The most crucial part of the immune system is made up of Foxp3 + regulatory T cells( Tregs ). No other cell population, taken individually, plays such a crucial part in the immune system’s proper operation. Trepts are known to prevent an unsuitable immune response against commensal microbiota, nonself pathogens, and self-antigens. & nbsp, I firmly believe that the data make it very clear.
I therefore want to understand the specifics of a well-designed research paper as soon as I see something that is contrary. Consider this recent article from The Journal of Clinical Investigation ( JCI ). It asserts and provides data that is fairly reliable that the removal of T follicular regulatory cells ( Tfr ) from the immune system in Foxp3-cre Bcl6-fl mice paradoxically decreases, rather than increases, peanut-specific IgE responses. & nbsp,
And if you believe that their knockout mice are oddballs of some sort, you are mistaken. Additionally, their model demonstrates that total IgE is rising as anticipated. Therefore, the system that the authors are employing complies with accepted standards. In addition, & nbsp,
The authors continued by demonstrating the significance of IL-10, which is derived from Tfr cells, in fostering the production of IgE that causes peanut allergies. & nbsp,
These findings are completely at odds with the entire theory regarding the function of Tfr cells and even IL-10 because the authors hypothesize that we should block il-10 in order to lessen peanut allergies rather than inject it, as everyone currently believes( IL-10 ) is a less well-known cytokine but is generally recognized as an immunosuppressant.
How should we then interpret these findings? In essence, what is happening? Is it possible to interpret these findings within the parameters of the accepted theory?
There is at least one possibility, in my opinion, that the authors did not take into account during their discussions. In this case, the authors are looking for primary adaptive T / B cell response to a novel antigen, in this instance, peanut. In this case, it is obvious that Tfr cells are not necessary to reduce the IgE response that peanut allergy promotes. However, the level of total IgE( representing unidentified antigen-specific IGE responses ) has risen at the same time. Instead of coming from the primary immune response, as peanut IgE does, we could say that total ige is derived from a well-established memory T / B system. When the brakes used by Tfrs are removed, these memory T / B / plasma cells then increase total IgE levels. However, the primary T / B response to peanut allergen does not follow the same rule. Why is that the case? It’s possible that the primary T / B cooperation is hampered specifically by the absence of Tfr. Due to the activation of other immune system components when brakes are removed, it is not a direct effect but rather an indirect one. Therefore, a lack of Tfr cells will undermine primary T / B responses, and it would seem that if they were promoting primary IgE responses and were absent, their production would be reduced. & nbsp,
Particularly when applied to human clinical data, the proper interpretation is crucial. By the time the allergic individuals are examined by a doctor, peanut allergy IgE has already become ingrained in humans’ memory systems. In that case, the authors’ proposed Tfr or IL – 10 system manipulation could be harmful rather than advantageous. In addition to & nbsp,
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