Splenic dendritic cells from the non-obese diabetic mouse induce a prolonged proliferation of syngeneic T cells. A role for an impaired apoptosis of NOD T cells?

Important note: Information in this article was accurate in 2000. The state of the art may have changed since the publication date.

Splenic dendritic cells from the non-obese diabetic mouse induce a prolonged proliferation of syngeneic T cells. A role for an impaired apoptosis of NOD T cells?

J Autoimmun. 1999 Dec;13(4):373-82. Unique Identifier : AIDSLINE MED/20054046
Radosevic K; Casteels KM; Mathieu C; Van Ewijk W; Drexhage HA; Leenen PJ; Department of Immunology, Erasmus University Rotterdam, The; Netherlands. radosevic@immu.fgg.eur.nl

Abstract: In this study we have tried to detect abnormalities in the immunophenotype and/or function of dendritic cells from the non-obese diabetic mouse (NOD DC), that might be related to islet autoimmunity. The immunophenotype of NOD splenic DC did not show significant abnormalities as compared with the immunophenotype of splenic DC from C57BL/10 mice. Furthermore, NOD splenic and lymph node DC stimulated proliferation of syngeneic T cells as efficiently as DC from C57BL/10 and BALB/c mice. The allogeneic response induced by NOD DC was similar to or only slightly lower than the response induced by C57BL/10 DC. Both a normal immunophenotype of NOD DC and efficient T cell stimulation were observed regardless of the stage of diabetes development. However, the syngeneic T cell proliferation induced by NOD splenic DC, but not by C57BL/10 splenic DC, was significantly prolonged, and it was accompanied by an increased proportion of activated/memory CD4(+)cells. We demonstrated that during the interaction of NOD cells fewer apoptotic cells were generated as compared with the interaction of C57BL/10 cells. Thus, the prolonged T cell response during the syngeneic interaction between NOD DC and T cells might be due to an impaired apoptosis induction. The impaired apoptosis might be of critical importance in the development of islet autoimmunity in the NOD mouse. Copyright 1999 Academic Press.

Keywords: JOURNAL ARTICLE Animal Antigens, CD45/IMMUNOLOGY Apoptosis/*IMMUNOLOGY Cell Division Cells, Cultured CD4-CD8 Ratio CD4-Positive T-Lymphocytes/IMMUNOLOGY Dendritic Cells/CYTOLOGY/*IMMUNOLOGY Diabetes Mellitus, Experimental/*IMMUNOLOGY Diabetes Mellitus, Insulin-Dependent/*IMMUNOLOGY Immunologic Memory Immunophenotyping Lymphocyte Culture Test, Mixed Lymphocyte Transformation Mice Mice, Inbred C57BL Mice, Inbred NOD Spleen/CYTOLOGY T-Lymphocytes/*IMMUNOLOGY
000530
A0052247

AEGiS is a 501(c)3, not-for-profit, tax-exempt, educational corporation. AEGiS is made possible through unrestricted funding from Elton John AIDS Foundation, the National Library of Medicine, and donations from users like you. Always watch for outdated information. This article first appeared in 2000. This material is designed to support, not replace, the relationship that exists between you and your doctor.

AEGiS presents published material, reprinted with permission and neither endorses nor opposes any material. All information contained on this website, including information relating to health conditions, products, and treatments, is for informational purposes only. It is often presented in summary or aggregate form. It is not meant to be a substitute for the advice provided by your own physician or other medical professionals. Always discuss treatment options with a doctor who specializes in treating HIV.

Copyright ©1980, 2000. AEGiS. All materials appearing on AEGiS are protected by copyright as a collective work or compilation under U.S. copyright and other laws and are the property of AEGiS, or the party credited as the provider of the content. .