Immunologic parameters in Chronic Fatigue Syndrome (CFS), major depression, & multiple sclerosis

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The purpose of this study was to evaluate the immune

dysfunction hypothesis of chronic fatigue syndrome (CFS) by

comparing immunologic data from patients with CFS with data

from patients with other fatiguing illnesses–major depression

and multiple sclerosis (MS)–and with data from healthy

sedentary controls. The subjects were 65 healthy sedentary

controls, 71 CFS patients (41 with no axis-I diagnosis), 23

patients with mild MS, and 21 patients with major depression.

Blood was sampled and assayed for the following: (1)

immunologic serologic variables–circulating immune complexes

(i.e., Raji cell and C1q binding), immunoglobulins A, E, G,

and M, and IgG subclasses; (2) cell surface activation

markers–the proportion of CD4+ cells expressing CD45RA+ and

CD45RO+ and the proportion of CD8+ cells expressing CD38+,

CD11b-, HLA-DR+ and CD28+; and (3) natural killer (NK) total

cell count as well as the proportion of lymphocytes expressing

NK cell surface markers (i.e., CD3-/CD16+ and CD56+. Of the 18

variables studied, differences between CFS patients and

controls were found only for IgG1 and IgG3. When CFS patients

were stratified by the presence or absence of concurrent

axis-I disease, it was the group with axis-I disorder that had

the lowest IgG1 values-contrary to expectation.

When data from

patients with MS and major depression were also evaluated, the

subclass deficiency was no longer significant. The one group

to show evidence for immune activation (i.e., an elevated

proportion of CD4+ cells expressing the CD45RA+ activation

marker) was the group with mild MS. These data support neither

immune dysfunction nor immune activation in CFS or in major

depression, for the variables studied. The reductions in IgG

subclasses may be an epiphenomenon of patient or control

subject composition. In contrast, MS, even in the mild and

early stages, as in the patients studied here, is associated

with immune activation.

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