Abstract
Guillain-Barré syndrome (GBS) is an acute inflammatory polyradiculoneuropathy that usually develops following a respiratory or intestinal infection. Although the pathogenic mechanisms of GBS have not been fully established, both humoral and cell-mediated immune factors have been shown to contribute to the disease process. Several antiglycosphingolipid (anti-GSL) antibodies have been found in the sera of patients with GBS or related diseases. Measurements of these antibody titers are very important in the diagnosis of GBS and in evaluating the effectiveness of treatments in clinical trials. The most common treatment strategies for these disorders involve plasmapheresis and the use of steroids for reducing anti-GSL antibody titers to ameliorate patients' clinical symptoms. Administration of intravenous immunoglobulin may also be beneficial in the treatment of neuropathies by suppressing the immune-mediated processes that are directed against antigenic targets in myelin and axons. In certain demyelinating neuropathies, the destruction or malfunctioning of the blood-nerve barrier, which results in the leakage of circulating antibodies into the peripheral nerve parenchyma, has been considered to be an initial step in development of the disease process. In addition, anti-GSL antibodies, such as anti-GM1, may cause nerve dysfunction and injury by interfering with the ion channel function at the nodes of Ranvier, where carbohydrate epitopes of glycoconjugates are located. These malfunctions thus contribute to the pathogenic mechanisms of certain demyelinating neuropathies.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1-17 |
| Number of pages | 17 |
| Journal | Journal of Neuroscience Research |
| Volume | 80 |
| Issue number | 1 |
| DOIs | |
| State | Published - Apr 1 2005 |
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Keywords
- Antiglycolipid antibodies
- Glycosphingolipids
- Guillain-Barré syndrome
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience
Cite this
Antiglycolipid antibodies in Guillain-Barré syndrome and related diseases : Review of clinical features and antibody specificities. / Ariga, Toshio; Yu, Robert K.
In: Journal of Neuroscience Research, Vol. 80, No. 1, 01.04.2005, p. 1-17.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Antiglycolipid antibodies in Guillain-Barré syndrome and related diseases
T2 - Review of clinical features and antibody specificities
AU - Ariga, Toshio
AU - Yu, Robert K.
PY - 2005/4/1
Y1 - 2005/4/1
N2 - Guillain-Barré syndrome (GBS) is an acute inflammatory polyradiculoneuropathy that usually develops following a respiratory or intestinal infection. Although the pathogenic mechanisms of GBS have not been fully established, both humoral and cell-mediated immune factors have been shown to contribute to the disease process. Several antiglycosphingolipid (anti-GSL) antibodies have been found in the sera of patients with GBS or related diseases. Measurements of these antibody titers are very important in the diagnosis of GBS and in evaluating the effectiveness of treatments in clinical trials. The most common treatment strategies for these disorders involve plasmapheresis and the use of steroids for reducing anti-GSL antibody titers to ameliorate patients' clinical symptoms. Administration of intravenous immunoglobulin may also be beneficial in the treatment of neuropathies by suppressing the immune-mediated processes that are directed against antigenic targets in myelin and axons. In certain demyelinating neuropathies, the destruction or malfunctioning of the blood-nerve barrier, which results in the leakage of circulating antibodies into the peripheral nerve parenchyma, has been considered to be an initial step in development of the disease process. In addition, anti-GSL antibodies, such as anti-GM1, may cause nerve dysfunction and injury by interfering with the ion channel function at the nodes of Ranvier, where carbohydrate epitopes of glycoconjugates are located. These malfunctions thus contribute to the pathogenic mechanisms of certain demyelinating neuropathies.
AB - Guillain-Barré syndrome (GBS) is an acute inflammatory polyradiculoneuropathy that usually develops following a respiratory or intestinal infection. Although the pathogenic mechanisms of GBS have not been fully established, both humoral and cell-mediated immune factors have been shown to contribute to the disease process. Several antiglycosphingolipid (anti-GSL) antibodies have been found in the sera of patients with GBS or related diseases. Measurements of these antibody titers are very important in the diagnosis of GBS and in evaluating the effectiveness of treatments in clinical trials. The most common treatment strategies for these disorders involve plasmapheresis and the use of steroids for reducing anti-GSL antibody titers to ameliorate patients' clinical symptoms. Administration of intravenous immunoglobulin may also be beneficial in the treatment of neuropathies by suppressing the immune-mediated processes that are directed against antigenic targets in myelin and axons. In certain demyelinating neuropathies, the destruction or malfunctioning of the blood-nerve barrier, which results in the leakage of circulating antibodies into the peripheral nerve parenchyma, has been considered to be an initial step in development of the disease process. In addition, anti-GSL antibodies, such as anti-GM1, may cause nerve dysfunction and injury by interfering with the ion channel function at the nodes of Ranvier, where carbohydrate epitopes of glycoconjugates are located. These malfunctions thus contribute to the pathogenic mechanisms of certain demyelinating neuropathies.
KW - Antiglycolipid antibodies
KW - Glycosphingolipids
KW - Guillain-Barré syndrome
UR - http://www.scopus.com/inward/record.url?scp=17744396351&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=17744396351&partnerID=8YFLogxK
U2 - 10.1002/jnr.20395
DO - 10.1002/jnr.20395
M3 - Review article
C2 - 15668908
AN - SCOPUS:17744396351
VL - 80
SP - 1
EP - 17
JO - Journal of Neuroscience Research
JF - Journal of Neuroscience Research
SN - 0360-4012
IS - 1
ER -