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What is the role of mPGES-1 in regulating the immune response to mycobacterium tuberculosis infection? 


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mPGES-1, a key enzyme in prostaglandin E2 (PGE2) synthesis, plays a crucial role in regulating the immune response to Mycobacterium tuberculosis (Mtb) infection. Studies have shown that mPGES-1-derived PGE2 promotes wound-induced angiogenesis by producing TGFβ and VEGF in accumulated regulatory T cells (Tregs) . Additionally, in human macrophages infected with Mtb, there is a significant increase in mPGES-1 expression and PGE2 production, which is associated with the activation of the NF-κB pathway . Furthermore, extracellular vesicles (EVs) released by Mtb-infected cells can modulate the immune response by regulating inflammatory cytokine release and antigen presentation, highlighting the intricate role of mPGES-1 and PGE2 in the immune response to Mtb infection .

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mPGES-1 plays a role in regulating immune responses to Mycobacterium tuberculosis infection by influencing IL-1 responses, as highlighted in the study on TB-induced immune-metabolic pathways.
mPGES-1, upregulated by M.tb infection, contributes to PGE2 production in human macrophages. Sulfasalazine inhibits this pathway, potentially modulating the immune response against M.tb.
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