       Document 0674
 DOCN  M9620674
 TI    Decreased cell-mediated immunity in patients with non-insulin-dependent
       diabetes mellitus.
 DT    9602
 AU    Chang FY; Shaio MF; Department of Internal Medicine, Tri-Service General
       Hospital,; National Defense Medical Center, Taipei, Taiwan, Republic of;
       China.
 SO    Diabetes Res Clin Pract. 1995 May;28(2):137-46. Unique Identifier :
       AIDSLINE MED/96030009
 AB    Peripheral blood mononuclear cells from patients with
       non-insulin-dependent diabetes mellitus (NIDDM) show reduced
       proliferative response to phytohemagglutinin (PHA) and other mitogens.
       This study was undertaken to determine whether this reduced lymphocyte
       proliferation is mediated by a decreased production of cytokine or
       decreased expression of interleukin-2 receptor (IL-2R). Mononuclear
       cells from NIDDM patients (n = 34) and healthy controls (n = 22) were
       cultured in RPMI-1640 media containing PHA, concanavalin-A and phorbol
       myristate acetate. NIDDM patients showed reduced [3H]thymidine uptake
       (57% of controls, P < 0.01), reduced percentage of IL-2R-positive cells
       (61% of controls, P < 0.02) and increased level of tumor necrosis factor
       (TNF)-alpha (200% of controls, P < 0.05). The percentage of complement
       receptor (CR) 3-positive monocytes from NIDDM patients was also
       decreased (72% of controls, P < 0.05). However, the production of IL-1
       beta, IL-2 and interferon-gamma, the percentages of pan T cells (CD3), T
       helper cells (CD4), T suppressor cells (CD8), the ratio of CD4/CD8 and
       the expression of CR1 and Fc receptors for immunoglobulin G (Fc gamma
       RII and Fc gamma RIII) were not significantly different between NIDDM
       patients and healthy subjects. Human recombinant IL-2 was unable to
       restore the [3H]thymidine uptake by PHA-stimulated mononuclear cells
       from NIDDM patients. Elevation of glucose concentration up to 27.8
       mmol/l in the culture medium did not suppress the [3H]thymidine uptake
       and IL-2R expression by activated lymphocytes from healthy subjects. The
       decreased expression of IL-2R on activated lymphocytes might be
       responsible for the insufficient lymphocyte proliferation in NIDDM
       patients. These findings suggest that decreased expression of CR3 on
       monocytes, decreased lymphocyte proliferation and decreased IL-2R
       expression despite a higher production of TNF-alpha may explain the
       impaired cell-mediated immunity seen in NIDDM patients.
 DE    Cells, Cultured  Comparative Study  Concanavalin A
       Cytokines/*BIOSYNTHESIS  CD4-CD8 Ratio  Diabetes Mellitus,
       Non-Insulin-Dependent/*IMMUNOLOGY  Female  Human  Immunity, Cellular
       *Lymphocyte Transformation  Male  Middle Age  Phytohemagglutinins
       Receptors, Interleukin-2/*BIOSYNTHESIS  Reference Values  Support,
       Non-U.S. Gov't  T-Lymphocyte Subsets/*IMMUNOLOGY  T-Lymphocytes/DRUG
       EFFECTS/*IMMUNOLOGY  Tetradecanoylphorbol Acetate/PHARMACOLOGY
       Thymidine/METABOLISM  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

