Immuunsysteem
Geplaatst: Ma 25 Sep 2017, 21:22
Hét forum over de ziekte van Lyme (Lyme-Borreliose)
https://www.lymeforum.nl/forum/
Borrelia burgdorferi lipoproteins activate inflammatory cells through Toll-like receptor 2 (TLR2), suggesting that TLR2 could play a pivotal role in the host response to B. burgdorferi. TLR2 does play a critical role in host defense, as infected TLR2−/− mice harbored up to 100-fold more spirochetes in tissues than did TLR2+/+ littermates. Spirochetes persisted at extremely elevated levels in TLR2-deficient mice for at least 8 wk following infection. Infected TLR2−/− mice developed normal Borrelia-specific Ab responses, as measured by quantity of Borrelia-specific Ig isotypes, the kinetics of class switching to IgG, and the complexity of the Ags recognized. These findings indicate that the failure to control spirochete levels in tissues is not due to an impaired acquired immune response. While macrophages from TLR2−/− mice were not responsive to lipoproteins, they did respond to nonlipoprotein components of sonicated spirochetes. These TLR2-independent responses could play a role during the inflammatory response to B. burgdorferi, as infected TLR2−/− mice developed greater ankle swelling than wild-type littermates. Thus, while TLR2-dependent signaling pathways play a major role in the innate host defense to B. burgdorferi, both inflammatory responses and the development of the acquired humoral response can occur in the absence of TLR2.
Another interesting observation about this bacteria is how it interacts with our body’s immune system; Dr. David Dorward of Rocky Mountain Labs made a video tape of how Borrelia burgdorferi acts when surrounded by B-cells. (The type of white blood cell that makes antibody.) The spirochete attached tip first, entered the B lymphocyte, multiplied and ruptured the cell. It repeated this process for three days until the B-cells were able to come to an equilibrium. A matter of concern was that some of the spirochetes were able to strip away part of the B-cell’s membrane, and wear it like a cloak. (Dorward, Hulinska 1994 LDF Conference Vancouver BC) This means: If this spirochete is evolved enough to attack our B-lymphocytes, then it may also be evolved in other ways that we do not yet understand. It is for certain that
its ability to kill B-lymphocytes, evolved as part of a defense mechanism to evade its own destruction. The observation that it can use the B-cell’s own membrane as camouflage, indicates that it may be able to go undetected by our immune system.