TSC1 deletion in the myeloid lineage constitutively activated mechanistic target of rapamycin complex 1 (mTORC1), increased M1 polarisation in synovial macrophages and exacerbated experimental OA in both CIOA and DMM models, while Rheb deletion inhibited mTORC1, enhanced M2 polarisation and alleviated CIOA in mice.
This study aims to investigate the effect of enriched plasma cells on the production of inflammatory cytokines and development of osteoarthritis (OA) in mice with B-cell-specific conditional deletion of the tuberous sclerosis 1 gene (TSC1).
Then mice with chondrocyte-specific mTORC1 activation (Tsc1 CKO and Tsc1 CKO<sup>ER</sup> ) or inhibition (Raptor CKO<sup>ER</sup> ) and their littermate controls were subjected to OA induced by destabilization of the medial meniscus (DMM) or not.