Is pancreas development abnormal in the non-obese diabetic mouse, a spontaneous model of type I diabetes?
Despite extensive genetic and immunological research, the complex etiology and pathogenesis of type I diabetes remains unresolved. During the last few years, our attention has been focused on factors such as abnormalities of islet function and/or microenvironment, that could interact with immune par...
| Main Author: | |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Associação Brasileira de Divulgação Científica
2001-04-01
|
| Series: | Brazilian Journal of Medical and Biological Research |
| Subjects: | |
| Online Access: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2001000400002 |
| _version_ | 1818882470584516608 |
|---|---|
| author | F. Homo-Delarche |
| author_facet | F. Homo-Delarche |
| author_sort | F. Homo-Delarche |
| collection | DOAJ |
| description | Despite extensive genetic and immunological research, the complex etiology and pathogenesis of type I diabetes remains unresolved. During the last few years, our attention has been focused on factors such as abnormalities of islet function and/or microenvironment, that could interact with immune partners in the spontaneous model of the disease, the non-obese diabetic (NOD) mouse. Intriguingly, the first anomalies that we noted in NOD mice, compared to control strains, are already present at birth and consist of 1) higher numbers of paradoxically hyperactive ß cells, assessed by in situ preproinsulin II expression; 2) high percentages of immature islets, representing islet neogenesis related to neonatal ß-cell hyperactivity and suggestive of in utero ß-cell stimulation; 3) elevated levels of some types of antigen-presenting cells and FasL+ cells, and 4) abnormalities of extracellular matrix (ECM) protein expression. However, the colocalization in all control mouse strains studied of fibroblast-like cells (anti-TR-7 labeling), some ECM proteins (particularly, fibronectin and collagen I), antigen-presenting cells and a few FasL+ cells at the periphery of islets undergoing neogenesis suggests that remodeling phenomena that normally take place during postnatal pancreas development could be disturbed in NOD mice. These data show that from birth onwards there is an intricate relationship between endocrine and immune events in the NOD mouse. They also suggest that tissue-specific autoimmune reactions could arise from developmental phenomena taking place during fetal life in which ECM-immune cell interaction(s) may play a key role. |
| first_indexed | 2024-12-19T15:18:16Z |
| format | Article |
| id | doaj.art-0ea8a785c5a147a0ae3e446fa624ecf1 |
| institution | Directory Open Access Journal |
| issn | 0100-879X 1414-431X |
| language | English |
| last_indexed | 2024-12-19T15:18:16Z |
| publishDate | 2001-04-01 |
| publisher | Associação Brasileira de Divulgação Científica |
| record_format | Article |
| series | Brazilian Journal of Medical and Biological Research |
| spelling | doaj.art-0ea8a785c5a147a0ae3e446fa624ecf12022-12-21T20:16:04ZengAssociação Brasileira de Divulgação CientíficaBrazilian Journal of Medical and Biological Research0100-879X1414-431X2001-04-0134443744710.1590/S0100-879X2001000400002Is pancreas development abnormal in the non-obese diabetic mouse, a spontaneous model of type I diabetes?F. Homo-DelarcheDespite extensive genetic and immunological research, the complex etiology and pathogenesis of type I diabetes remains unresolved. During the last few years, our attention has been focused on factors such as abnormalities of islet function and/or microenvironment, that could interact with immune partners in the spontaneous model of the disease, the non-obese diabetic (NOD) mouse. Intriguingly, the first anomalies that we noted in NOD mice, compared to control strains, are already present at birth and consist of 1) higher numbers of paradoxically hyperactive ß cells, assessed by in situ preproinsulin II expression; 2) high percentages of immature islets, representing islet neogenesis related to neonatal ß-cell hyperactivity and suggestive of in utero ß-cell stimulation; 3) elevated levels of some types of antigen-presenting cells and FasL+ cells, and 4) abnormalities of extracellular matrix (ECM) protein expression. However, the colocalization in all control mouse strains studied of fibroblast-like cells (anti-TR-7 labeling), some ECM proteins (particularly, fibronectin and collagen I), antigen-presenting cells and a few FasL+ cells at the periphery of islets undergoing neogenesis suggests that remodeling phenomena that normally take place during postnatal pancreas development could be disturbed in NOD mice. These data show that from birth onwards there is an intricate relationship between endocrine and immune events in the NOD mouse. They also suggest that tissue-specific autoimmune reactions could arise from developmental phenomena taking place during fetal life in which ECM-immune cell interaction(s) may play a key role.http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2001000400002NOD micepostnatal pancreas developmentantigen-presenting cellextracellular matrix |
| spellingShingle | F. Homo-Delarche Is pancreas development abnormal in the non-obese diabetic mouse, a spontaneous model of type I diabetes? Brazilian Journal of Medical and Biological Research NOD mice postnatal pancreas development antigen-presenting cell extracellular matrix |
| title | Is pancreas development abnormal in the non-obese diabetic mouse, a spontaneous model of type I diabetes? |
| title_full | Is pancreas development abnormal in the non-obese diabetic mouse, a spontaneous model of type I diabetes? |
| title_fullStr | Is pancreas development abnormal in the non-obese diabetic mouse, a spontaneous model of type I diabetes? |
| title_full_unstemmed | Is pancreas development abnormal in the non-obese diabetic mouse, a spontaneous model of type I diabetes? |
| title_short | Is pancreas development abnormal in the non-obese diabetic mouse, a spontaneous model of type I diabetes? |
| title_sort | is pancreas development abnormal in the non obese diabetic mouse a spontaneous model of type i diabetes |
| topic | NOD mice postnatal pancreas development antigen-presenting cell extracellular matrix |
| url | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2001000400002 |
| work_keys_str_mv | AT fhomodelarche ispancreasdevelopmentabnormalinthenonobesediabeticmouseaspontaneousmodeloftypeidiabetes |