bioRxiv Science⌕ Search

Biology subjects

Pereira, M. S.

Publications and source records attributed to Pereira, M. S..

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↗

CDK4/6 inhibition sensitizes breast cancer to NK cell therapy by inducing immune-interactive surface proteins

CDK4/6 inhibitors are standard-of-care for metastatic estrogen receptor-positive (ER+) breast cancer, yet the development of resistance remains a significant clinical hurdle. While CDK4/6 inhibitors are primarily recognized for their ability to induce cytostasis, their role in modulating innate immune responses remains poorly defined. Here, we demonstrated that CDK4/6i treatment remodels the tumor cell surface to favor recognition and elimination by Natural Killer (NK) cells. Using a diverse biobank of patient-derived organoids (PDOs), we found that CDK4/6 inhibition robustly upregulated the adhesion molecule ICAM-1 and the NKG2D stress ligands (ULBP2/5/6 and MICA/B). This NK-engaging cell surface phenotype was driven by a bifurcated signaling network: NF-{kappa}B signaling orchestrated ICAM-1 induction, while the PI3K/mTOR pathway regulated the expression of stress ligands. Functional assays confirmed that these ligands were indispensable for NK cell-mediated elimination of breast cancer cells. In vivo studies using ER+ PDX models revealed that a brief seven-day primer treatment with the CDK4/6 inhibitor abemaciclib was sufficient to sensitize tumors to NK cell therapy, significantly inhibiting tumor growth and prolonging survival. We also observed efficacy with a concurrent dosing strategy that delayed the onset of acquired resistance. These findings provide a mechanistic rationale for combining CDK4/6 inhibitors with NK cell therapy. This "prime and kill" approach offers a promising strategy to overcome therapeutic resistance and improve outcomes for patients with metastatic ER+ breast cancer.

cancer biology↗