The human immune system typically produces both T cells and B cells that are capable of being reactive with self-protein, but these self-reactive cells are usually either killed prior to becoming active within the immune system, placed into a state of anergy (silently removed from their role within the immune system due to over-activation), or removed from their role within the immune system by regulatory cells. When any one of these mechanisms fail, it is possible to have a reservoir of self-reactive cells that become functional within the immune system. The mechanisms of preventing self-reactive T cells from being created take place through negative selection process within the thymus as the T cell is developing into a mature immune cell. Some infections, such as Campylobacter jejuni, have antigens that are similar (but not identical) to our own self-molecules. In this case, a normal immune response to C. jejuni can result in the production of antibodies that also react to a lesser degree with gangliosides of myelin sheath surrounding peripheral nerves' axons (i.e., Guillain–Barré). A major understanding of the underlying pathophysiology of<unk> s has been the application of genome-wide association scans that have identified a degree of genetic sharing among the<unk> s.<unk> ty, on the other hand, is the presence of self-reactive immune response (e.g., auto-antibodies, self-reactive T cells), with or without damage or pathology resulting from it. For this reason, autoantibodies are a hallmark of most<unk>  disorders. This may be restricted to certain organs (e.g. in<unk>  thyroiditis) or involve a particular tissue in different places (e.g. Goodpasture's disease which may affect the basement membrane in both the lung and the kidney). There are many different theories as to how an<unk>  state arises. Some common ones are listed below.
Autoimmune disease
Adhesive capsulitis of the shoulder
Neurodegenerative disease
Degenerative disease
Viral disease
Neuromuscular disease
Autoinflammatory diseases
Immune disorder