Deletion of both ICAM-1 and C3 enhances severity of experimental autoimmune encephalomyelitis compared to C3-deficient mice

Neuroscience Letters

Volumn 442, Issue 2, 2008, Pages 158-160

  Smith, Sherry S ^a   Ludwig, Michael ^a   Wohler, Jillian E ^a   Bullard, Daniel C ^b   Szalai, Alex J ^c   Barnum, Scott R ^a,d  

^a University of Alabama at Birmingham   (United States)

^b UNIVERSITY OF ALABAMA AT BIRMINGHAM   (United States)

^c University of Alabama at Birmingham   (United States)

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

Author keywords

Adhesion molecules; Complement; Experimental autoimmune encephalomyelitis; Neuroimmunology

Indexed keywords

ANTIGEN; CELL ADHESION MOLECULE; GAMMA INTERFERON; INTERCELLULAR ADHESION MOLECULE 1; MYELIN OLIGODENDROCYTE GLYCOPROTEIN; TUMOR NECROSIS FACTOR ALPHA;

ALLERGIC ENCEPHALOMYELITIS; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CELL HOMING; CELL INFILTRATION; CELL ISOLATION; CELL MIGRATION; CONTROLLED STUDY; CYTOKINE PRODUCTION; DISEASE SEVERITY; GENE DELETION; LEUKOCYTE; MOUSE; NONHUMAN; PRIORITY JOURNAL; SPINAL CORD; T LYMPHOCYTE;

ANIMALS; ANTIGENS, CD; CELL PROLIFERATION; COMPLEMENT C3; DISEASE MODELS, ANIMAL; DOSE-RESPONSE RELATIONSHIP, DRUG; ENCEPHALOMYELITIS, AUTOIMMUNE, EXPERIMENTAL; GENE EXPRESSION REGULATION; INTERCELLULAR ADHESION MOLECULE-1; LEUKOCYTES; MICE; MICE, KNOCKOUT; MYELIN-ASSOCIATED GLYCOPROTEIN; SEVERITY OF ILLNESS INDEX; SPINAL CORD; T-LYMPHOCYTES;

EID: 48149091591     PISSN: 03043940     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.neulet.2008.07.005     Document Type: Article

References (15)

1. Archelos J.J., Previtali S.C., and Hartung H.P. The role of integrins in immune-mediated diseases of the nervous system. Trends Neurosci. 22 (1999) 30-38
2. Barnum S.R., and Szalai A.J. Complement and demyelinating disease: no MAC needed?. Brain Res. Rev. 52 (2006) 58-68
3. Boackle S.A., and Holers V.M. Role of complement in the development of autoimmunity. Curr. Dir. Autoimmun. 6 (2003) 154-168
4. Bullard D.C., Hu X., Adams J.E., Schoeb T.R., and Barnum S.R. p150,95 (CD11c/CD18) expression is required for the development of experimental autoimmune encephalomyelitis. Am. J. Pathol. 170 (2007) 2001-2008
5. Bullard D.C., Hu X., Schoeb T.R., Axtell R.C., Raman C., and Barnum S.R. Critical requirement of CD11b (Mac-1) on T cells and accessory cells for development of experimental autoimmune encephalomyelitis. J. Immunol. 175 (2005) 6327-6333
6. Bullard D.C., Hu X., Schoeb T.R., Collins R.G., Beaudet A.L., and Barnum S.R. Intercellular adhesion molecule-1 expression is required on multiple cell types for the development of experimental autoimmune encephalomyelitis. J. Immunol. 178 (2007) 851-857
7. Casciola-Rosen L., Anhalt G.J., and Rosen A. Autoantigens targeted in systemic lupus erythematusus are clustered in two populations of surface structures on apoptotic keratinocytes. J. Exp. Med. 179 (1994) 1317-1330
8. Casciola-Rosen L.A., Anhalt G.J., and Rosen A. DNA-dependent protein kinase is one of a subset of autoantigens specifically cleaved early during apoptosis. J. Exp. Med. 182 (1995) 1625-1634
9. Casciola-Rosen L.A., Miller D.K., Anhalt G.J., and Rosen A. Specific cleavage of the 70-kDa protein component of the U1 small nuclear ribonucleoprotein is a characteristic biochemical feature of apoptotic cell death. J. Biol. Chem. 269 (1994) 30757-30760
10. Circolo A., Garnier G., Fukuda W., Wang X., Hidvegi T., Szalai A.J., Briles D.E., Volanakis J.E., Wetsel R.A., and Colten H.R. Genetic disruption of the murine complement C3 promoter region generates deficient mice with extrahepatic expression of C3 mRNA. Immunopharmacology 42 (1999) 135-149
11. Engelhardt B. Molecular mechanisms involved in T cell migration across the blood-brain barrier. J. Neural Transm. 113 (2006) 477-485
12. Rosen A., Casciola-Rosen L., and Ahearn J. Novel packages of viral and self-antigens are generated during apoptosis. J. Exp. Med. 181 (1995) 1557-1561
13. Smith S.S., and Barnum S.R. Differential expression of b2-integrins and cytokine production between gd and ab T cells in experimental autoimmune encephalomyelitis. J. Leukoc. Biol. 83 (2008) 71-79
14. Szalai A.J., Hu X., Adams J.E., and Barnum S.R. Complement in experimental autoimmune encephalomyelitis revisited: C3 is required for development of maximal disease. Mol. Immunol. (2007)
15. Utz P.J., Hottelet M., Schur P.H., and Anderson P. Proteins phosphorylated during stress-induced apoptosis are common targets for autoantibody production in patients with systemic lupus erythematosus. J. Exp. Med. 185 (1997) 843-854