Transient decomplementation of mice delays onset of experimental autoimmune encephalomyelitis and impairs MOG-specific T cell response and autoantibody production.

Multiple sclerosis (MS) is the most common inflammatory and demyelinating disease of the central nervous system. In both MS and its animal model experimental autoimmune encephalomyelitis (EAE), it is thought that infiltrating CD4(+) T cells initiate an inflammatory process and collect other immune effectors to mediate tissue damage. The pathophysiology of the disease however remains unclear.

On-chip complement activation adds an extra dimension to antigen microarrays.

Antibody profiling on antigen microarrays helps us in understanding the complexity of responses of the adaptive immune system. The technique, however, neglects another, evolutionarily more ancient apparatus, the complement system, which is capable of both recognizing and eliminating antigen and serves to provide innate defense for the organism while cooperating with antibodies on multiple levels. Complement components interact with both foreign substances and self molecules, including antibodies, and initiate a cascade of proteolytic cleavages that lead to the covalent attachment of complement components to molecules in nanometer proximity.