Complement activation and expression during chronic relapsing experimental autoimmune encephalomyelitis in the Biozzi...

Area of Science:

• Neuroimmunology
• Innate Immunity

Background:

• Chronic relapsing experimental autoimmune encephalomyelitis (crEAE) is a mouse model for multiple sclerosis (MS).
• While adaptive immunity is implicated in MS and crEAE, the role of innate immunity and complement is emerging.
• The activation and significance of complement in crEAE remain to be fully elucidated.

Purpose of the Study:

• To investigate complement activation in the central nervous system (CNS) during crEAE.
• To determine the importance of complement in the pathogenesis of crEAE.

Main Methods:

• Induction of crEAE in Biozzi ABH mice.
• Assessment of complement activation products and complement gene/protein expression in the spinal cord at various disease stages.
• Analysis included complement components (C1q, C3, C9) and regulators (CD55, Crry, CD59a).

Main Results:

• Complement activation products were abundant in the CNS during acute relapse and progressive phases of crEAE, but not in early remission.
• Local expression of C1q and C3 increased across all disease stages.
• C9 expression was elevated in acute disease, while expression of complement regulators CD55, Crry, and CD59a was reduced throughout the disease course.

Conclusions:

• Complement is activated within the CNS during crEAE.
• The findings support the exploration of anti-complement agents as a potential therapeutic strategy for multiple sclerosis.