Abstract
In this issue, we are hosting several reviews on topics of broad interests, such as therapeutic or prophylactic antibodies, and the role of autophagy in autoimmunity.
In the first review, Simonetta Salemi and colleagues provide a historical perspective on antibodies as a means to control or prevent diseases. This review covers the importance of hyperimmune polyclonal globulin in the pre- and postantibiotic era, as a companion to other approaches designed to control infectious diseases. With the discovery of monoclonal antibodies, the field evolved dramatically, witnessing a standard of care today in autoimmune diseases, oncology and microbiology that comprise or rely heavily on antibodies.
In the second review dedicated to antibody therapy, Misato Hashizume and colleagues showcase a relatively new therapeutic antibody—against IL-6 receptor (IL-6R)—that is applicable to the treatment of rheumatoid arthritis (RA). The authors discuss the pleiotropic functions of IL-6 and their importance to RA pathogenesis, building the case for the anti-IL-6R monoclonal antibody Tocilizumab®. They highlight the clinical experience to date with this antibody that binds and neutralizes IL-6R, resulting in the inhibition of various IL-6-mediated biological activities, including inflammation-related, immunomodulatory and tissue/matrix remodeling effects.
Last but not the least, Xu-jie Zhou and colleagues discuss the interesting subject of autophagy in systemic lupus erythematosus (SLE). The authors explain the mechanism of autophagy and its role in successful clearance of self-antigens that could otherwise initiate or amplify autoimmune processes. As SLE is an autoimmune disease largely caused by failure to control immune reactions against antigens released by dying cells, the aspect of autophagy garnered significant interest from both biomarker, translational and therapeutic standpoint.
Declaration of Interest
The author reports no conflict of interest. The authors alone are responsible for the content and writing of the article.