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Preserving β Cells in Type 1 Diabetes mellitus: the role of immunological tolerance
Author(s) -
Pillemer Stanley R.
Publication year - 2008
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.20240
Subject(s) - immunology , monoclonal antibody , immune system , immune tolerance , medicine , type 1 diabetes , effector , antibody , inflammation , diabetes mellitus , endocrinology
Type 1 diabetes mellitus (T1DM) is characterized by an autoimmune attack on beta cells of the islets of Langerhans. This immunological attack is mediated by effector T‐lymphocytes and results in the destruction of the β cells. One approach to abrogating the immunological attack is to use immunosuppressive treatments. Such treatments tend to broadly suppress the immune system. A better approach is to develop treatments that induce tolerance. Autoimmune diseases are associated with the presence of inadequate numbers of functionally active regulatory T cells (Tregs). Tregs can induce a state of immunological tolerance and suppress the inflammation and destruction of target tissues. Teplizumab, also known as hOKT3 γ 1 (Ala‐Ala), is a humanized monoclonal antibody that induces Tregs. In clinical trials, treatment with this antibody preserved insulin production and improved metabolic control during the first year of T1DM. A pivotal multinational trial is in progress to determine the efficacy and safety of teplizumab in the treatment of new onset T1DM. Drug Dev Res 69:153–157, 2008. ©2008 Wiley‐Liss, Inc.