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Theileria

ABSTRACT: Comparision of Theileria annulata and Theileria parva genomes

PROVIDER: PRJNA14000 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR3001169_1.fastq.gz	Fastqsanger.gz
	SRR3001169_2.fastq.gz	Fastqsanger.gz

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miRNA profiling of extracellular vesicles from Theileria annulata infected B cells (TBL20) and their uninfected control counterparts (BL20)

Project description:We report significant changes in six bovine miRNA in vesicles from Theileria annulata infected cells

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Systemic proteomic and small RNA profile analysis of extracellular vesicles derived from Theileria annulata

Project description:Extracellular vesicles (EVs) are key mediators of intercellular communication, and often play critical roles in host-parasite interactions by facilitating parasite’s physiology and pathogenesis. Theileria annulata, an apicomplexan parasite, induces profound changes in host cells, leading to uncontrolled proliferation, apoptosis resistance, and increased invasiveness. In this study, we performed the comprehensive proteomic and small RNA analysis of EVs isolated from a T. annulata Kashi isolate-infected bovine lymphocyte cell line (TaXJS), B cell line (TaBC), dendritic cell line (TaDC), and from the sera of cattle before and after infection. Our label-free LC-MS/MS proteomics identified 2580 proteins, while small RNA sequencing revealed 6635 miRNAs associated with parasite development, host invasion, and immune evasion. Functional enrichment analyses recognized vesicular components involved in key pathways of the parasite-host such as ECM-receptor interaction, oxidative phosphorylation, and proton transport. These findings highlight the potential of Theileria-derived EVs in modulating host responses and their potential as therapeutic and vaccine targets.

2025-10-21 | GSE279977 | GEO

Novel roles for GZMA and RASGRP1 in suppressing dissemination of both Theileria annulata-transformed macrophages and human B-lymphoma cells

Project description:Theileria annulata is a tick-transmitted apicomplexan parasite that infects and transforms bovine leukocytes into disseminating tumors that cause a disease called tropical theileriosis. Using comparative transcriptomics we identified genes transcriptionally perturbed during Theileria-induced transformation and highlighted a small set of genes associated with leukocyte dissemination. CRISPR/Cas9-mediated knock-down of GZMA and RASGRP1 in macrophages attenuated for dissemination led to a regain in their dissemination in Rag2/gC mice confirming their suppressor roles in vivo. Comparing the transcriptomes of 934 human cancer cell lines to that of Theileria-transformed bovine B cells again highlighted GZMA and RASGRP1 and CRISPR-mediated overexpression of GZMA and RASGRP1 dampened the dissemination potential of human B-lymphomas. The ensemble provide evidence for a novel suppressor function in the dissemination of both T. annulata-transformed bovine leukocytes and human B-lymphomas.

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Theileria parasites sequester host eIF5A to escape elimination by host-mediated autophagy

Project description:Intracellular pathogens develop elaborate mechanisms to survive within the hostile environments of host cells. Theileria parasites infect bovine leukocytes and cause devastating diseases in cattle in developing countries. Theileria spp. have evolved sophisticated strategies to hijack host leukocytes, inducing proliferative and invasive phenotypes characteristic of cell transformation. Intracellular Theileria parasites secrete proteins into the host cell and recruit host proteins to induce oncogenic signaling for parasite survival. It is unknown how Theileria parasites evade host cell defense mechanisms, such as autophagy, to survive within host cells. Here, we show that Theileria annulata parasites sequester the host eIF5A protein to their surface to escape elimination by autophagic processes. We identified a small-molecule compound that reduces parasite load by inducing autophagic flux in host leukocytes, thereby uncoupling Theileria parasite survival from host cell survival. We took a chemical genetics approach to show that this compound induced host autophagy mechanisms and the formation of autophagic structures via AMPK activation and the release of the host protein eIF5A which is sequestered at the parasite surface. The sequestration of host eIF5A to the parasite surface offers a strategy to escape elimination by autophagic mechanisms. These results show how intracellular pathogens can avoid host defense mechanisms and identify a new anti-Theileria drug that induces autophagy to target parasite removal.

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