Abstract
Toll-like receptors are typically expressed in immune cells to regulate innate immunity. We found that functional Toll-like receptor 7 (TLR7) was expressed in C-fiber primary sensory neurons and was important for inducing itch (pruritus), but was not necessary for eliciting mechanical, thermal, inflammatory and neuropathic pain in mice. Our results indicate that TLR7 mediates itching and is a potential therapeutic target for anti-itch treatment in skin disease conditions.
Publication types
-
Comparative Study
-
Research Support, N.I.H., Extramural
MeSH terms
-
Aminoquinolines / toxicity
-
Animals
-
Cells, Cultured
-
Dose-Response Relationship, Drug
-
Female
-
Histamine / physiology
-
Imiquimod
-
Male
-
Membrane Glycoproteins / adverse effects*
-
Membrane Glycoproteins / deficiency
-
Membrane Glycoproteins / physiology
-
Mice
-
Mice, Inbred C57BL
-
Mice, Knockout
-
Mice, Transgenic
-
Nerve Fibers, Unmyelinated / physiology
-
Pain Measurement / methods
-
Pruritus / chemically induced
-
Pruritus / etiology*
-
Pruritus / metabolism*
-
Toll-Like Receptor 7 / deficiency
-
Toll-Like Receptor 7 / physiology
Substances
-
Aminoquinolines
-
Membrane Glycoproteins
-
Tlr7 protein, mouse
-
Toll-Like Receptor 7
-
Histamine
-
Imiquimod