Low CTLA-4 expression in CD4+ helper T-cells in patients with fulminant type 1 diabetes.

Abstract

Fulminant type 1 diabetes is a novel subtype of type 1 diabetes characterized by a remarkably abrupt onset of insulin-deficient hyperglycemia. An accelerated immune reaction has been suggested as the cause of markedly rapid beta cell loss in this disease, but the precise mechanism has not been clarified. We analyzed the expression of cytotoxic T lymphocyte antigen 4 (CTLA-4) in CD4(+) helper T-cells in 16 patients with fulminant type 1 diabetes, 14 patients with type 1A diabetes, 10 patients with type 2 diabetes and 20 normal control subjects. There was a significant reduction in CTLA-4 expression in CD4(+) helper T-cells from patients with fulminant type 1 diabetes (P<0.05) compared with the other three groups. Low CTLA-4 expression was also observed in both CD4(+)CD25(high) T-cells and CD4(+)CD25(-) T-cells. There was a significant negative correlation between the proliferation of CD4(+)CD25(-) T-cells and the levels of CTLA-4. Intracellular expression of CTLA-4 in CD4(+) helper T-cells was not correlated with two CTLA-4 polymorphisms. In conclusion, the expression of CTLA-4 in CD4(+) helper T-cells was low in patients with fulminant type 1 diabetes.

• Authors: Fumitaka Haseda, Akihisa Imagawa, Yuko Murase-Mishiba, Hiroyuki Sano, Suzue Hirano-Kuwata, Hironori Ueda, Jungo Terasaki, Toshiaki Hanafusa
• Journal: Immunology letters (Immunol Lett) Vol. 139 Issue 1-2 Pg. 80-6 (Sep 30 2011) ISSN: 1879-0542 [Electronic] Netherlands
• PMID: 21620894 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2011 Elsevier B.V. All rights reserved.

Chemical References

• Antigens, CD
• CTLA-4 Antigen
• FOXP3 protein, human
• Forkhead Transcription Factors
• RNA, Messenger

Topics

• Adult
• Aged
• Antigens, CD (immunology, metabolism)
• CTLA-4 Antigen (genetics, metabolism)
• Cell Proliferation
• Diabetes Mellitus, Type 1 (genetics, immunology, metabolism)
• Female
• Forkhead Transcription Factors (immunology, metabolism)
• Gene Expression Regulation (immunology)
• Humans
• Intracellular Space (metabolism)
• Lymphocyte Activation (immunology)
• Male
• Middle Aged
• Polymorphism, Single Nucleotide (genetics)
• RNA, Messenger (genetics, metabolism)
• T-Lymphocytes, Helper-Inducer (immunology, metabolism)
• Young Adult