Publications by authors named "Cecile M Fremond"
Article Synopsis
- MyD88 is crucial for managing acute Mycobacterium tuberculosis (MTB) infection, with IL-1R signaling showing a significant role in early immune response.
- Disruption of IL-1R1 leads to severe MTB infection outcomes, while IL-18R and TIRAP deficiencies do not have the same impact, indicating they are not essential for acute response.
- The findings suggest IL-1 signaling is central to MyD88-mediated resistance against MTB, highlighting its importance in the body's initial defense mechanisms.
Toll-like receptors (TLRs) such as TLR2 and TLR4 have been implicated in host response to mycobacterial infection. Here, mice deficient in the TLR adaptor molecule myeloid differentiation factor 88 (MyD88) were infected with Mycobacterium tuberculosis (MTB). While primary MyD88(-/-) macrophages and DCs are defective in TNF, IL-12, and NO production in response to mycobacterial stimulation, the upregulation of costimulatory molecules CD40 and CD86 is unaffected.
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- Live mycobacteria, specifically Mycobacterium bovis (BCG), engage pattern recognition receptors like TLR4 and TLR2, impacting immune responses in vitro and in vivo.
- In experiments with TLR4 mutant mice, macrophages showed reduced TNF levels during BCG infection, but both mutant and control mice managed to control the infection over time, despite the mutants facing increased inflammation and other complications.
- Findings suggest that while TLR4 signaling isn't crucial for the initial fight against BCG, it plays an important role in managing inflammation during the chronic phase of the infection.