Phenotype and Functional Characteristics of Islet-Infiltrating B-Cells Suggest the Existence of Immune Regulatory Mechanisms in Islet Milieu
- Maria Carmen Puertas1,
- Jorge Carrillo1,
- Xavier Pastor1,
- Rosa Maria Ampudia1,
- Aurora Alba1,
- Raquel Planas1,
- Ricardo Pujol-Borrell1,
- Marta Vives-Pi1 and
- Joan Verdaguer12
- 1Laboratory of Immunobiology for Research and Diagnosis (LIRAD) and Center for Transfusion and Tissue Bank (BST), Institut d'Investigacio Germans Trias i Pujol, Carretera de Can Ruti, Badalona, Barcelona, Spain
- 2Immunology Unit, Department of Ciencies Mediques Basiques, Faculty of Medicine, University of Lleida, Lleida, Catalonia, Spain
- Address correspondence and reprint requests to Dr. Joan Verdaguer, Unit of Immunology, Departament de Ciencies Mediques Basiques, Facultat de Medicina, Universitat de Lleida, Carrer Montserrat Roig 2, 25008 Lleida, Catalonia, Spain. E-mail: joan.verdaguer{at}cmb.udl.es
Abstract
B-cells participate in the autoimmune response that precedes the onset of type 1 diabetes, but how these cells contribute to disease progression is unclear. In this study, we analyzed the phenotype and functional characteristics of islet-infiltrating B-cells in the diabetes-prone NOD mouse and in the insulitis-prone but diabetes-resistant (NOD×NOR)F1 mouse. The results indicate that B-cells accumulate in the islets of both mice influenced by sex traits. Phenotypically and functionally, these B-cells are highly affected by the islet inflammatory milieu, which may keep them in a silenced status. Moreover, although islet-infiltrating B-cells seem to be antigen experienced, they can only induce islet-infiltrating T-cell proliferation when they act as accessory cells. Thus, these results strongly suggest that islet-infiltrating B-cells do not activate islet-infiltrating T-cells in situ, although they may affect the progression of the disease otherwise.
- APC, antigen-presenting cell
- CFSE, carboxy-fluorescein diacetate succinimidyl ester
- CTL, cytotoxic T-cell
- FITC, fluorescein isothiocyanate
- IFN-γ, γ-interferon
- IL, interleukin
- LPS, lipopolysaccharide
- mAb, monoclonal antibody
- MHC, major histocompatibility complex
Footnotes
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- Accepted December 21, 2006.
- Received March 30, 2006.
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