TY - JOUR
T1 - Recombinant human β-galactoside binding lectin suppresses clinical and histological signs of experimental autoimmune encephalomyelitis
AU - Offner, Halina
AU - Celnik, Bozena
AU - Bringman, Timothy S.
AU - Casentini-Borocz, Denise
AU - Nedwin, Glenn E.
AU - Vandenbark, Arthur A.
N1 - Funding Information:
The authors wish to thank Louise Richardson for excellent technical assistance in production and purification of rlML-1, Janet Drakes for preparation of the manuscript, and Alex Lin for preparation of the figures. This work was supported by the Department of Veterans Affairs and by IDEON Corporation.
PY - 1990/7
Y1 - 1990/7
N2 - Human placental tissue contains regulatory molecules that may prevent allo-sensitization. Recently, a 14 kDa β-galactoside binding protein with demonstrated immunoregulatory properties has been cloned using cDNA from human placenta and expressed in Escherichia coli. The present study assesses the ability of this recombinant immunomodulatory lectin (rIML-1), to prevent experimental autoimmune encephalomyelitis (EAE), a paralytic T cell-mediated disease directed against myelin basic protein (BP). Injection or rIML-1 into Lewis rats inhibited the induction of both clinical and histological signs of EAE, apparently by blocking sensitization of encephalitogenic BP-specific T cells and inducing BP-dependent suppressor cells. Because it is neither immunogenic nor toxic, rIML-1 may have application in humans, and would have distinct advantages over unselective cytotoxic immunosuppressive agents used currently in the treatment of autoimmune diseases and transplantation.
AB - Human placental tissue contains regulatory molecules that may prevent allo-sensitization. Recently, a 14 kDa β-galactoside binding protein with demonstrated immunoregulatory properties has been cloned using cDNA from human placenta and expressed in Escherichia coli. The present study assesses the ability of this recombinant immunomodulatory lectin (rIML-1), to prevent experimental autoimmune encephalomyelitis (EAE), a paralytic T cell-mediated disease directed against myelin basic protein (BP). Injection or rIML-1 into Lewis rats inhibited the induction of both clinical and histological signs of EAE, apparently by blocking sensitization of encephalitogenic BP-specific T cells and inducing BP-dependent suppressor cells. Because it is neither immunogenic nor toxic, rIML-1 may have application in humans, and would have distinct advantages over unselective cytotoxic immunosuppressive agents used currently in the treatment of autoimmune diseases and transplantation.
KW - Delayed-type hypersensitivity
KW - Experimental autoimmune encephalomyelitis
KW - Immunosuppression
KW - Myelin basic protein
KW - Recombinant β-galactoside binding human immunolectin
KW - T cell line
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U2 - 10.1016/0165-5728(90)90032-I
DO - 10.1016/0165-5728(90)90032-I
M3 - Article
C2 - 1694534
AN - SCOPUS:0025309457
SN - 0165-5728
VL - 28
SP - 177
EP - 184
JO - Journal of Neuroimmunology
JF - Journal of Neuroimmunology
IS - 2
ER -