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Passweg, J.

Publications and source records attributed to Passweg, J..

2 recordsLinked to original sources

Longitudinal profiling of tumor-reactive T cells during TIL therapy in metastatic melanoma

Adoptive cell therapy (ACT) with expanded autologous tumor-infiltrating lymphocytes (TILs) can induce durable responses in metastatic melanoma, yet many patients relapse. We profiled tumor-reactive T cell dynamics during TIL therapy using single-cell RNA and TCR sequencing from seven patients to elucidate underlying reasons. We found that tumor-reactive T cells preferentially expanded early during ex vivo TIL culture, transitioning from exhausted to reinvigorated effector states. Particularly, CD8+ exhausted T cells (Tex) and CD4+ follicular helper T cell (Tfh), but not CD4+ Tex, were efficiently reinvigorated. Further, we resolved the heterogeneity of tumor-reactive CD8+ and CD4+ subsets, defining unique signatures for their identification during TIL expansion. In addition, non-responders (NRs) exhibit increased levels of Type 17 T cells in TIL products, suggesting a potential association with resistance to therapy. After transfer, tumor-reactive clones rapidly extravasated and established a stem-like reservoir. However, in NRs, CD4+ regulatory T cells (Tregs) expanded de novo and tumor-reactive CD8+ T cells reacquired exhaustion markers, limiting their functionality. By contrast, responders (Rs) retained a pool of less differentiated, stem-like cells. Collectively, these data provide a comprehensive analysis of T cell fates during TIL-ACT providing the basis for new approaches to enhance therapeutic strategies.

immunology↗

IL-1β promotes MPN disease initiation by favoring early clonal expansion of JAK2-mutant hematopoietic stem cells

JAK2-V617F is the most frequent somatic mutation causing myeloproliferative neoplasm (MPN). However, JAK2-V617F can also be found in healthy individuals with clonal hematopoiesis of indeterminate potential (CHIP) with a frequency much higher than the prevalence of MPN. The factors controlling the conversion of JAK2-V617F CHIP to MPN are largely unknown. We hypothesized that IL-1{beta} mediated inflammation is one of the factors that favors this progression. We examined mono- or oligoclonal evolution of MPN by performing bone marrow transplantations at limiting dilutions with only 1-3 JAK2-mutant HSCs per recipient. Genetic loss of IL-1{beta} in JAK2-mutant hematopoietic cells or inhibition by a neutralizing anti-IL-1{beta} antibody restricted the early clonal expansion of these JAK2-mutant HSCs resulting in a reduced frequency of a CHIP-like state and a lower rate of conversion to MPN. The MPN disease-promoting effects of IL-1{beta} were associated with damage to sympathetic innervation leading to loss of nestin-positive mesenchymal stromal cells and required the presence of IL-1R1 on bone marrow stromal cells. The anti-IL-1{beta} antibody protected these mesenchymal stromal cells from IL-1{beta} mediated damage and limited the expansion of the JAK2-mutant clone. Our results identify IL-1{beta} as a potential therapeutic target for preventing the transition from JAK2-V617F CHIP to MPN. Brief summaryIn a mouse model of oligo-clonal myeloproliferative neoplasm (MPN), IL-1{beta} produced by JAK2-mutant cells favored expansion of sub-clinical JAK2-V617F clones and initiation of MPN disease.

cancer biology↗