pathogenesis autoimmunity

Why does autoimmunity occur? In RHD,the antigenic epitope [against which anti streptococcus antibody and anti heart antibody are created after streptococcal pharyngitis } is always there in heart valve and is always exposed to APCs and lymphocytes. Then why suddenly antibody [ against heart] is produced only when this antigenic epitope is presented by streptcocci?

Immediately after antigenic stimuli, there is production of plasma cells that produce IgM [primary immune response] and 7-10day later , the mRNA [of these plasma cells } producing the IgM, undergoes splicing and the spliced mRNA now produces IgG [instead of IgM}[secondary immune response] . However the variable region [i.e. antigen binding site , Fv ] of these IgG remains same as that of the original IgM.

Now the plasma cells produced during primary immune response are monoclonal or almost monoclonal -- i.e. the antibodies [Ig M } produced by them have a unique paratope. I mean that these Ig M antibodies can bind to one specific antigen only -- and NOT to the other SIMILAR antigens. In eg of RHD , the plasma cells [ that are produced during primary immune response due to stimulation by say M-5 protein of streptococcus cell wall} can produce antibodies [obviously Ig M and NOT Ig G } that have the capability to bind to ONLY streptococcal M-5 protein ........ and neither to even streptococcal M-6 protein , nor to cardiac myosin Protein.

Now as time of about 7-10 days goes, two things happen-
[i] The plasma cells produce Ig G, instead of IgM [mechanism discussed already]

[ii] In these 7-10 days , the plasma cells undergo numerous cell divisions and with every cell division, there is the chance of a mutation in the DNA coding for that specific immunoglobulin. As a result of these mutations, m RNA also alters a bit, and the resultant Ig G molecule has a variable region [antigen binding site ..i.e. Fv } that is slightly different from the variable region of the original IgM. This process results in a polyclonal production of Ig G [ as opposed to the monoclonal nature of the initial Ig M molecules } that serve dual result—

[i] it protects body from the other antigenic mutant types of the attacking pathogen [like from streptococci bearing M-6 , M-8 etc and not only from those bearing M- 5]
[ii] it makes a chance that the antibody molecule may acquire a paratope against an epitope of a closely resembling host tissue . [e.g. cardiac myosin and streptococcal M protein]