The development of tertiary lymphoid organs in the central nervous system facilitates determinant spreading of the MP4-specific T cell response (P4164)
TL;DRAbstract
Abstract Accumulating evidence indicates that B cells aggregate into tertiary lymphoid organs (TLOs) in the central nervous system (CNS) in the human autoimmune disease multiple sclerosis (MS). In patients with secondary-progressive MS the presence of ectopic B cell aggregates has been linked to more severe clinical disease and cortical pathology. Here we demonstrate the formation of TLOs in myelin basic protein (MBP)-proteolipid protein (PLP) fusion protein MP4-induced experimental autoimmune encephalomyelitis (EAE) of C57BL/6 mice. TLOs were a characteristic feature of the chronic disease stage and most prevalent in the cerebellum, while also being present in the spinal cord and cerebrum, but absent in the brain stem. TLOs were characterized by B and T cell compartmentalization, the presence of high endothelial venules and germinal center formation. An association with TH17, but not TH1 cells was evident. In addition, results obtained from ELISPOT analysis of the antigen-specific T c
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Abstract Accumulating evidence indicates that B cells aggregate into tertiary lymphoid organs (TLOs) in the central nervous system (CNS) in the human autoimmune disease multiple sclerosis (MS). In patients with secondary-progressive MS the presence of ectopic B cell aggregates has been linked to more severe clinical disease and cortical pathology. Here we demonstrate the formation of TLOs in myelin basic protein (MBP)-proteolipid protein (PLP) fusion protein MP4-induced experimental autoimmune encephalomyelitis (EAE) of C57BL/6 mice. TLOs were a characteristic feature of the chronic disease stage and most prevalent in the cerebellum, while also being present in the spinal cord and cerebrum, but absent in the brain stem. TLOs were characterized by B and T cell compartmentalization, the presence of high endothelial venules and germinal center formation. An association with TH17, but not TH1 cells was evident. In addition, results obtained from ELISPOT analysis of the antigen-specific T c
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