Auto-immunity and infection

AUTO-IMMUNITY AND INFECTION – CURRENT CONCEPTS

An auto-immune disease is defined as an inflammatory response due auto-antigens. There is information about some infectious antigens can elicit auto-immune response. This is probably a regulatory fail, like negative selection in immune maturation. Hence, BC and TC have an elevated affinity for auto-antigens.

There are many mechanisms described which explain some auto-immune diseases:

• Molecular mimicry: In this case, the infection allows the immune system to perform a response but some antigens are very similar to auto-antigens, so, the immune system reacts against body proteins. (i.e. rheumatic fever, Guillain Barre Syndrome, E.lyme arthritis)
• Super antigenic response: There are proteins usually belong to gram + bacteria and virus that can link the MHC-II in his native way on the outside and can link non specifically TCR on his β chain in the variable region, with this union the BC and TC proliferate clonally. Hence, those superantigen proteins can stimulate auto reactive cells to proliferate and be deleterious. (i.e. B enteric toxin can stimulate TC proliferation against MBP (myelin basic protein) and elicits an experimental allergic encephalomyelitis).
• Spectator Effect: Some immune cells don’t react against antigens but can proliferate because the cytokines release, in some cases the cells could be auto-reactive.
• APC activation: Could happen that antigen presenting cells don’t recognize some kind of antigens on his immature phase, so, when they mature can recognize them and present them to TC that are very reactive against them because they don’t knew them.
• Antigen release and transformation: Some apoptotic cells can express antigens on their membrane like ribonucleoprotein in erythematous lupus, this antigen elicit anti-DNA antibody production. Therefore, some proteins like anti-bodies, signaling proteins and others, are changed by biochemical mechanisms like acylation, citrulination, glycolization, and others. There is evidence that very proteins are changed in auto-immune diseases, like arthritis, multiple sclerosis, SEL.
• Epitope Spread: When the TC reacts against some epitope of certain antigen, it could happen that this epitope change, so, the cell chooses another peptide region to link. In this way, TC could have more chances for develop a molecular mimicry response.
• Immune complexes Deposit: The immunity complexes can be deposited in vessels, joints, kidneys and lungs. This complex can develop an inflammatory response on the deposit site. (i.e. group a streptococcus acute glomerulonephritis has been very studied)
  

Referencies:

¿La infección: inductor o reguladora de autoinmunidad? – Toro, Fabiola – 2004 – Anuario de enfermedades infecciosas – Universidad de Antioquia