CCL26 and CCR3 are associated with the acute inflammatory response in the CNS in experimental autoimmune encephalomyelitis.

Chemokine ligand 26 (CCL26) is a member of the eotaxin family. It works by interacting exclusively with chemokine receptor 3 (CCR3) and acts as an eosinophil-selective chemoattractant. There is an emerging role for eotaxins in autoimmune diseases. Studies have reported that chemokine ligand 11 (CCL11) and CCL26 are upregulated in patients with neuromyelitis optica spectrum disorder (NMOSD) during remission, CCL26 levels appear to be decreased in relapsing-remitting multiple sclerosis (RRMS), whereas CCL26 levels are significantly increased in secondary progressive multiple sclerosis (SPMS), indicating that CCL26 participates in the pathogenesis of multiple sclerosis (MS). We investigated the levels of CCL26, CCR3 and claudin-5 (a marker of changes in BBB (blood-brain barrier) permeability) at different stages of experimental autoimmune encephalomyelitis (EAE) to explore the underlying immune mechanisms of EAE. Our results showed that the levels of CCL26 and CCR3 in EAE rats were significantly increased compared with those in the control group. The levels of CCL26 in the serum and in brain tissues as well as the protein expression of CCR3 in brain tissues were positively correlated with the inflammatory scores of brain tissues from EAE rats and were negatively correlated with the protein expression of claudin-5. We concluded that CCL26, which in turn binds to the receptor CCR3, showed pro-inflammatory effects and aggravated tissue damage involving BBB impairment, especially in the acute stage of EAE. Our study uncovers another possible immunopathological mechanism of MS and provides a possible target for immune therapy.

IL-23 and IL-27 Levels in Serum are Associated with the Process and the Recovery of Guillain-Barré Syndrome.

IL-23 and IL-27 are believed to be involved in the pathogenesis of Guillain-Barré syndrome (GBS). However, changes in these cytokines during the dynamic pathological and recovery processes of GBS are not well described. In the present study, plasma was collected from 83 patients with various stages of GBS, 70 patients with central nervous system demyelinating diseases,70 patients with other neurological diseases (OND) and 70 age- and sex-matched healthy volunteers. Serum levels of IL-23, IL-27, and Campylobacter jejuni (CJ) IgM were assessed using enzyme linked immunosorbent assay (ELISA). We found that serum IL-23 levels of patients during the acute phase of GBS were significantly higher followed by a decreasing trend during the recovery phase of the disease. Serum IL-27 levels significantly increased during the acute phase of GBS, and gradually increased during the recovery phase. Interestingly, both the severity and subtype of GBS were closely associated with the two cytokines. IL-23 levels were positively correlated with IL-27 levels, prognosis, and other clinical parameters. Our findings confirm that IL-23 may show pro-inflammatory effects, especially at the early stage of GBS. IL-27 appears to have a dual role in GBS, with initial pro-inflammatory effects, followed by anti-inflammatory properties during recovery.

Polymorphisms in exon 2 of CD1 genes are associated with susceptibility to Guillain-Barré syndrome.

Guillain-Barré syndrome (GBS) is a post-infectious autoimmune peripheral neuropathy. Studies have shown that a T cell-mediated immune response to peripheral nerve is associated with the pathogenesis of GBS. CD1 molecules are MCH-like glycoproteins specialized to capture and present glycolipids to T cells. Polymorphisms of CD1 genes may affect susceptibility to GBS. We investigated the polymorphisms of CD1 genes in GBS patients in a Chinese Han population. In 126 patients and in 138 controls we genotyped exon 2 of the CD1A and CD1E genes. The results indicated that polymorphisms of CD1A genes are associated with GBS. Furthermore, subjects with CD1A*01/02 had a 2.9 times lower risk of developing GBS, and those with CD1A*02/02 had a 2.5 times higher risk to developing GBS than the controls, while there was no association between polymorphisms of CD1E genes and the susceptibilities to GBS.