Immunologische Kreuzreaktivität zwischen dem Myelin-Oligodendrozyten-Glykoprotein (MOG) und Butyrophilin (BTN) bei Multipler Sklerose
Beschreibung
vor 21 Jahren
The aetiology of multiple sclerosis (MS) is believed to involve
environmental factors that disrupt self-tolerance to myelin
autoantigens but their identity and mode of action are unknown.
This study reports that the epitope specificity of autoantibodies
to the myelin oligodendrocyte glycoprotein (MOG), an important
candidate autoantigen in MS, is heterogeneous and that MOG exhibits
extensive immunological cross-reactivity with the bovine milk
protein butyrophilin (BTN), an ubiquitous dietary antigen. In a
subset of MS patients this cross-reactive antibody response is
significantly enhanced and are selectively sequestered in the
central nervous system (CNS) suggesting that this cross-reactive
immune response may play an active role in the pathogenesis of MS.
Immunological cross-reactivity between MOG and BTN may modulate the
composition and pathogenicity of the MOG-specific autoimmune
response. In one scenario this response might be innocuous or even
protective due to the induction of oral tolerance by BTN that
cross-reacts with MOG. Alternatively, cross-reactive antibodies and
pro-inflammatory Th1 T cell responses may target humoral and
cellular effector mechanisms to attack white matter tracts in the
CNS of susceptible patients.
environmental factors that disrupt self-tolerance to myelin
autoantigens but their identity and mode of action are unknown.
This study reports that the epitope specificity of autoantibodies
to the myelin oligodendrocyte glycoprotein (MOG), an important
candidate autoantigen in MS, is heterogeneous and that MOG exhibits
extensive immunological cross-reactivity with the bovine milk
protein butyrophilin (BTN), an ubiquitous dietary antigen. In a
subset of MS patients this cross-reactive antibody response is
significantly enhanced and are selectively sequestered in the
central nervous system (CNS) suggesting that this cross-reactive
immune response may play an active role in the pathogenesis of MS.
Immunological cross-reactivity between MOG and BTN may modulate the
composition and pathogenicity of the MOG-specific autoimmune
response. In one scenario this response might be innocuous or even
protective due to the induction of oral tolerance by BTN that
cross-reacts with MOG. Alternatively, cross-reactive antibodies and
pro-inflammatory Th1 T cell responses may target humoral and
cellular effector mechanisms to attack white matter tracts in the
CNS of susceptible patients.
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