From parasite chromatin to host immune reprogramming: linking developmental state, effector regulation, and persistence in Toxoplasma gondii
- 1Department of Molecular and Life Science, Hanyang University
- 2Department of Molecular Medicine, School of Biopharmaceutical Convergence, Hanyang University
- 3Biopeptics Inc.
Abstract
Toxoplasma gondii establishes persistent infection despite sustained cell-mediated immune pressure, requiring coordinated regulation of parasite development and host immune responses. Parasite developmental states are controlled by sequence-specific transcription factors and chromatin regulators, including apicomplexan AP2 proteins and ATP-dependent chromatin remodelers, which establish stage-specific transcriptional programs. These developmental programs are accompanied by changes in the expression and delivery of host-modulatory effectors, although effector abundance does not necessarily predict their delivery into host cells. This review examines the emerging mechanistic link between parasite-intrinsic transcriptional and chromatin states, stage-dependent effector regulation, and host immune reprogramming during T. gondii infection. We discuss how rhoptry and dense-granule effectors alter host signaling, STAT-dependent transcription, transcriptional cofactor and corepressor function, histone modification, and chromatin accessibility. These activities can suppress interferon-responsive and cell-death pathways or induce inflammatory and migration-associated transcriptional programs, with outcomes that depend on the combination of effectors, host cell identity, and parasite genetic background. We further consider how stage-specific effector activity contributes to immune containment, persistence, reactivation, and tissue pathology in the central nervous system, ocular tissues, and placenta. Although individual parasite transcriptional regulators and host-targeting effectors have been characterized in considerable detail, direct regulatory connections between parasite developmental chromatin states and stage-specific effector expression and delivery remain incompletely defined. Defining these connections across parasite stages, host cell types, genetic backgrounds, and infected tissues will be important for understanding how parasite developmental programs shape tissue-specific immune modulation and pathogenesis.
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BibTeX
@article{kim2026from,
title = {{From parasite chromatin to host immune reprogramming: linking developmental state, effector regulation, and persistence in Toxoplasma gondii}},
author = {Yebom Kim and Yu Seong Ham and Jihyeon Yun and Seungbin Han and Chul-Su Yang},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.2000150},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.2000150/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - From parasite chromatin to host immune reprogramming: linking developmental state, effector regulation, and persistence in Toxoplasma gondii
AU - Yebom Kim
AU - Yu Seong Ham
AU - Jihyeon Yun
AU - Seungbin Han
AU - Chul-Su Yang
PY - 2026
DA - 2026/10/15
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.2000150
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.2000150/full
AB - Toxoplasma gondii establishes persistent infection despite sustained cell-mediated immune pressure, requiring coordinated regulation of parasite development and host immune responses. Parasite developmental states are controlled by sequence-specific transcription factors and chromatin regulators, including apicomplexan AP2 proteins and ATP-dependent chromatin remodelers, which establish stage-specific transcriptional programs. These developmental programs are accompanied by changes in the expression and delivery of host-modulatory effectors, although effector abundance does not necessarily predict their delivery into host cells. This review examines the emerging mechanistic link between parasite-intrinsic transcriptional and chromatin states, stage-dependent effector regulation, and host immune reprogramming during T. gondii infection. We discuss how rhoptry and dense-granule effectors alter host signaling, STAT-dependent transcription, transcriptional cofactor and corepressor function, histone modification, and chromatin accessibility. These activities can suppress interferon-responsive and cell-death pathways or induce inflammatory and migration-associated transcriptional programs, with outcomes that depend on the combination of effectors, host cell identity, and parasite genetic background. We further consider how stage-specific effector activity contributes to immune containment, persistence, reactivation, and tissue pathology in the central nervous system, ocular tissues, and placenta. Although individual parasite transcriptional regulators and host-targeting effectors have been characterized in considerable detail, direct regulatory connections between parasite developmental chromatin states and stage-specific effector expression and delivery remain incompletely defined. Defining these connections across parasite stages, host cell types, genetic backgrounds, and infected tissues will be important for understanding how parasite developmental programs shape tissue-specific immune modulation and pathogenesis.
SN - 1664-3224
ER -