Laquinimod, a prototypic quinoline-3-carboxamide and aryl hydrocarbon receptor agonist, utilizes a CD155-mediated natural killer/dendritic cell interaction to suppress CNS autoimmunity

被引：0

作者：

Martina Ott

Erika Avendaño-Guzmán

Evelyn Ullrich

Carolin Dreyer

Judith Strauss

Markus Harden

Margarete Schön

Michael P. Schön

Günter Bernhardt

Christine Stadelmann

Christiane Wegner

Wolfgang Brück

Stefan Nessler

机构：

[1] University Medical Center Göttingen,Institute of Neuropathology

[2] Goethe University,LOEWE Center for Cell and Gene Therapy

[3] Hospital of the Goethe University Frankfurt,Division of Stem Cell Transplantation and Immunology, Department for Children and Adolescents Medicine

[4] University Medical Center Göttingen,Institute for Multiple Sclerosis Research and Neuroimmunology

[5] University Medical Center Göttingen,Department of Medical Statistics

[6] University Medical Center Göttingen,Department of Dermatology, Venereology and Allergology

[7] University Medical Center Göttingen and University of Osnabrück,Lower Saxony Institute of Occupational Dermatology

[8] Hannover Medical School,Institute of Immunology

[9] University Medical Center Göttingen,Present Address: Institute of Pathology

来源：

Journal of Neuroinflammation | / 16卷

关键词：

Quinoline-3-carboxamide; Laquinimod; Natural killer cells; Aryl hydrocarbon receptor; Dendritic cells; DNAM-1/CD155 interactions; B16F10 melanoma cells; Experimental autoimmune encephalomyelitis; CNS autoimmunity;

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