NDLI: Forced expression of programmed death-1 gene on T cell decreased the incidence of type 1 diabetes.

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Forced expression of programmed death-1 gene on T cell decreased the incidence of type 1 diabetes.

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Forced expression of programmed death-1 gene on T cell decreased the incidence of type 1 diabetes.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Won, Tae Joon Jung, Yu Jin Kwon, Seok Joong Lee, Yoon Jeong Lee, Do Ik Min, Hyeyoung Park, Eon Sub Joo, Seong Soo Hwang, Kwang Woo
Description	Author Affiliation: Won TJ ( Chung-Ang University, Seoul, Korea.)
Abstract	Programmed death-1 (PD-1) is a co-inhibitory receptor of the CD28/CTLA-4 family which is expressed on activated T cells and inhibits T cell activation after binding to PD-1 ligands. In animal models, PD-1 regulates autoimmune disease and induces tolerance in pancreas. In this study the effects of PD-1 on type 1 diabetes were examined using PD-1 transgenic mice (Tg). The incidence of autoimmune diabetes induced by multiple low dose of streptozotocin (STZ) was reduced in PD-1 Tg mice. Although the expression of CTLA-4, PD-1 and FoxP3, which are inhibitory molecules of activated T cells, is reduced only on STZ injected wild type (WT) mice, CD4, CD8 and regulatory T cell populations were not changed in all experimental groups. When splenocytes were re-stimulated in ex vivo, the production of IL-2 and IFN-Î³ and the T cell proliferation were increased in all STZ injected mice, but the increment rate was less in PD-1 Tg groups. Interestingly, macrophages were observed in splenocytes of STZ injected PD-1 Tg at somewhat lower level than macrophage in diabetic wild type mice. In this research, we found out that total numbers of T cell in the experimental groups are not changed, but T cell function is changed, and FoxP3 expression is decreased in pancreas and spleen of diabetes-induced groups. Macrophage frequency might also affects on type 1 diabetes. Although more experimental evidence needs to be provided, these results suggest that ligation of PD-1 and PD-L1/2 may have an effect on macrophages as well as does T cells.
File Format	HTM / HTML
ISSN	02536269
Issue Number	11
Volume Number	33
e-ISSN	19763786
Journal	Archives of Pharmacal Research
Language	English
Publisher	Springer
Publisher Date	2010-11-01
Publisher Place	Korea (South)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Pharmacology Antigens, Cd Metabolism Antigens, Surface Apoptosis Regulatory Proteins Diabetes Mellitus, Experimental Prevention & Control Diabetes Mellitus, Type 1 Lymphocyte Activation T-lymphocytes Animals Immunology Antigens, Cd274 Antigens, Cd80 Genetics Cd4-positive T-lymphocytes Cd8-positive T-lymphocytes Ctla-4 Antigen Gene Expression Immune Tolerance Interferon-gamma Interleukin-2 Macrophages Male Membrane Glycoproteins Mice Mice, Inbred C57bl Mice, Transgenic Peptides Programmed Cell Death 1 Ligand 2 Protein Programmed Cell Death 1 Receptor Journal Article Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Organic Chemistry Drug Discovery Molecular Medicine

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