Serum Interleukin-2, Soluble Interleukin-2 Receptors and Neopterin Concentrations in Guillain-Barre Syndrome.
- Author:
Jeong Geun LIM
1
;
Young Choon PARK
;
Jung Chul KIM
Author Information
1. Department of Neurology, Keimyung University School of Medicine, Korea.
- Publication Type:Original Article
- MeSH:
Autoimmune Diseases;
Cytokines;
Follow-Up Studies;
Guillain-Barre Syndrome*;
Humans;
Immune System;
Immunity, Cellular;
Interleukin-2*;
Macrophage Activation;
Neopterin*;
Plasmapheresis;
Polyradiculoneuropathy;
Receptors, Interleukin-2*;
T-Lymphocytes
- From:Journal of the Korean Neurological Association
1994;12(2):279-288
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Guillain-Barre syndrome (GBS) is an autoimmune disease with an acute evolution of inflammatory demyelinating polyradiculoneuropathy. Although the precise immune mechanisms and involved antigens are uncertain, both humoral and cellular immune mechanisms are thought to be involved. Interactions between the various compartments of the immune system are governed by cytokines. Laboratory investigations have shown that immune activation can be quantified by measurement of cytokines and soluble immune activation products in serum. Interleukin-2(IL-2) is probably the best characterized among the many cytokines and soluble interleukin-2 receptor (sIL-2R) and neopterin are major immune activation products. In order to observe activities of cellular immunity of GBS, we measured serum concentrations of IL-2, sIL-2R and neopterin in 28 patients with GBS and in 22 healthy controls. Serial serum samples were drawn 2 to 25 days after motor onset of the disease, 2 to 3 days after treatment with plasmapheresis and 43-300days of follow-up. The occurences of IL-2 positive serum samples were 41.7%, 23.8% and 18.2% in each time in GBS but none in healthy controls. Initial serum sIL-2R and neopterin level were elevated in 21% and 17% of patients with GBS compared with healthy controls. After plasmapheresis, both serum sIL-2R and neopterin level were significantly elevated in GBS compared with initial serum samples and healthy controls. Thus, T-cell and macrophage activation may play a role in the pathogenesis of GBS. However, further study is needed to evaluate the effect of plasmapheresis and clinical severity on the serum concentration of IL-2, sIL-2R and neopterin in GBS.
