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MCP-1 production regulated by ATG5 in inflammatory monocytes selectively modulates anti-malarial CD4+ Th1 response

ABSTRACT: MCP-1 production regulated by ATG5 in inflammatory monocytes selectively modulates anti-malarial CD4+ Th1 response

PROVIDER: PRJNA949962 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24003400_1.fastq.gz	Fastqsanger.gz
	SRR24003400_2.fastq.gz	Fastqsanger.gz
	SRR24003401_1.fastq.gz	Fastqsanger.gz
	SRR24003401_2.fastq.gz	Fastqsanger.gz
	SRR24003402_1.fastq.gz	Fastqsanger.gz

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ATG5-regulated MCP-1 production in myeloid cells selectively modulates anti-malarial CD4+ Th1 responses

Project description:Induction of parasite-specific CD4+ Th1 cell responses is a promising strategy for designing effective blood-stage malaria vaccines; however, the underlying regulatory mechanisms remain largely unknown. This study demonstrated that ATG5 deficiency in myeloid cells can significantly inhibit the growth of rodent blood-stage malarial parasites by enhancing parasite-specific CD4+ Th1 cell responses. This effect was independent of ATG5-mediated canonical and non-canonical autophagy. Mechanistically, ATG5 deficiency promoted myeloid cell (Ly6G-CD11b+F4/80-) survival and subsequently increased MCP-1 production in parasite-infected mice. Ly6G-CD11b+F4/80- cell-derived MCP-1 interacted with CCR2 on CD4+ Th1 cells for their optimized responses through the JAK2/STAT4 pathway. Notably, recombinant MCP-1 significantly improved parasite-specific CD4+ Th1 responses of the whole-killed blood-stage vaccine. Conclusively, our study highlights the previously unrecognized role of ATG5 in modulating myeloid cell survival via MCP-1 production, which selectively promotes CD4+ Th1 cell responses. Our findings provide new insights into the development of effective antimalarial vaccines.

2023-12-16 | GSE239405 | GEO

MCP-1 production regulated by ATG5 in inflammatory monocytes selectively modulates anti-malarial CD4+ Th1 response

Project description:A promising strategy to design effective malaria blood-stage vaccines is to induce parasite-specific CD4+ Th1 cell responses, but the regulatory mechanism of which is still largely unknown. Here, we showed that the ATG5-deficiency in myeloid cells significantly inhibit the growth of rodent blood-stage malaria parasites through specifically enhancing parasite-specific CD4+ Th1 cell responses. This effect was independent of ATG5-mediated canonical autophagy and non-canonical autophagy. Mechanistically, the deficiency of ATG5 promoted the survival of inflammatory monocytes (CD11b+F4/80- cells), and sequentially increased the generation of chemokine MCP-1 in parasite-infected mice. The interaction of CD11b+F4/80- cells-derived MCP-1 with CCR2 on CD4+ Th1 cells for its optimized differentiation dependent on Jak2/stat4 pathway. Therefore, we highlight the previously unrecognized role of ATG5 in the modulation of the survival of inflammatory monocytes to produce MCP-1, and the selective promoting effect of MCP-1 on CD4+ Th1 cell differentiation, which shed new lights on effective malaria vaccine designation.

2024-03-01 | GSE228461 | GEO

ATG5-regulated MCP-1 production in myeloid cells selectively modulates anti-malarial CD4+ Th1 responses

Project description:ATG5-regulated MCP-1 production in myeloid cells selectively modulates anti-malarial CD4+ Th1 responses

| PRJNA999227 | ENA

ATG5-regulated CCL2/MCP-1 production in myeloid cells selectively modulates anti-malarial CD4<sup>+</sup> Th1 responses.

Project description: Not available

| S-EPMC11210915 | biostudies-literature

Transcriptomic analysis of ATG5 induced hepatocellular carcinoma in zebrafish

Project description:ATG5 is a key autophagy effect in autophagosome formation; however, it also mediates autophagy-independent processes. ATG5 has been intricately linked to cancer where both tumor-promoting and tumor-suppressing functions of ATG5 have been described. We established a stable transgenic zebrafish to promote ATG5 functions in liver and found that overexpression of ATG5 in liver contributed to hepatocellular carcinoma.

2026-06-01 | GSE278167 | GEO

Genome-wide expression analysis in Control and Atg5-deficient eosinophils.

Project description:Depletion of autophagy-associated protein 5 (Atg5), specifically within the eosinophil lineage in mice, resulted in increased body weight, impaired glucose metabolism, and structural alterations in adipose tissue. Our findings highlight that Atg5 influences the functional activity of eosinophils within adipose tissue rather than their quantity. To gain a deeper understanding of the molecular mechanisms underlying ATG5's role in eosinophils, we conducted total RNA-seq analyses on control and Atg5-deficient eosinophils isolated from both bone marrow and blood of mice.

2023-11-21 | GSE245134 | GEO

Atg5 Deletion in Macrophages Protects Against Kidney Fibrosis in Mice

Project description:To identify the factors or genes associated with macrophages in a condition of ATG5 deficiency, we isolated F4/80+ cells from kidney single-cell suspensions of MΦ Atg5 -/- and WT mice(10 mouse per group) by immunomagnetic positive selection. we performed RNA-seq and heatmap analysis to identify the expression of chemokine receptor genes in MΦ Atg5-/- and WT mice.

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Next Generation Sequencing analysis atg5 gene expression in zebrafish model

Project description:Purpose: study of function of ATG5 protein on zebrafish larvae development Methods: Using morpholino oligos for atg5 gene knock down and overexpression, injected into one- to four-cell-stage embryos,extracted total RNA, then sending to RNA sequencing. Results: we compared to Wildtype, 5MO and atg5 mRNA groups, we analyza autophagy related gene mRNA expression, there are obvious different. Conclusion: our study showed the function of autophagy related gene 5 on zebrafish larvae, it has an important significant for understanding the affection of autophagy on embryo development

2019-04-30 | GSE120170 | GEO

Expression data from MCP-1-treated human kidney cancer CRL-1932 cell line

Project description:Microarray analysis revealed MCP-1 treatment altered protein folding processes in RCC CRL1932 cells. In response to MCP-1 treatment, CRL1932 cells and xenograft tumors expressed MCP-1-induced protein (MCPIP) which was reported to cause endoplasmic reticulum (ER) stress-induced apoptosis in human cardiomyocytes. In line with MCPIP induction, the expression of ER stress mediators, such as GRP78, PERK, IRE1α, and PDI, as well as molecules involved in ER stress-induced apoptosis, CHOP, calnexin, and Ero1α, presented in MCP-1 treated RCC cell line and xenograft tumors whereas absent or downregulated in untreated controls. TUNEL assay confirmed apoptosis of MCP-1 treated CRL1932 cells. MCPIP ectopically expressed in HEK293 cell resulted in apoptosis. Meta-analysis showed low level of MCP-1 associated with lower one year-survival rate after nephrectomy in RCC. In this dataset, we include the expression array data from human kidney cancer CRL-1932 cell line with or without the treatment of MCP-1. These data were used to obtain genes upregulated in MCP-1-treated CRL-1932 cells.

2019-12-31 | GSE127996 | GEO

ATG5 suppresses type I interferon-dependent neutrophil swarming and NET release

Project description:Inflammation is critical for controlling infections but can cause disease when unchecked. For tuberculosis, the leading cause of death by infection, neutrophil-dominated inflammation is associated with disease progression, emphasizing the need to understand how neutrophil functions are regulated during Mycobacterium tuberculosis infection. Atg5 was the first gene shown to specifically function within neutrophils to promote control of M. tuberculosis. ATG5 is best studied for its role in autophagy, however, the protective activity of ATG5 in neutrophils was unexpectedly independent of other autophagy proteins and remained elusive. We report that ATG5 is required in neutrophils to suppress type I interferon-induced neutrophil extracellular trap (NET) release and swarming during M. tuberculosis infection. Elevated NET release contributes to the early susceptibility of Atg5fl/fl-LysM-Cre mice during infection. These findings identify ATG5 as a master regulator of how type I interferon influences neutrophil responses during infection, revealing a new potential target for host-directed therapies.

2025-03-07 | GSE280193 | GEO

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