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1996-02-26
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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).