Toll-like receptor 4 and MAIR-II/CLM-4/LMIR2 immunoreceptor regulate VLA-4-mediated inflammatory monocyte migration

Nature Communications

Volumn 5, Issue , 2014, Pages

  Totsuka, Naoya ^a,b   Kim, Yun Gi ^a,c   Kanemaru, Kazumasa ^a   Niizuma, Kouta ^a   Umemoto, Eiji ^d   Nagai, Kei ^a   Tahara Hanaoka, Satoko ^a   Nakahasi Oda, Chigusa ^a   Honda, Shin Ichiro ^a   Miyasaka, Masayuki ^d   Shibuya, Kazuko ^a   Shibuya, Akira ^a  

^a UNIVERSITY OF TSUKUBA   (Japan)

^b FUKUSHIMA MEDICAL UNIVERSITY   (Japan)

^c UNIVERSITY OF MICHIGAN MEDICAL SCHOOL   (United States)

^d OSAKA UNIVERSITY   (Japan)

Author keywords

[No Author keywords available]

Indexed keywords

IMMUNOGLOBULIN RECEPTOR; LIPOPOLYSACCHARIDE; MYELOID ASSOCIATED IMMUNOGLOBULIN LIKE RECEPTOR II; TOLL LIKE RECEPTOR 4; UNCLASSIFIED DRUG; VERY LATE ACTIVATION ANTIGEN 4; LMIR2 PROTEIN, MOUSE; MYD88 PROTEIN, MOUSE; MYELOID DIFFERENTIATION FACTOR 88; MYELOID-ASSOCIATED IG-LIKE RECEPTOR , MOUSE; SECRETORY COMPONENT; TLR4 PROTEIN, MOUSE;

BLOOD; IMMUNOASSAY; INFECTIOUS DISEASE; POLYSACCHARIDE; SIGNALING; SURVIVAL;

ADOPTIVE TRANSFER; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CELL ADHESION; CELL MIGRATION; CONTROLLED STUDY; FEMALE; HOST RESISTANCE; IMMUNE RESPONSE; IN VIVO STUDY; INFLAMMATORY MONOCYTE; MACROPHAGE; MALE; MONOCYTE; MOUSE; NONHUMAN; PERITONEAL CAVITY; PERITONITIS; PROTEIN EXPRESSION; REGULATORY MECHANISM; STIMULATION; SURVIVAL; ANIMAL; BAGG ALBINO MOUSE; C57BL MOUSE; CECUM; CELL MOTION; DEFICIENCY; DISEASE MODEL; GENETICS; INFLAMMATION; KNOCKOUT MOUSE; LIGATION; PATHOLOGY; PATHOPHYSIOLOGY; PHYSIOLOGY; SIGNAL TRANSDUCTION;

ANIMALS; CECUM; CELL ADHESION; CELL MOVEMENT; DISEASE MODELS, ANIMAL; FEMALE; INFLAMMATION; INTEGRIN ALPHA4BETA1; LIGATION; LIPOPOLYSACCHARIDES; MALE; MICE; MICE, INBRED BALB C; MICE, INBRED C57BL; MICE, KNOCKOUT; MONOCYTES; MYELOID DIFFERENTIATION FACTOR 88; PERITONITIS; RECEPTORS, IMMUNOLOGIC; RECEPTORS, POLYMERIC IMMUNOGLOBULIN; SIGNAL TRANSDUCTION; TOLL-LIKE RECEPTOR 4;

EID: 84907318928     PISSN: None     EISSN: 20411723     Source Type: Journal    
DOI: 10.1038/ncomms5710     Document Type: Article

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