Evaluating the effect of TLR7-deficiency on B cell responses in autoimmunity

Abstract

The immune system is a well-honed machinery that is able to walk the fine line of balance between pathology and protection. Its ability to differentiate the various pathogen associated microbes from itself is largely thanks to its specificity. However, in certain cases where this machinery breakdown and the mechanism gets entangled and confused itself as a pathogen, it leads to autoimmune disease such as SLE. Thus, in this dissertation, we investigate the contribution of TLRs and TLR7 especially in lupus prone mice model. We do so by comparing two lupus like mice strain that are similar with one another with just one difference in which one has its TLR7 ablated through knockout. We carried out an aged cohort study between the two mice strains and also carried out B cell culture in both and subjected them with various treatments of synthetic ligands that conforms to the various TLRs signals in vitro. We observed that the TLR7 deficient mice experienced a better outcome with respect to the SLE disease progression and showed a lower activation levels of B cells growth.