Authors:
Powers, JM
Rosenblatt, DS
Schmidt, RE
Cross, AH
Black, JT
Moser, AB
Moser, HW
Morgan, DJ
Citation: Jm. Powers et al., Neurological and neuropathologic heterogeneity in two brothers with cobalamin C deficiency, ANN NEUROL, 49(3), 2001, pp. 396-400
Citation: Ah. Cross et G. Ku, Astrocytes and central nervous system endothelial cells do not express B7-1 (CD80) or B7-2 (CD86) immunoreactivity during experimental autoimmune encephalomyelitis, J NEUROIMM, 110(1-2), 2000, pp. 76-82
Citation: Bm. Segal et Ah. Cross, Fas(t) track to apoptosis in MS - TNF receptors may suppress or potentiateCNS demyelination, NEUROLOGY, 55(7), 2000, pp. 906-907
Citation: Ah. Cross et al., CTLA-4-Fc treatment of ongoing EAE improves recovery, but has no effect upon relapse rate. Implications for the mechanisms involved in disease perpetuation, J NEUROIMM, 96(2), 1999, pp. 144-147
Citation: Ka. Sabelko-downes et al., Role of Fas-FasL interactions in the pathogenesis and regulation of autoimmune demyelinating disease, J NEUROIMM, 100(1-2), 1999, pp. 42-52
Citation: Jl. Trotter et al., Increased frequency of recognition of delipidated versus intact CNS myelinin multiple sclerosis and control subjects, J NEUR SCI, 166(1), 1999, pp. 23-27
Authors:
Benson, JM
Stuckman, SS
Cox, KL
Wardrop, RM
Gienapp, IE
Cross, AH
Trotter, JL
Whitacre, CC
Citation: Jm. Benson et al., Oral administration of myelin basic protein is superior to myelin in suppressing established relapsing experimental autoimmune encephalomyelitis, J IMMUNOL, 162(10), 1999, pp. 6247-6254
Citation: Ka. Sabelko-downes et al., Dual role for Fas ligand in the initiation of and recovery from experimental allergic encephalomyelitis, J EXP MED, 189(8), 1999, pp. 1195-1205
Citation: Ja. Lyons et al., B cells are critical to induction of experimental allergic encephalomyelitis by protein but not by a short encephalitogenic peptide, EUR J IMMUN, 29(11), 1999, pp. 3432-3439
Authors:
Cross, AH
Lyons, JA
San, M
Keeling, RM
Ku, G
Racke, MK
Citation: Ah. Cross et al., T cells are the main cell type expressing B7-1 and B7-2 in the central nervous system during acute, relapsing and chronic experimental autoimmune encephalomyelitis, EUR J IMMUN, 29(10), 1999, pp. 3140-3147