One hypothesis that couples infection with autoimmune disease is molecular mimicry.

One mechanism by which self-destruction can be triggered is molecular mimicry.

Many pathogenic bacteria scavenge sialic acids from their host and use them for molecular mimicry.

This further raises the possibility of pathogenic mechanisms such as antigenic cross-reactivity and molecular mimicry.

MG is an immune-mediated disorder caused by molecular mimicry and autoantibodies against the neuromuscular junction.

In a process called molecular mimicry, many bacterial pathogens decorate their cell surface glycolipids with Neu5Ac.

Such cross-reactivities suggest that ' molecular mimicry' could exist between p18 of HIV and normal constituents of human cells.

Finally, animal models are available in which the onset, progression and control of molecular mimicry can be evaluated.

This suggests that those viruses, possibly by molecular mimicry, play a role in the induction of the disease.

These data demonstrate the importance of molecular mimicry between an infecting agent and hnRNP-A1 in autoimmune disease of the CNS.

These reconstructions reveal how steric hindrance and molecular mimicry are used to prevent both premature folding states and binding of later factors.

Pathways that are common to these disorders include microglial activation, pro-inflammatory cytokines, molecular mimicry, anti-neuronal autoantibodies, self-reactive T cells and disturbance of the blood-brain barrier.

Autoimmune reactions due to molecular mimicry of bacterial epitopes by host proteins cause acute rheumatic fever (ARF) and subsequent disease progression to RHD.

The immune response resulting in anti-U1-snRNP seems antigen driven and may result from molecular mimicry between U1-snRNP and certain viral proteins.

Molecular mimicry of host proteins by pathogens can lead to autoimmune disease.

Molecular mimicry of self-epitopes by viral antigens is one possible pathogenic mechanism underlying induction of autoimmunity.