The American Autoimmune Related Diseases Association estimates that approximately 50 million Americans have an autoimmune disease. The impact factor of these diseases on our country creates an additional and personal motivation for understanding the mechanisms that underlie autoimmune disease in general. Seeking a deeper understanding of autoimmunity can also contrast with and reinforce the ideas we have about the normal immune response. The AM 14 model of Systemic Lupus Erythematosus continues to reveal mechanisms underlying systemic autoimmunity. It has been validated as a model using genuine autoantigens and the prevalence of disease only in the presence of that autoantigen. It has been further manipulated in our system by injecting the autoantigen to circumvent the variability that exists with stochastic spontaneous autoimmunity. To study autoimmune memory in this defined system, AM14 transgenic Rheumatoid Factor B cells will be transferred to a non-transgenic, non-autoimmune prone background. We will follow this defined population of cells to determine mechanisms of memory development and whether Toll-like receptors are involved in memory-mediated disease propagation. ? ? ?
| Sweet, Rebecca A; Nickerson, Kevin M; Cullen, Jaime L et al. (2017) B Cell-Extrinsic Myd88 and Fcer1g Negatively Regulate Autoreactive and Normal B Cell Immune Responses. J Immunol 199:885-893 |
| Sweet, Rebecca A; Cullen, Jaime L; Shlomchik, Mark J (2013) Rheumatoid factor B cell memory leads to rapid, switched antibody-forming cell responses. J Immunol 190:1974-81 |
| Sweet, Rebecca A; Ols, Michelle L; Cullen, Jaime L et al. (2011) Facultative role for T cells in extrafollicular Toll-like receptor-dependent autoreactive B-cell responses in vivo. Proc Natl Acad Sci U S A 108:7932-7 |
