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Interferon gamma suppresses T follicular helper cells and antibody responses upon viral infection

ABSTRACT: Interferon gamma suppresses T follicular helper cells and antibody responses upon viral infection

PROVIDER: PRJNA1052674 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27209819_1.fastq.gz	Fastqsanger.gz
	SRR27209819_2.fastq.gz	Fastqsanger.gz
	SRR27209820_1.fastq.gz	Fastqsanger.gz
	SRR27209820_2.fastq.gz	Fastqsanger.gz
	SRR27209821_1.fastq.gz	Fastqsanger.gz

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Interferon gamma suppresses T follicular helper cells and antibody responses upon viral infection

Project description:Interferon gamma suppresses T follicular helper cells and antibody responses upon viral infection

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Interferon gamma suppresses T follicular helper cells and antibody responses upon viral infection

Project description:Humoral and cellular immunity upon viral infections usually co-exist; however, sometimes, one of the two responses emerges as dominant and is responsible for most of the antiviral activity. For example, infection with lymphocytic choriomeningitis virus (LCMV) induces very strong cellular responses, but weak and inefficient neutralizing Ab (nAb) responses. Lack of nAb responses is an important issue for complete clearance of LCMV and other similar viruses, which in some instances tend to establish chronic infections. Recent work from our group has shown that this unbalance is observed also at the level of CD4 T cells responses, with subcutaneous LCMV infection leading almost exclusively to TH1 but no TFH differentiation. Here, we report that LCMV-induced TH1 cells are heterogeneous and comprise a Tcf-1+ subset and a GzmB+ subset. We found that none of the subsets is dependent on the major TH1-polarizing cytokine IL-12. Instead, IFN-gamma (IFN-g) was found to promote the development of GzmB+ cells and to suppress the commitment of the Tcf-1+ population into fully differentiated TFH. As a result, blockade of IFN-g led to a rescue in the TFH population, germinal center B cells and antibody responses. Our results shed light on new mechanisms underlying the inefficient nAbs production in response to non-cytopathic viruses such as LCMV and are promising for the design of new vaccination strategies.

2025-03-25 | GSE250209 | GEO

Interferon gamma suppresses T follicular helper cells and antibody responses upon viral infection

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Transcription profiling of mouse vivo follicular helper CD4 T cells (TFH) versus non follicular helper CD4 T cells (non-TFH)

Project description:Analysis of in vivo antigen-specific (LCMV-specific, SMARTA TCR transgenic) follicular helper CD4 T cells (CXCR5high),versus non-follicular helper CD4 T cells (CXCR5low), eight days after viral infection. A paper including data analysis of these experiments has been accepted for publication (Robert J. Johnston et al. Bcl6 and Blimp-1 are reciprocal and antagonistic regulators of follicular helper CD4 T cell differentiation). Experiment Overall Design: Analysis of in vivo antigen-specific (LCMV-specific, SMARTA TCR transgenic) follicular helper CD4 T cells (CXCR5high), versus non-follicular helper CD4 T cells (CXCR5low), eight days after viral infection.

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CD4 T Follicular Helper 1 Cells Promote HIV-1 Env Antibody Persistence

Project description:CD4 T Follicular Helper 1 Cells Promote HIV-1 Env Antibody Persistence

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Murine follicular helper T cells

Project description:Murine follicular helper T cells

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CD4 T Follicular Helper 1 Cells Promote HIV-1 Env Antibody Persistence

Project description:CD4 T follicular helper cells (Tfh) are essential for establishing serological memory and have distinct helper attributes that impact both the quantity and quality of the antibody response. Therefore, gaining insights into Tfh subsets promoting antibody persistence and functional capacity is crucial for vaccine design. We investigated the potential of inducing a mixed Tfh1/17 response to enhance HIV-1 Envelope (Env) antibodies to a DNA-prime/protein boost platform, utilizing rhesus macaques as our experimental model. Following immunization with Clade C gp140 protein formulated with cationic liposome-based formulation (CAF01), we successfully generated germinal center (GC) Tfh1/17 cells, in contrast to the predominance of GC Tfh1 cells induced with gp140 formulated in monophosphoryl lipid A+QS-21 (MPLA). Analysis of lymph nodes, employing proteomic and transcriptional approaches, demonstrated robust induction of GC responses across vaccine platforms with distinct qualitative and quantitative effects elicited by MPLA versus CAF01. While the induction of GC Tfh1 cells with MPLA and GC Tfh1/17 cells with CAF01 resulted in comparable peak HIV-Env antibody levels, there was a notable difference in antibody persistence. The MPLA group demonstrated significantly greater antibody persistence at week 8 and up to 30 weeks after final immunization compared to CAF01. Inducing GC Tfh1 cells with MPLA furthermore enhanced tier 1 neutralization titers, antibody functions, and Env-specific IgG in the rectal mucosa. Notably, IFNγ+ Env-specific Tfh responses, both in blood and lymph nodes, were higher with MPLA and correlated with Env antibody persistence. These findings suggest that vaccine platforms maximizing GC Tfh1 induction may confer protective immunity against HIV.

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Migratory CD11b+ conventional dendritic cells induce T follicular helper cell dependent antibody responses

Project description:Migratory CD11b+ conventional dendritic cells induce T follicular helper cell dependent antibody responses

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Expression Data from in vivo follicular helper CD4 T cells (TFH) versus non follicular helper CD4 T cells (non-TFH)

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