How does B-Cell tolerance contribute to the protective effects of diabetes following induced mixed chimerism in autoimmune diabetes?

Wong, Florence ORCID: https://orcid.org/0000-0002-2812-8845 2014. How does B-Cell tolerance contribute to the protective effects of diabetes following induced mixed chimerism in autoimmune diabetes? Diabetes 63 (6) , pp. 1855-1857. 10.2337/db14-0327

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Abstract

In type 1 diabetes, autoimmune-mediated damage and destruction of insulin-producing β-cells lead to a raised blood glucose. Glucose itself is toxic and some recovery of β-cell function is expected in the honeymoon phase after insulin treatment is instituted, but it was previously believed that all β-cells will ultimately be lost. In fact, there are individuals who continue to have some functioning β-cells, even many years after the onset of type 1 diabetes (1,2). This raises the hope that treatment to induce replication or regeneration of β-cells could be instituted in patients with long-standing diabetes, and makes it even more imperative that means of halting autoimmunity are found. Although nonmyeloablative autologous stem cell transplantation has been carried out, with long-term insulin independence successfully achieved in type 1 diabetes (3,4), many would feel that the risk-benefit ratio of this treatment is not acceptable for general use. Many other strategies, both nonantigen- and antigen-specific therapies, have been trialed in patients with new-onset type 1 diabetes, but none, as yet, has provided a long-term solution to the autoimmune attack on remaining β-cells (5). However, short-term slowing of β-cell loss was seen with T-cell−targeted therapy using nondepleting anti-CD3 (6,7), which was shown to temporarily reduce T cells, but, more importantly, to increase T-cell regulation. In addition, anti-CD20 treatment (rituximab) that targets B cells also temporarily slowed loss of endogenous insulin production (8,9 …

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Medicine Systems Immunity Research Institute (SIURI)
Subjects:	Q Science > QR Microbiology > QR180 Immunology
Publisher:	American Diabetes Association
ISSN:	0012-1797
Last Modified:	28 Oct 2022 10:28
URI:	https://orca.cardiff.ac.uk/id/eprint/78418

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