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Defective autologous mixed leukocyte reaction in newly diagnosed type 1 diabetes mellitus
Insights
Autologous mixed leukocyte reaction (AMLR) is impaired in type 1 diabetes patients, showing reduced IL-2 production. Supplementing IL-2 partially restored AMLR, suggesting a role in type 1 diabetes pathogenesis.
Area of Science:
- Immunology
- Endocrinology
Background:
- Type 1 diabetes (T1D), or insulin-dependent diabetes mellitus (IDDM), is an autoimmune disease.
- Autologous mixed leukocyte reaction (AMLR) is a measure of T-cell immune function.
Purpose of the Study:
- To investigate AMLR in patients with T1D.
- To explore the role of Interleukin-2 (IL-2) in T1D immune dysfunction.
Main Methods:
- Blood samples were collected from T1D patients, their healthy siblings, and healthy controls.
- AMLR was measured, along with IL-2 production.
- Exogenous IL-2 was added to patient cultures to assess restoration of AMLR.
Main Results:
- AMLR was significantly depressed in T1D patients compared to healthy controls and siblings.
- IL-2 production during AMLR was impaired in T1D patients.
- Adding exogenous IL-2 restored AMLR in some patients, but not all.
- T1D patients often had elevated activated T lymphocytes, with some showing particularly high levels.
Conclusions:
- Defective AMLR and elevated activated T cells may contribute to the pathogenesis of T1D.
- IL-2 plays a role in the immune dysregulation observed in T1D.
Abstract:
We studied autologous mixed leukocyte reaction (AMLR) in type 1 (insulin-dependent) diabetes mellitus (IDDM) patients, their healthy siblings and healthy schoolchildren, Blood samples from the patients were drawn within 1 week after hospitalization and 2 months later. AMLR was significantly depressed in the patients when compared to healthy siblings or other healthy controls. In addition, the mean AMLR responsiveness of the healthy control group exceeded that of healthy siblings. The production of IL-2 in AMLR was impaired in the patient group and the defective AMLR could be restored by addition of exogenous IL-2 in 7-10 patient cultures. However, in 3-10 patients addition of IL-2 induced no enhancement of proliferation. While the patients in general had raised levels of activated T lymphocytes these three patients had higher numbers of activated T cells than other patients. Defective AMLR and presence of activated T cells may be related and may play a role in the pathogenesis of IDDM.