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Decreased CD57 lymphocyte subset in patients with chronic Lyme disease.

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Abstract

BACKGROUND:

Chronic
Lyme disease (LD) is a debilitating illness caused by tickborne infection with the spirochete Borrelia burgdorferi. Although immunologic abnormalities appear to play a role in this
disease, specific immunologic markers of chronic LD have not been identified.

METHODS:

We evaluated 73 patients with chronic LD for lymphocyte subset abnormalities using flow cytometry. Of these, 53 patients had predominant musculoskeletal symptoms, while 20 patients had predominant neurologic symptoms. The estimated duration of infection ranged from 3 months to 15 years, and all patients had positive serologic tests for B. burgdorferi. Ten patients with acute LD (infection less than 1 month) and 22 patients with acquired immunodeficiency syndrome (AIDS) served as
disease controls.

RESULTS:

All 31 chronic LD patients who were tested prior to antibiotic treatment had significantly decreased CD57 lymphocyte counts (mean, 30+/-16 cells per microl; normal, 60-360 cells per microl, P<0.001). Nineteen of 37 patients (51%) who were tested after initiating antibiotic therapy had decreased CD57 levels (mean, 66+/-39 cells per microl), and all five patients tested after completing antibiotic treatment had normal CD57 counts (mean, 173+/-98 cells per microl). In contrast, all 10 patients with acute LD and 82% of AIDS patients had normal CD57 levels, and the difference between these groups and the pre-treatment patients with chronic LD was significant (P<0.001). Patients with chronic LD and predominant neurologic symptoms had significantly lower mean CD57 levels than patients with predominant musculoskeletal symptoms (30+/-21 vs. 58+/-37 cells per microl, P=0.002). CD57 levels increased in chronic LD patients whose symptoms improved, while patients with refractory
disease had persistently low CD57 counts.

CONCLUSIONS:

A decrease in the CD57 lymphocyte subset may be an important marker of chronic LD. Changes in the CD57 subset may be useful to monitor the response to therapy in this
disease.

Immunol Lett. 2001 Feb 1;76(1):43-8.

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