Upregulation of chemokines and their receptors show likely immunomodulatory effects
THURSDAY, Oct. 15 (HealthDay News) -- The effects of interferon beta on chemokine receptor genes and chemokine expression in peripheral immune cells may provide the therapeutic effect seen in multiple sclerosis treatment, according to a German study in the October issue of the Archives of Neurology.
Sabine Cepok, Ph.D., of Technische Universitat in München, Germany, and colleagues evaluated blood samples from untreated and interferon beta-treated multiple sclerosis patients, both positive and negative for neutralizing antibodies (NABs). The study evaluated the expression of 14 chemokines and 14 chemokine receptor genes. The main study outcomes were gene expression and chemokine protein levels in the blood.
The researchers found upregulation of CCL1, CCL2, CCL7, CXCL10, CXCL11, and CCR1 gene expression in interferon beta-treated patients who were negative for NABs. However, gene expression in treated patients who were positive for NABs was the same as for untreated multiple sclerosis patients. In addition, serum chemokine protein levels were shown to be higher in treated multiple sclerosis patients who were negative for NABs than in treated multiple sclerosis patients who were positive for NABs or untreated patients.
"We demonstrate that interferon beta strongly upregulates a set of chemokines and CCR1 in peripheral immune cells. The peripheral upregulation of these chemokines may reduce the chemoattraction of immune cells to the central nervous system and thus add to the therapeutic effects of interferon beta," the authors conclude.
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