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Time course of the lymphopenia in BB rats. Relation to the onset of diabetes
Insights
Spontaneously diabetic BB rats exhibit early lymphopenia (low lymphocyte counts), affecting T-cell subsets. This genetically determined defect may predispose rats to diabetes development.
Area of Science:
- Immunology
- Endocrinology
- Genetics
Background:
- The BB rat syndrome, a model for Type 1 diabetes, is characterized by lymphopenia.
- Lymphopenia may be a prerequisite for diabetes development in these rats.
Purpose of the Study:
- To investigate the early time course of peripheral blood lymphocyte counts and subsets in BB rats from birth to 66 days.
- To determine if lymphocyte subset changes predict diabetes onset.
Main Methods:
- Peripheral blood lymphocyte counts and subsets (T-cells, helper/inducer, suppressor/cytotoxic, B-cells) were assessed from birth to 66 days of age.
- Rats were monitored for diabetes onset.
Main Results:
- At birth, total lymphocytes, T-cells (W3/13+, OX19+), helper/inducer (W3/25+), and suppressor/cytotoxic (OX8+) subsets were decreased.
- Lymphocyte counts showed a subnormal rise over time.
- No significant differences in lymphocyte counts at 66 days predicted subsequent diabetes development.
- No concurrent changes in lymphocyte counts were observed at diabetes onset.
Conclusions:
- A genetically determined defect in lymphocyte numbers exists in BB rats, leading to a lifelong subnormal lymphocyte count.
- This defect may predispose rats to diabetes by interacting with an unidentified factor causing beta-cell cytotoxicity.
Abstract:
The spontaneously diabetic BB rat syndrome is associated with a marked lymphopenia, which affects all members of litters of diabetes-prone rats, and may be a necessary condition for the development of the disease. We assessed peripheral blood lymphocyte counts and subsets from birth to 66 days of age with a view to assessing the early time course. At birth, total numbers were decreased, as were total T-cells (monoclonal antibody W3/13+, with an even greater deficit in OX19+ cells), the helper/inducer subset (W3/25+), and the suppressor/cytotoxic subset (OX8+), but Ia+ (B, OX6+) cells were not reduced. There was a less-than-normal rise in these values with time, and a similar pattern was observed at 66 days. Rats followed thereafter to onset of diabetes showed no differences at 66 days that were predictive of subsequent diabetes development. Another set of rats studied at the same age and again at onset of diabetes showed no changes concurrent with diabetes onset. The data are consistent with a genetically determined defect in lymphocyte numbers that leads to a subnormal rise in circulating cells later in life, and may predispose to another unidentified factor responsible for precipitation of the beta cell cytotoxicity.
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