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Impact of ECTV C15 expression on the development of CD8+ effector T cells

ABSTRACT: Orthopoxviruses, such as variola and Mpox, encode a myriad of immunomodulatory proteins to promote pathogenesis. One notable family is the B22 family of proteins, which are highly conserved surface glycoproteins that potently inhibit T cell activation in vitro and ex vivo. However, there has been limited work investigating the impact of B22 proteins on both CD4+ and CD8+ T cell responses in vivo. Therefore, we used ectromelia (ECTV) as a natural host-pathogen model to investigate the impact of its B22 protein, C15, on T cell responses in vivo. To broadly investigate the impact of C15 on CD8+ effector (CD62L-CD44+) T cell development, we performed bulk RNA-seq on splenic CD8+ effector T cells 7 days post-infection with either WT ECTV or ECTV∆C15.

ORGANISM(S): Mus musculus

PROVIDER: GSE308808 | GEO | 2026/03/12

REPOSITORIES: GEO

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Impact of ECTV C15 expression on the development of CD8+ effector T cells [d10]

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Impact of ECTV C15 expression on the early immune response in the popliteal lymph node (bulk RNA-seq)

Project description:Orthopoxviruses, such as variola and Mpox, encode a myriad of immunomodulatory proteins to promote pathogenesis. One notable family is the B22 family of proteins, which are highly conserved surface glycoproteins that potently inhibit T cell activation in vitro and ex vivo. Using the model poxvirus, ectromelia (ECTV), our lab has demonstrated that its B22 protein, C15, is capable of inhibiting both CD4+ and CD8+ T cells both in vitro and ex vivo, similar to other B22 proteins. Furthermore, we have also identified an additional function of C15: antagonism of NK cells during early infection. Specifically, C15 antagonizes the engagement of NK cells with infected cells in the popliteal lymph node during the innate immune response to infection. This inhibition by C15 promotes viral dissemination and replication, such that in the absence of C15, viral replication is significantly stunted. To date, there has not been any work investigating the mechanisms underlying this NK cell inhibition. To broadly explore the transcriptional changes occurring during this critical window, we performed bulk RNA-seq on popliteal lymph nodes at 48 hours post-infection.

2026-03-12 | GSE309219 | GEO

Impact of ECTV C15 expression on the early immune response in the popliteal lymph node (scRNA-seq)

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2026-03-12 | GSE309220 | GEO

Impact of ECTV C15 expression on the development of CD8+ effector T cells

Project description:Impact of ECTV C15 expression on the development of CD8+ effector T cells

| PRJNA1332742 | ENA

Impact of ECTV C15 expression on the development of CD8+ effector T cells [d10]

Project description:Impact of ECTV C15 expression on the development of CD8+ effector T cells [d10]

| PRJNA1332741 | ENA

Impact of ECTV C15 expression on the development of CD4+ effector T cells

Project description:Impact of ECTV C15 expression on the development of CD4+ effector T cells

| PRJNA1332747 | ENA

Impact of ECTV C15 expression on the early immune response in the popliteal lymph node (scRNA-seq)

Project description:Impact of ECTV C15 expression on the early immune response in the popliteal lymph node (scRNA-seq)

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Project description:Impact of ECTV C15 expression on the early immune response in the popliteal lymph node (bulk RNA-seq)

| PRJNA1334365 | ENA

Comparison of host gene expression profiles in spleen tissues of genetically susceptible and resistant mice during ECTV infection

Project description:Ectromelia virus (ECTV) has emerged as a valuable model for investigating the host-orthopoxvirus relationship as it relates to pathogenesis and the immune response. ECTV causes mousepox in most strains of mice, including BALB/c and DBA/2, and these are therefore classified as susceptible mice. Conversely, C57BL/6 and certain 129 strains display limited pathology and a very low mortality, and are thus classified as resistant. To understand the host genetic factors of different mouse strains in response to ECTV infection, we carried out a microarray analysis using Affymetrix Gene-Chip Mouse Genome Arrays of spleen tissues from BALB/c and C57BL/6 mice at 3 and 10 days post-ECTV infection. Differential Expression of Genes (DEGs) analyses revealed distinct differences in the gene profiles of resistant and susceptible mice infected with ECTV. Gene ontology and KEGG pathway analysis showed that the DEGs of susceptible mice were involved mainly in immunity, apoptosis, spliceosomes and cancer-related pathways, while the DEGs of resistant mice were largely involved in MAPK signaling and leukocyte transendothelial migration. This suggests that the susceptible BALB/c mice have a stronger response than the resistant C57BL/6 mice to ECTV infection. The BALB/c mice showed a strong induction of interferon-induced genes (ISGs), including guanylate binding proteins (GBPs), myxovirus resistance protein (Mx) GTPases, oligoadenylate synthetase (OAS) and IFN-induced protein with tetratricopeptide repeats (IFIT) family proteins, while the C57BL/6 mice upregulated more genes related to metabolic pathways. This suggests that the susceptible BALB/c mice have a stronger response than the resistant C57BL/6 mice to ECTV infection.

2018-02-16 | GSE100644 | GEO

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