The LPS receptor, CD14, in experimental autoimmune encephalomyelitis and multiple sclerosis.
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.
Department of Neurology, Saarland University Hospital, Homburg, Germany.
Silke
S
Walter
Axinia
A
Doering
Maryse
M
Letiembre
Yang
Y
Liu
Wenlin
W
Hao
Ricarda
R
Diem
Christian
C
Bernreuther
Markus
M
Glatzel
Britta
B
Engelhardt
Klaus
K
Fassbender
D000818:Animals; D015551:Autoimmunity; D004195:Disease Models, Animal; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000139:chemically induced / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D005260:Female; D007113:Immunity, Innate; D007150:Immunohistochemistry; D018950:Lipopolysaccharide Receptors / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D009103:Multiple Sclerosis
D018950:Lipopolysaccharide Receptors