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Chromatin accessibility profile of splenic LCMV-specific memory B cells following type I or II interferon blockade in acute versus chronic LCMV infection

ABSTRACT: Dynamics of interferon signalling impact the adaptive immune response. We used ATAC sequencing (ATAC-seq) to analyze chromatin accessibility in memory B cells from mice infected with acute or chronic LCMV infection, treated with type I or type II interferon blocking antibodies.

ORGANISM(S): Mus musculus

PROVIDER: GSE226485 | GEO | 2024/02/17

REPOSITORIES: GEO

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Chromatin accessibility profile of splenic LCMV-specific memory B cells following type I or II interferon blockade in acute versus chronic LCMV infection

Project description:Chromatin accessibility profile of splenic LCMV-specific memory B cells following type I or II interferon blockade in acute versus chronic LCMV infection

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Chromatin accessibility profile at the single cell level of splenic LCMV-specific B cells in acute versus chronic LCMV infection [scATAC-seq]

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Project description:Type I interferons (IFN-I) are critical for antiviral immunity; however, chronic IFN-I signaling is associated with hyperimmune activation and disease progression in persistent infections. We demonstrated in mice that blockade of IFN-I signaling diminished chronic immune activation and immune suppression, restored lymphoid tissue architecture, and increased immune parameters associated with control of virus replication, ultimately facilitating clearance of the persistent infection. The accelerated control of persistent infection induced by blocking IFN-I signaling required CD4 T cells and was associated with enhanced IFN-γ production. Thus, we demonstrated that interfering with chronic IFN-I signaling during persistent infection redirects the immune environment to enable control of infection.

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Project description:During persistent viral infections, chronic immune activation, negative immune regulator expression, an elevated interferon signature, and lymphoid tissue destruction correlate with disease progression. We demonstrated that blockade of type I interferon (IFN-I) signaling using an IFN-I receptor neutralizing antibody reduced immune system activation, decreased expression of negative immune regulatory molecules, and restored lymphoid architecture in mice persistently infected with lymphocytic choriomeningitis virus. IFN-I blockade before and after establishment of persistent virus infection resulted in enhanced virus clearance and was CD4 T cell-dependent. Hence, we demonstrate a direct causal link between IFN-I signaling, immune activation, negative immune regulator expression, lymphoid tissue disorganization, and virus persistence. Our results suggest that therapies targeting IFN-I may help control persistent virus infections.

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