Deletion of both the C3a and C5a receptors fails to protect against experimental autoimmune encephalomyelitis

Neuroscience Letters

Volumn 467, Issue 3, 2009, Pages 234-236

  Ramos, Theresa N ^a   Wohler, Jillian E ^a   Barnum, Scott R ^a,b  

^a University of Alabama at Birmingham   (United States)

^b The University of Alabama at Birmingham   (United States)

Author keywords

Anaphylatoxin receptors; Complement; Experimental autoimmune encephalomyelitis; Neuroimmunology

Indexed keywords

COMPLEMENT COMPONENT C3 RECEPTOR; COMPLEMENT COMPONENT C3A RECEPTOR; COMPLEMENT COMPONENT C5A RECEPTOR; GAMMA INTERFERON; INTERLEUKIN 12; INTERLEUKIN 17; TUMOR NECROSIS FACTOR ALPHA; UNCLASSIFIED DRUG;

ALLERGIC ENCEPHALOMYELITIS; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIGEN SPECIFICITY; ARTICLE; ATTENUATION; CD4+ T LYMPHOCYTE; CD8+ T LYMPHOCYTE; CELL ISOLATION; COMPLEMENT SYSTEM; CONTROLLED STUDY; CYTOKINE PRODUCTION; DISEASE COURSE; DISEASE SEVERITY; GENE DELETION; IMMUNOMODULATION; KNOCKOUT MOUSE; LYMPHOCYTE MIGRATION; LYMPHOCYTIC INFILTRATION; MOUSE; NEUROMODULATION; NEUROPATHOLOGY; NEUROPROTECTION; NONHUMAN; PRIORITY JOURNAL; WILD TYPE;

ANIMALS; CD4-POSITIVE T-LYMPHOCYTES; CELL MOVEMENT; COMPLEMENT C3A; CYTOKINES; DISEASE MODELS, ANIMAL; ENCEPHALOMYELITIS, AUTOIMMUNE, EXPERIMENTAL; FEMALE; GENE DELETION; GENETIC PREDISPOSITION TO DISEASE; MALE; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; MULTIPLE SCLEROSIS; RECEPTOR, ANAPHYLATOXIN C5A; RECEPTORS, COMPLEMENT;

EID: 70350761549     PISSN: 03043940     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.neulet.2009.10.045     Document Type: Article

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