PD-L1 is increased in the spinal cord and infiltrating lymphocytes in experimental allergic encephalomyelitis

Experimental allergic encephalomyelitis is a mouse model of human multiple sclerosis with similar pathology and pathogenesis. Thl cells play an important role in the pathogenesis of experimental allergic encephalomyelitis. This study determined the potential effect of programmed cell death 1 ligand 1 in the pathogenesis of experimental allergic encephalomyelitis induced by injecting myelin oligodendrocyte glycoprotein, complete Freund＇s adjuvant and Bordetella pertussis toxin into C57BL/6J mice. Experimental allergic encephalomyelitis mice developed disease and showed in- flammatory changes in the central nervous system by hematoxylin-eosin staining of spinal cord pathological sections, demyelination by Luxol fast-blue staining and clinical manifestations. The expression of programmed cell death 1 ligand 1 in mice was detected by immunohistochemistry, flow cytometry and western blot anatysis. The expression of programmed cell death 1 ligand 1 in the spinal cord and splenocytes of mice was significantly increased compared with normal mice. Our findings suggest the involvement of programmed cell death 1 ligand 1 in the pathogenesis of ex- perimental allergic encephalomyelitis and suggest this should be studied in multiple sclerosis.

Expression of ICAM-1,B7.1 and TPO on human thyrocytes induced by IFN-α

Objective To detect expression of intercellular adhesion molecule 1 (ICAM 1), B7.1 and thyroid peroxidase (TPO) on thyrocyte and study the possible mechanism of interferon alpha (IFN α) in the pathogenesis of autoimmune thyroid disease (AITD). Methods Thyrocytes were cultured from 6 normal persons. Antigen expression on thyrocytes induced by cytokines was examined using immunofluorescence staining with flow cytometer. Results IFN α significantly stimulated the expression of ICAM 1, B7.1 and TPO, as compared with those of control group. IFN γ markedly enhanced the expression of HLA DR and ICAM 1, but not B7.1. Prolactin (PRL) resulted in increased expression of ICAM 1, B7.1, as well as overexpression of TPO, which is more significant than that stimulated by IFN α. Conclusions Thyroid autoimmunity induced by IFN α is associated with the expression of ICAM 1, B7.1 and TPO. IFN γ could not induce the expression of B7.1, therefore it is not an initiator in AITD. In addition, we should pay more attention to PRL which possibly plays an important role in the initiation and perpetuation of postpartum thyroiditis.