Anti–CD3 Antibody Treatment: a Promising Immunotherapeutic for Type 1 Diabetes

نویسندگان

  • Riyasat Ali
  • Sudhir Kumar
چکیده

Type 1 diabetes (T1D) is an autoimmune disease characterized by spontaneous pancreatic beta cells destruction. The central cause of T1D is mainly the weakening of central and peripheral tolerance. So, the induction of tolerance is a major goal for most of the immunotherapies. Investigations over the last couple of decades have shown that anti–CD3 monoclonal antibodies (mAbs) and their therapeutic variants effectively treat autoimmune disease in animal models, and have also shown promise in clinical trials. Tolerance induction by anti–CD3 mAbs is mainly related to the induction of Th2 type immune response and regulatory T cells (Tregs) development that control pathogenic autoimmune responses. Here, we review main findings of last couple of decades research, and current scenario of anti–CD3 mediated immune tolerance, and preclinical and clinical studies in which anti–CD3 mAbs have been used.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Anti‐CD3 treatment up‐regulates programmed cell death protein‐1 expression on activated effector T cells and severely impairs their inflammatory capacity

T cells play a key role in the pathogenesis of type 1 diabetes, and targeting the CD3 component of the T-cell receptor complex provides one therapeutic approach. Anti-CD3 treatment can reverse overt disease in spontaneously diabetic non-obese diabetic mice, an effect proposed to, at least in part, be caused by a selective depletion of pathogenic cells. We have used a transfer model to further i...

متن کامل

Endocytosis and Degradation of Murine Anti-Human CD3 Monoclonal Antibodies by Normal and Malignant T-Lymphocytes1

Treatment of lymphoid malignancies with monoclonal antibodies (mAbs) and immunoconjugates is a promising new immunotherapeutic approach. However, few published studies have examined in detail the subcellular fate of antibodies following binding to lymphocyte cell surface antigens. In this study, we have investigated the disposition of monoclonal anti-CD3 antibody 64.1 following binding to norma...

متن کامل

Endocytosis and degradation of murine anti-human CD3 monoclonal antibodies by normal and malignant T-lymphocytes.

Treatment of lymphoid malignancies with monoclonal antibodies (mAbs) and immunoconjugates is a promising new immunotherapeutic approach. However, few published studies have examined in detail the subcellular fate of antibodies following binding to lymphocyte cell surface antigens. In this study, we have investigated the disposition of monoclonal anti-CD3 antibody 64.1 following binding to norma...

متن کامل

Glucagon-like peptide 1 and type 1 diabetes: NOD ready for prime time?

Diabetes mellitus is considered the epidemic of the 21st century, affecting close to 170 million people in 2000, and expected to double in incidence by 2030 (1). The two major types of diabetes (types 1 and 2) are characterized by chronic hyperglycemia due to a loss of insulin secretion and/or defective insulin action; however, the etiopathogenesis of each type is distinct. Type 1 diabetes mell...

متن کامل

Immunotherapeutic effects of pentoxifylline in type 1 diabetic mice and its role in the response of T-helper lymphocytes

Objective(s):Pentoxifylline is an immunomodulatory and anti-inflammatory agent and is used in vascular disorders. It has been shown that pentoxifylline inhibits proinflammatory [d1] cytokines production. The purpose of this study was to investigate the therapeutic effects of pentoxifylline on the treatment of autoimmune diabetes in mice. Materials and Methods: Diabetes was induced by multiple l...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2016