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Bosteels, V.

Publications and source records attributed to Bosteels, V..

2 recordsLinked to original sources

Beyond a binary view of cystic fibrosis: systemic immunity and inflammation across the spectrum of CFTR dysfunction

Cystic fibrosis is traditionally framed as a dichotomy between affected individuals and clinically unaffected carriers, yet the systemic immune consequences across the spectrum of CFTR functionality remain incompletely defined. The advent of highly effective CFTR modulators now provides a unique momentum to examine whether partial restoration of CFTR function can influence systemic immunity. Using multimodal immune profiling, we constructed a single-cell atlas of circulating immune cells in people with cystic fibrosis (pwCF), healthy F508del carriers and non-carriers. In pwCF, systemic immunity was markedly altered following in vivo CFTR modulation with elexacaftor-tezacaftor-ivacaftor, with broad reductions in pro-inflammatory cytokines linked to improved clinical outcomes. Notably, healthy F508del carriers exhibited a CF-like immune signature characterised by low-grade systemic inflammation, including elevated IL-6, reduced mucosal-associated invariant T cells, and inflammatory monocyte features overlapping with pwCF. Together, these findings show that CFTR-related immune dysregulation extends beyond classical cystic fibrosis, challenging a strict dichotomy between health and disease.

immunology↗

Distinct cDC subsets co-operate in CD40 agonist response while suppressive microenvironments and lack of antigens subvert efficacy

Agonistic CD40 therapy has shown to inhibit cancer progression, but only in a fraction of patients. Hence, understanding the cancer cell-intrinsic and microenvironmental determinants of CD40 therapy response is crucial to identify responsive patient populations and design efficient combination treatments. Here, we showed that the therapeutic efficacy of CD40 in responder melanoma tumours, relied on pre-existing cDC1-primed CD8+ T cells, however cDC1s were dispensable after CD40 administration. Surprisingly, in response to CD40 the abundance of activated cDCs, potentially derived from cDC2s increased, thereby further activating antitumour CD8+ T cells. Hence, distinct cDC subsets are required to induce CD40 responses. By contrast, lung tumours, characterised by a high abundance of macrophages, were resistant to CD40 therapy. Combining CD40 therapy with macrophage depletion led to tumour growth inhibition only in the presence of strong neoantigens. Accordingly, treatment with immunogenic cell-death inducing chemotherapy sensitised non-immunogenic tumours to CD40 therapy.

cancer biology↗