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Objective  To confirm  CXCL 10 over production in bone marrow mesenchymal stem cells ( MSC s) and circulating monocytes isolated from multiple sclerosis patients ( MS ) and identify predate cell molecular signature; to extend this analysis after autologous hematopoietic stem cell transplantation ( AHSCT ) to test if therapy has modifying effects on  MSC s and circulating monocytes.    Methods   MSC s and monocytes were isolated from 19 MS patients who undergone  AHSCT  before and seven of them at least 3 years after transplant.  CXCL 10 production was detected after  LPS / IFN ‐ γ  stimulation.  TLR 4 signaling pathways were investigated by means of transcription factors phosphorylation/activation level.  RT ‐ PCR  of activated transcription factors was performed to quantify their expression. All experiments were conducted in parallel with 24 matched healthy donors ( HD ).    Results  CXCL10 expression was significantly increased in both peripheral circulating monocytes and BM MSCs compared to HD. We showed that CXCL10 production is determined by an altered signaling pathway downstream TLR4, with the involvement of STAT‐1, NF‐ κ B, p38, JNK, and CREB. All upregulated transcription factors are more phosphorylated in MS patient sample. These features are not modified after AHSCT.    Interpretation  We demonstrated that in  MS  two different cell lineages are characterized by significantly increased production of  CXCL 10, due to altered signaling pathways of innate immune reaction mediated by  TLR 4, probably associated with disease phenotype. This characteristic is not modified by  AHSCT , suggesting that when T and B lymphocytes are reset, other possible components of  MS  pathology, such as  CXCL 10 over production, do not determine therapy outcome.

Increased CXCL10 expression in MS MSCs and monocytes is unaffected by AHSCT