells migrated under the guidance of leukotriene B4 and D4. The migration of Th17 cells was more efficient than that of Th1 and Th2 cells, and it was blocked by specific inhibitors of LTB4R1 or CysLTR1. Studies in an animal model of experimental autoimmune encephalomyelitis revealed that treatment with montelukast alleviated disease symptoms and inhibited the recruitment of Th17 cells to the central nervous system. Thus, leukotrienes may act as chemoattractants for Th17 cells.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Acetates / pharmacology
-
Animals
-
Benzophenones / pharmacology
-
Cell Movement / drug effects
-
Cells, Cultured
-
Cyclopropanes
-
Encephalomyelitis, Autoimmune, Experimental / immunology
-
Encephalomyelitis, Autoimmune, Experimental / therapy*
-
Humans
-
Leukotriene B4 / antagonists & inhibitors
-
Leukotriene D4 / antagonists & inhibitors
-
Mice
-
Mice, Inbred C57BL
-
Multiple Sclerosis / immunology
-
Multiple Sclerosis / therapy*
-
Quinolines / pharmacology
-
Receptors, Leukotriene / metabolism
-
Receptors, Leukotriene B4
-
Signal Transduction
-
Sulfides
-
Th1 Cells / immunology*
-
Th17 Cells / immunology*
-
Th2 Cells / immunology*
Substances
-
Acetates
-
Benzophenones
-
Cyclopropanes
-
Ltb4r1 protein, mouse
-
Quinolines
-
Receptors, Leukotriene
-
Receptors, Leukotriene B4
-
Sulfides
-
LY 223982
-
Leukotriene B4
-
Leukotriene D4
-
leukotriene D4 receptor
-
montelukast