The LPS receptor, CD14, in experimental autoimmune encephalomyelitis and multiple sclerosis.
Standard
The LPS receptor, CD14, in experimental autoimmune encephalomyelitis and multiple sclerosis. / Walter, Silke; Doering, Axinia; Letiembre, Maryse; Liu, Yang; Hao, Wenlin; Diem, Ricarda; Bernreuther, Christian; Glatzel, Markus; Engelhardt, Britta; Fassbender, Klaus.
in: CELL PHYSIOL BIOCHEM, Jahrgang 17, Nr. 3-4, 3-4, 2006, S. 167-172.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - The LPS receptor, CD14, in experimental autoimmune encephalomyelitis and multiple sclerosis.
AU - Walter, Silke
AU - Doering, Axinia
AU - Letiembre, Maryse
AU - Liu, Yang
AU - Hao, Wenlin
AU - Diem, Ricarda
AU - Bernreuther, Christian
AU - Glatzel, Markus
AU - Engelhardt, Britta
AU - Fassbender, Klaus
PY - 2006
Y1 - 2006
N2 - Innate immune receptors are crucial for defense against microorganisms. Recently, a cross-talk between innate and adaptive immunity has been considered. Here, we provide first evidence for a role of the key innate immune receptor, LPS receptor (CD14) in pathophysiology of experimental autoimmune encephalomyelitis, the animal model of multiple sclerosis. Indicating a functional importance in vivo, we show that CD14 deficiency increased clinical symptoms in active experimental autoimmune encephalomyelitis. Consistent with these observations, CD14 deficient mice exhibited a markedly enhanced infiltration of monocytes and neutrophils in brain and spinal cord. Moreover, we observed an increased immunoreactivity of CD14 in biopsy and post mortem brain tissues of multiple sclerosis patients compared to age-matched controls. Thus, the key innate immune receptor, CD14, may be of pathophysiological relevance in experimental autoimmune encephalomyelitis and multiple sclerosis.
AB - Innate immune receptors are crucial for defense against microorganisms. Recently, a cross-talk between innate and adaptive immunity has been considered. Here, we provide first evidence for a role of the key innate immune receptor, LPS receptor (CD14) in pathophysiology of experimental autoimmune encephalomyelitis, the animal model of multiple sclerosis. Indicating a functional importance in vivo, we show that CD14 deficiency increased clinical symptoms in active experimental autoimmune encephalomyelitis. Consistent with these observations, CD14 deficient mice exhibited a markedly enhanced infiltration of monocytes and neutrophils in brain and spinal cord. Moreover, we observed an increased immunoreactivity of CD14 in biopsy and post mortem brain tissues of multiple sclerosis patients compared to age-matched controls. Thus, the key innate immune receptor, CD14, may be of pathophysiological relevance in experimental autoimmune encephalomyelitis and multiple sclerosis.
U2 - 10.1159/000092078
DO - 10.1159/000092078
M3 - SCORING: Zeitschriftenaufsatz
VL - 17
SP - 167
EP - 172
JO - CELL PHYSIOL BIOCHEM
JF - CELL PHYSIOL BIOCHEM
SN - 1015-8987
IS - 3-4
M1 - 3-4
ER -