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Systemic bias of cytokine production toward cell-mediated immune regulation in IDDM and toward humoral immunity in Graves' disease
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Systemic bias of cytokine production toward cell-mediated immune regulation in IDDM and toward humoral immunity in Graves' disease
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Journal Article
Systemic bias of cytokine production toward cell-mediated immune regulation in IDDM and toward humoral immunity in Graves' disease
1997
Overview
Systemic bias of cytokine production toward cell-mediated immune regulation in IDDM and toward humoral immunity in Graves'
disease.
B A Kallmann ,
M Hüther ,
M Tubes ,
J Feldkamp ,
J Bertrams ,
F A Gries ,
E F Lampeter and
H Kolb
Clinical Department of the Diabetes Research Institute, Heinrich-Heine-University of Dusseldorf, Germany.
Abstract
Disturbed immune regulation has been postulated to be crucial in the pathogenesis of IDDM and other autoimmune or allergic
diseases. We therefore tested the hypothesis of a general bias in the peripheral immune system in patients with recent-onset
IDDM or Graves' disease in comparison to healthy control subjects by studying whole blood cultures stimulated with phytohemagglutinin.
Cells from IDDM patients (n = 53) produced significantly higher amounts of Th1 cytokines gamma-interferon (IFN-gamma) (P =
0.028) and tumor necrosis factor alpha (TNF-alpha) (P = 0.007) than normal control subjects (n = 56), while Th2 cytokine levels
(interleukin [IL]-4, IL-10) were similar. Low levels of islet cell antibodies (ICAs) in IDDM patients were associated with
high levels of Th1 and Th2 cytokines. Antibodies to GAD, ICA512, or insulin did not correlate with individual cytokine profiles.
Also, HLA-DQ types did not significantly correlate with either Th1 or Th2 cytokine production. Conversely, whole blood cultures
from patients with Graves' disease (n = 18) produced significantly less TNF-alpha and IL-4 than normal subjects (P = 0.001-0.006).
However, when the balance between Th1 and Th2 cytokine production was analyzed in individuals, the ratio between IFN-gamma
or TNF-alpha and IL-4 or IL-10 was clearly biased toward Th1 reactivity in patients with IDDM (P = 0.0001), while a dominance
of Th2 cytokine production was seen in Graves' disease (P = 0.0001). The ratio of counterregulatory cytokines appeared to
be the most reliable marker of the individual disease process. This study provides first evidence of a systemic bias in the
immune regulation of humans, which might be either toward cell-mediated immunity (Th1) in IDDM or humoral immunity (Th2) in
Graves' disease.
Publisher
American Diabetes Association
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