Help..Anyone know what this means?

In childhood ITP, the key pathologic event may be failure to suppress these previously sequestered autoantibodies.14 Specifically, it has been proposed that the T lymphocyte pathways characterized by the CD25+ T regulatory cells may not be fully mature in children 2–5 years of age, thus permitting autoimmune antibody production and antigen presentation by B lymphocytes that had escaped thymic deletion due to their crossreactivity with viral antigens. The T cell profile and cytokines in these patients, at presentation, are most consistent with a protracted T cell helper 1 (TH1) response with elevated interleukin (IL)-1α or IL-1β and decreased IL-4 as has been described in juvenile rheumatoid arthritis (JRA) and early onset diabetes.6,7,9 In general, it is a polyclonal response with many children producing both IgG and IgM autoantibodies to a variety of platelet epitopes including the more common glycoproteins α2 β3 and GPIb complex. Certain Fc gamma receptor IIa and IIIa polymorphisms have an increased association with childhood ITP. This observation may point toward individual differences in the clearance of autoantibody-bound platelets in the onset and duration of ITP. Early studies suggest that these Fc gamma receptor polymorphisms may play a role in predicting response to therapy as well.

Just came off nights so brain not functioning. I hope someone can help you out. That said I can look in my books and see if I can find an answer for you when I wake up from sleep.

Is there more to the article?

Does the article by chance mention Rituxan/ Rituximab? or a variation of that treatment?


Basically it talking about proteins that trigger or send messages that create an immune responses. The book I had that would of helped me with this is gone meaning I must of sold it.


If you have more of the article I'd would love to read it.

asheducationbook.hematologylibrary.org/content/2006/1/97.full

Yes, I was researching my dear friend Rituxan...I was worried since their cells aren't mature it might cause long term effects?

The article is titled :
Immune Thrombocytopenic Purpura of Childhood
Diane J. Nugent Hematology 2006 P.97

The paragraph you cite cannot be taken out of the context of the previous paragraph:

Given the diversity of immunoglobulin specificity, every child and adult has the potential to form autoantibodies to platelets. For unclear reasons, these self-reactive antiplatelet clones are not deleted during fetal development and persist in the antibody repertoire of the mature individual.13 In vivo, some antiplatelet antibodies are “naturally occurring” antibodies that are kept under tight control by a form of natural immune suppression called peripheral tolerance.

Neither paragraph appears to be discussing Rituxan or any treatment in particular. They appear to suggest an explanation (or at least a theory) of the mechanism by which ITP occurs in children. The final sentences are stating that there are individual differences in children that might determine which interventions might be most effective for a given child. The author seems to suggest that future work with "Fc gamma receptor polymorphisms" might prove beneficial in choosing the best treatment for a specific child. The english and greek alphabet soup is over my head.

Farther down, the section headed, "Treatment Options in Childhood ITP" may be more useful. It is certainly more readable!
I think you will find that Rituxan is discussed only in terms of CHRONIC ITP.

I hope this helps you, Crystal Lee.