Murine Models of Systemic Lupus Erythematosus

Abstract

Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disorder. The study of diverse mouse models of lupus has provided clues to the etiology of SLE. Spontaneous mouse models of lupus have led to identification of numerous susceptibility loci from which several candidate genes have emerged. Meanwhile, induced models of lupus have provided insight into the role of environmental factors in lupus pathogenesis as well as provided a better understanding of cellular mechanisms involved in the onset and progression of disease. The SLE-like phenotypes present in these models have also served to screen numerous potential SLE therapies. Due to the complex nature of SLE, it is necessary to understand the effect specific targeted therapies have on immune homeostasis. Furthermore, knowledge gained from mouse models will provide novel therapy targets for the treatment of SLE.

Carbon monoxide inhibits T cell activation in target organs during systemic lupus erythematosus

“…This apparent discrepancy might be due to genetic background differences between the lupus mice models used in each study conferring distinctive characteristics to each model [39]. Although CO could modulate CD11b 1 cell expansion in spleen from lupus FcgRIIb KO mice, CO treatment in MRL-Fas lpr lupus mice does not modulate this cell type population.…”

The Use of Filariae as a Therapeutic Agent for Hypersensitivity Diseases

“…Spontaneous lupus arises in BSXB/Yaa and MRL/lpr mouse strains, as well as from F1 hybrids between New Zealand White (NZW) and New Zealand Black (NZB) strains. These strains have predominantly been used to shed light on the genetic factors contributing to the development of SLE (172).…”

Interferons as Biomarkers and Effectors: Lessons Learned from Animal Models

“…The exact etiology of SLE is unknown, and mouse models with the development of lupus-like phenotypes have been crucial to uncovering cellular and genetic mechanisms of disease. Spontaneous (NZB/W F1, MRL/lps, BXSB/ Yaa) and induced (pristine and chronic graft-versus-host disease) mouse models of lupus have led to the identification of numerous susceptibility loci and provided identification of potential biomarkers for disease and prognosis [134]. Indeed, extensive animal and human studies have revealed a crucial role for type I IFN in the initiation and perpetuation of disease, and components of the IFN system, including transcription factors, are now putative drug targets and biomarkers in the treatment of SLE.…”