G09SecL04Tpc2: Difference between revisions
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====Inactivation of effector mechanisms==== | ====Inactivation of effector mechanisms==== | ||
Besides extensive down-regulation upon infection of the host, ''b.burgdorferi'' can make it even harder for the body to carry out a successful immune response. The borrelia can express complement-binding surface proteins, which prevents complement-mediated killing once inside the host regulated by the host’s immune system<ref name=art4>PMID:18097481</ref>. Although prior vaccination before infection is ideal, it is also important to develop and continue antibiotic research that can be administered after infection. In addition to eluding the immune system through these newly expressed surface proteins, borrelia also possesses the potential to activate anti-inflammatory cytokines such as Interleukin 10 (IL-10)<ref name=art4>PMID:18097481</ref>. Ultimately, this suggests that borrelia can decrease inflammation by inducing IL-10 and preventing the host immune system from marking regions of antigenic activity. This can also delay or possibly halt the attack of leukocytes. Lastly, recent studies have shown that ''b.burgdorferi'' releases antigens that are soluble. Aside from the irony, these antigens mingle with the antibodies that are specific for b.burgdorferi and prevent the antibodies from carrying out their role in defense. Not only does borrelia demonstrate abilities of suppressing the immune response, but also dramatically weakens the reliable effector mechanisms of the host immune system. | Besides extensive down-regulation upon infection of the host, ''b.burgdorferi'' can make it even harder for the body to carry out a successful immune response. The borrelia can express complement-binding surface proteins, which prevents complement-mediated killing once inside the host regulated by the host’s immune system<ref name=art4>PMID:18097481</ref>. Although prior vaccination before infection is ideal, it is also important to develop and continue antibiotic research that can be administered after infection. In addition to eluding the immune system through these newly expressed surface proteins, borrelia also possesses the potential to activate anti-inflammatory cytokines such as Interleukin 10 (IL-10)<ref name=art4>PMID:18097481</ref>. Ultimately, this suggests that borrelia can decrease inflammation by inducing IL-10 and preventing the host immune system from marking regions of antigenic activity. This can also delay or possibly halt the attack of leukocytes. Lastly, recent studies have shown that ''b.burgdorferi'' releases antigens that are soluble. Aside from the irony, these antigens mingle with the antibodies that are specific for b.burgdorferi and prevent the antibodies from carrying out their role in defense. Not only does borrelia demonstrate abilities of suppressing the immune response, but also dramatically weakens the reliable effector mechanisms of the host immune system. | ||
====Hiding in | ====Hiding in less accessible compartments such as the Extracellular Matrix==== | ||
===Crossing the Blood-Brain Barrier to the CNS=== | ===Crossing the Blood-Brain Barrier to the CNS=== | ||
