PATHOGENESIS OF AUTOIMMUNE DISORDER
MYSTERY IN PATHOGENESIS OF AUTOIMMUNE DISORDER
why does rheumatic carditis[RHD ] occur?
According to SelfNon Self model - Reason is Cross reaction with streptococcal M protein to which fetus is not exposed
Question - The entire antigenic epitope is always there in[heart ] valve .... so why suddenly antibody is created only when this antigen is presented by streptcocci? In other words since the antigenic epitopes of Strepto M and cardiac myosin are same [almost ] , so the antigenic epitope of strepto M-protein had been exposed to the humanFetus in his foetal life in form of cardiac myosin. I refer this argument henceforth as argument 1 .
Why is it occurring only in 3-16 yr age? Why only 3% patients of Strepto infection have RHD ..? This shows that there is not only a mechanical stereotype antigen antibody reaction in this but something apart
Danger pathway of matzinger xplain : “For autoimmunity, the Danger model offers
a unique suggestion that would not arise
from the SNS or the INS models. Starting
with the view that “bad” death or cell stress
can elicit an immune response, the model
suggests that some autoimmune diseases may
be caused by mutations in genes governing
the normal physiological death and clearance
processes, or by environmental pathogens or
toxins that cause cellular stress or death. In
these cases, the immune system is not at fault;
it is doing its job of responding to alarm
signals (but, in these cases, to the detriment
of the host).’’
Danger Model [of matzinger ] explains Streptococci is danger to body. So in Strepto infection , if body thinks that there is enough danger , then anti Strepto M-protein [and anti cardiac ] Ab is created. Now it follows that in people of 3-16 yr age and only 3 % of such people .. the body thinks that Strepto infection is a sufficient danger
Why so? What is the danger pathway that is fulfilled only in these handful people ?
Now if anyway i accept that danger impulse is coming because Strepto is causing cell lysis .. then question appears : When recombinant or extracted M protein of streptococcus is injected into lewis rat, then too there is RHD. Why so ? there is no cell destructn here because no live Streptococci hav been introduced into the rat
If i accept that danger impulse is coming just because the epitope is of an external organism [keeping in mind argument 1 ] then following query come
[I] When O positive [Rh positive ] blood from a donour is injected into an O positive recipient ..then there is no anti Rh antibody in the recipient. Why so ? Here also the Rh antigen is from an external organism viz donour
[II] we accept that antibody of blood group [like anti B and anti A ] do appear in blood of an infant for first time due to reaction with some alimentary tract bacterial antigens. It follows that our alimentary canal has bacteria that express both A and B antigens. Now let us take a A blood group subject. In his alimentary tract there is bacteria that express A antigens that are "cross reacting " with hiss group A RBCs. The situation is equal to Streptococci expressing protein "cross reacting " with cardiac valve. But we dont hear autoimmune disease of this type . Why so ?
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