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- W4285992465 abstract "Systemic lupus erythematosus (SLE) is a female-biased multisystem inflammatory disease with substantial morbidity and mortality and limited treatment options. Our lab previously found that VGLL3, a putative transcription co-factor with increased activity in female cells, can drive lupus-like systemic inflammation when overexpressed in mouse epidermis under the K5 promoter. IL-7 signaling was found to be elevated in the skin of lupus patients and K5-Vgll3+ mice alike. Our current results demonstrate that deleting peripheral Il7r in these mice prevents the development of disease phenotype, with amelioration of dermatitis, splenomegaly, lymphadenopathy, and kidney damage. Cell and molecular analyses indicate down-regulation of inflammatory signaling and dampened lymphocyte activation that accompany the ameliorated phenotype in the absence of Il7r. On the other hand, deleting Tlr7, an X-linked pro-inflammatory gene that has been hypothesized to promote lupus in women, not only fails to rescue the autoimmune phenotype in K5-Vgll3+ mice, but further exacerbates the severity of their disease. Therefore, VGLL3-driven systemic autoimmunity is dependent on IL-7 signaling and independent of TLR7. Further research is underway to determine whether neutralizing anti-IL-7 antibodies can halt or slow down the progression of end-organ damage in K5-Vgll3+ mice to better assess the therapeutic potential of targeting IL-7 signaling for treatment of SLE." @default.
- W4285992465 created "2022-07-21" @default.
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- W4285992465 date "2022-08-01" @default.
- W4285992465 modified "2023-09-28" @default.
- W4285992465 title "035 Blocking IL-7, but not TLR7, signaling prevents the development of lupus-like autoimmunity in mice" @default.
- W4285992465 doi "https://doi.org/10.1016/j.jid.2022.05.089" @default.
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