035 Blocking IL-7, but not TLR7, signaling prevents the development of lupus-like autoimmunity in mice
نویسندگان
چکیده
Systemic lupus erythematosus (SLE) is a female-biased multisystem inflammatory disease with substantial morbidity and mortality limited treatment options. Our lab previously found that VGLL3, putative transcription co-factor increased activity in female cells, can drive lupus-like systemic inflammation when overexpressed mouse epidermis under the K5 promoter. IL-7 signaling was to be elevated skin of patients K5-Vgll3+ mice alike. current results demonstrate deleting peripheral Il7r these prevents development phenotype, amelioration dermatitis, splenomegaly, lymphadenopathy, kidney damage. Cell molecular analyses indicate down-regulation dampened lymphocyte activation accompany ameliorated phenotype absence Il7r. On other hand, Tlr7, an X-linked pro-inflammatory gene has been hypothesized promote women, not only fails rescue autoimmune mice, but further exacerbates severity their disease. Therefore, VGLL3-driven autoimmunity dependent on independent TLR7. Further research underway determine whether neutralizing anti-IL-7 antibodies halt or slow down progression end-organ damage better assess therapeutic potential targeting for SLE.
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ژورنال
عنوان ژورنال: Journal of Investigative Dermatology
سال: 2022
ISSN: ['1523-1747', '0022-202X']
DOI: https://doi.org/10.1016/j.jid.2022.05.089