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Decreased cell-mediated immunity in patients with non-insulin-dependent diabetes mellitus

F Y Chang1, M F Shaio

  • 1Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Republic of China.

Diabetes Research and Clinical Practice
|May 1, 1995
PubMed

Insights

Non-insulin-dependent diabetes mellitus (NIDDM) impairs immune cell function, leading to reduced lymphocyte proliferation. This is linked to lower interleukin-2 receptor (IL-2R) expression and complement receptor 3 (CR3) on monocytes, suggesting compromised cell-mediated immunity in NIDDM patients.

Area of Science:

  • Immunology
  • Endocrinology
  • Cell Biology

Background:

  • Patients with non-insulin-dependent diabetes mellitus (NIDDM) exhibit diminished lymphocyte responsiveness to mitogens.
  • The underlying mechanisms for impaired cell-mediated immunity in NIDDM, such as altered cytokine production or receptor expression, require elucidation.

Purpose of the Study:

  • To investigate whether reduced lymphocyte proliferation in NIDDM is associated with decreased cytokine production or diminished interleukin-2 receptor (IL-2R) expression.
  • To explore the role of other immune cell markers, including complement receptor 3 (CR3), in NIDDM-related immune dysfunction.

Main Methods:

  • Peripheral blood mononuclear cells (PBMCs) from NIDDM patients and healthy controls were cultured with mitogens (PHA, concanavalin-A, phorbol myristate acetate).
  • Lymphocyte proliferation was assessed via [3H]thymidine uptake.
  • Expression of IL-2R, CR3, and other immune markers (CD3, CD4, CD8, CR1, Fc gamma RII/III) was quantified using flow cytometry. Cytokine levels (IL-1β, IL-2, IFN-γ, TNF-α) were measured.

Main Results:

  • NIDDM patients demonstrated significantly reduced [3H]thymidine uptake and lower percentages of IL-2R-positive cells compared to controls.
  • Elevated levels of tumor necrosis factor-alpha (TNF-α) and decreased expression of complement receptor 3 (CR3) on monocytes were observed in NIDDM patients.
  • No significant differences were found in IL-1β, IL-2, interferon-gamma production, T cell subset percentages, CD4/CD8 ratio, or Fc receptor expression.

Conclusions:

  • Decreased IL-2R expression on activated lymphocytes likely contributes to impaired lymphocyte proliferation in NIDDM.
  • Reduced CR3 expression on monocytes, coupled with decreased lymphocyte proliferation and IL-2R expression, may underlie the compromised cell-mediated immunity in NIDDM.
  • Elevated TNF-α production in NIDDM does not appear to compensate for the observed immune deficits.

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