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Gimaev, I.

Publications and source records attributed to Gimaev, I..

2 recordsLinked to original sources

CD19 CAR T cell therapy reshapes the host microbiota immune axis in autoimmune diseases

CD19 targeted CAR T cell therapy induces profound B cell depletion and clinical responses in autoimmune disease; however, whether it reshapes host microbiota interactions remains unknown. We longitudinally profiled gut microbiome composition and microbiota-specific humoral immunity in 20 patients with systemic lupus erythematosus, systemic sclerosis, or idiopathic inflammatory myopathy undergoing CAR T cell therapy, alongside 23 healthy controls, using shotgun metagenomics, IgA/IgG-bound microbiota profiling, and PhIP Seq. CAR T cell therapy reshaped microbiota directed humoral immunity, with reduced fecal IgA and serum anti commensal IgA and IgG accompanied by selective remodeling of microbiota-reactive antibody repertoires. This finding was paralleled by selective changes in gut microbial composition, including depletion of Bifidobacterium adolescentis, without uniform depletion of disease-associated pathobionts. Integrated host microbiome analyses identified altered predicted protein protein interactions involving the immunoproteasome and B cell plasma cell pathways, with interactions before CAR T cell intervention being significantly associated with subsequent relapse. Consistent with these findings, taxon specific IgA targeting, but not global diversity of IgA IgG coated microbiota, differed according to subsequent relapse. Lower baseline fecal IgA was also associated with delayed B-cell reconstitution, linking mucosal humoral immunity to immune recovery after CAR T cell therapy.

immunology↗

Mucosal innate immune activation as the trigger to Prevotella species-induced arthritis in genetically resistant mice

An altered gut microbiota, particularly the expansion of Prevotellaceae members, is increasingly implicated in the pathogenesis of rheumatoid arthritis (RA), yet the mechanisms hind this phenomenon remain unclear. Here, we demonstrate that Palleniella intestinalis, a member of the Prevotellaceae family, induces a 100% arthritis incidence in genetically resistant C57BL/6 mice. Inoculation with P. intestinalis modifies gut microbiota ecology, increases intestinal permeability, and selectively activates colonic CD11bCD11c myeloid cells, facilitating Th17 differentiation and driving joint inflammation. In vitro, outer membrane vesicles (OMV) from P. intestinalis and Segatella copri (formerly known as Prevotella copri) prime bone marrow-derived dendritic cells (BMDCs) to drive Th17 differentiation in an IL-6-dependent manner. Similar changes with increase in innate immune cell activation and IL-6 levels were shown in gut biopsies from new-onset RA patients. The transfer of Prevotellaceae-derived OMVs or Prevotellaeae-primed BMDCs replicates the hightened arthritis incidence in resistant mice, highlighting the critical role of intestinal immune activation in RA. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=130 SRC="FIGDIR/small/643707v1_ufig1.gif" ALT="Figure 1"> View larger version (36K): org.highwire.dtl.DTLVardef@1ce227corg.highwire.dtl.DTLVardef@3a2d0eorg.highwire.dtl.DTLVardef@16404b6org.highwire.dtl.DTLVardef@1717dc1_HPS_FORMAT_FIGEXP M_FIG C_FIG O_LIColonization with Paleniella intestinalis bypasses genetic resistance, consistently inducing arthritis incidence in non-susceptible C57BL/6 mice C_LIO_LIP. intestinalis activates colonic CD11b+CD11c+ myeloid cells, driving systemic Th17 cell differentiation C_LIO_LIIn vitro, outer membrane vesicles from P. intestinalis or RA-derived S. copri RPC01 primed DCs that drive Th17 differentiation in an IL-6-dependent manner C_LIO_LITransfer of P. intestinalis-primed DCs or its outer membrane vesicles alone increases arthritis incidence in non-susceptible C57BL/6 mice C_LI

immunology↗