Activation of surface TLR will produce cascade of reaction which will translocate cytoplasmic NFkb into nucleus which will bind to DNA and induce mRNAs of cytokine. So if NFkb will be translocated into nucleus then any TLR should produce similar types of cytokines. Is this correct? if not then what determines the variations in cytokine productions?
There are many kinds of Toll-like receptors and these have different stimulators, so one question is whether the variation in cytokine production comes from the difference of the TLR (for example some TLRS induce more importantly the cascade). Also, inflammasomes are involved in the production of cytokines, and depends on the stimulators of the priming and activation steps, and the type of inflammasome producing those cytokines so I think this variation can be explained.
Hey Kamlesh,
not all TLRs induce the translocation of NF-kB into the nucleus. Some activate other transcription factors (exlusively alone or in addition with others such as NF-kB. Moreover, the inflammasome, as a central component for the secretion of IL-1ß and IL-18, needs additional signals and not only TLR-mediated signals and a lot of cyto- and chemokines are completly independent of the inflammasome.
This review really helped me to get a general overview of TLRs and their subsequent signaling cascades:
O'Neill, L., Golenbock, D. & Bowie, A.
The history of Toll-like receptors — redefining innate immunity.
Nat Rev Immunol 13, 453–460 (2013). https://doi.org/10.1038/nri3446
All the best,
Marc
I highly appreciate for adding answers. Thank you Marc Herb for suggestive reading. I really need to clarify the theoretical knowledge of TLR activation.
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