TLR7 Activation Accelerates Cardiovascular Pathology in a Mouse Model of Lupus

Ahmed S. Elshikha, Xiang Yu Teng, Nathalie Kanda, Wei Li, Seung Chul Choi, Georges Abboud, Morgan Terrell, Kristianna Fredenburg, Laurence Morel

Producción científica: Articlerevisión exhaustiva

6 Citas (Scopus)

Resumen

We report a novel model of lupus-associated cardiovascular pathology accelerated by the TLR7 agonist R848 in lupus-prone B6.Sle1.Sle2.Sle3 (TC) mice. R848-treated TC mice but not non-autoimmune C57BL/6 (B6) controls developed microvascular inflammation and myocytolysis with intracellular vacuolization. This histopathology was similar to antibody-mediated rejection after heart transplant, although it did not involve complement. The TC or B6 recipients of serum or splenocytes from R848-treated TC mice developed a reactive cardiomyocyte hypertrophy, which also presents spontaneously in old TC mice as well as in TC.Rag-/- mice that lack B and T cells. Each of these cardiovascular lesions correspond to abnormalities that have been reported in lupus patients. Lymphoid and non-lymphoid immune cells as well as soluble factors contribute to lupus-associated cardiovascular lesions in TC mice, which can now be dissected using this model with and without R848 treatment.

Idioma originalEnglish (US)
Número de artículo914468
PublicaciónFrontiers in immunology
Volumen13
DOI
EstadoPublished - jul 4 2022
Publicado de forma externa

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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