Co-stimulation agonists as a new immunotherapy for autoimmune diseases.
Lymphocytes are important in the pathogenesis of many autoimmune diseases. Blocking co-stimulatory signals for T-cell activation has been widely used as an approach to treating autoimmunity, but it has encountered limited clinical success. Some agonistic monoclonal antibodies to co-stimulatory molecules greatly enhance immune responses mediated by T cells, such as antiviral, anti-tumor and alloresponses. Surprisingly, recent studies have demonstrated that these agonists have profound therapeutic effects on autoimmune diseases by potentially depleting autoreactive lymphocytes or by inhibiting their function. These findings imply that signaling through co-stimulatory molecules can have diametric outcomes in modulating immune responses, thereby providing a novel approach to the treatment of autoimmune diseases.
Sun
Yonglian
Y
Department of Pathology and Committee in Immunology, University of Chicago, Chicago, IL 60637, USA.
Subudhi
Sumit K
SK
Fu
Yang-Xin
YX
D000276:Adjuvants, Immunologic / Q000494:pharmacology*; D000818:Animals; D000911:Antibodies, Monoclonal / Q000494:pharmacology*; D015703:Antigens, CD; D001327:Autoimmune Diseases / Q000188:drug therapy* / Q000276:immunology; D019013:CD40 Antigens / Q000187:drug effects*; D006801:Humans; D008214:Lymphocytes / Q000187:drug effects; D051379:Mice; D017475:Receptors, Nerve Growth Factor / Q000819:agonists*; D018124:Receptors, Tumor Necrosis Factor / Q000819:agonists*; D053261:Tumor Necrosis Factor Receptor Superfamily, Member 9
D000276:Adjuvants, Immunologic; D000911:Antibodies, Monoclonal; D015703:Antigens, CD; D019013:CD40 Antigens; D017475:Receptors, Nerve Growth Factor; D018124:Receptors, Tumor Necrosis Factor; C505714:TNFRSF9 protein, human; C505715:Tnfrsf9 protein, mouse; D053261:Tumor Necrosis Factor Receptor Superfamily, Member 9