Inflammation, though naturally intended as a part of the immune response, is the misery part of having an autoimmune disorder. As well, the inflammation response can have a life of its own. Identification is the first order of an immune response, but targeting and orchestrating the inflammation activity itself is not only the source of the autoimmune disorder personal suffering, but can take on a life of its own. If the modulation of message passing is misdirected, primary targeting doesn't necessarily need to be the source of error. Inflammation can also vary with target identity beyond the point of B cell and T cell activity. Yet the article here treats inflammation response as a tangential activity. Normally the immune system is viewed as a response in the direction of antigen to killing and repair localization, but research also needs to turn to independent tissue attraction as a part of how the inflammation becomes locally active. How does floating increase and decrease of inflammation activity, as well as self-targeting occur? As a non-specific autoimmune sufferer and novice student, these are some conclusions and questions I have drawn.
Recent Comments