What adapter protein do TLR receptors activate in response to tuberculosis?

Toll-like receptors (TLRs) play a crucial role in the innate immune system by recognizing pathogen-associated molecular patterns, such as those found in Mycobacterium tuberculosis. Upon activation by these patterns, TLRs serve as a trigger for downstream signaling pathways that lead to an immune response.

In the case of tuberculosis, TLR receptors, specifically TLR2 and TLR4, primarily utilize the MyD88 adapter protein to propagate the signal. MyD88 is essential for the activation of several pro-inflammatory cytokine production, which ultimately helps in orchestrating the immune response against the infection. The MyD88-mediated pathway leads to the recruitment of various kinases and transcription factors that promote the expression of genes involved in inflammation and immune defense.

While other adapter proteins, such as TRIF and TRAM, are important for mediating signals from certain TLRs (such as TLR3 and TLR4 in specific contexts), they are not the primary adapters involved in the response to tuberculosis. Therefore, MyD88 is the most relevant and significant adapter protein in this scenario, emphasizing its critical role in initiating an effective immune response against Mycobacterium tuberculosis.