Maintenance of X chromosome inactivation after T cell activation requires NF-κB signaling.

X chromosome inactivation (XCI) balances X-linked gene dosage between sexes. Unstimulated T cells lack cytological enrichment of X-inactive specific transcript (Xist) RNA and heterochromatic modifications on the inactive X chromosome (Xi), which are involved in maintenance of XCI, and these modifications return to the Xi after stimulation. Here, we examined allele-specific gene expression and epigenomic profiles of the Xi in T cells.

NF-κB Signaling is Required for X-Chromosome Inactivation Maintenance Following T cell Activation.

X Chromosome Inactivation (XCI) is a female-specific process which balances X-linked gene dosage between sexes. Unstimulated T cells lack cytological enrichment of RNA and heterochromatic modifications on the inactive X chromosome (Xi), and these modifications become enriched at the Xi after cell stimulation. Here, we examined allele-specific gene expression and the epigenomic profiles of the Xi following T cell stimulation.

Dendritic cell-mediated responses to secreted effectors are required for parasite-specific CD8 T cell responses.

causes debilitating diarrheal disease in patients with primary and acquired defects in T cell function. However, it has been a challenge to understand how this infection generates T cell responses and how they mediate parasite control. Here, was engineered to express a parasite effector protein (MEDLE-2) that contains the MHC-I restricted SIINFEKL epitope which is recognized by TCR transgenic OT-I CD8 T cells.

A positive feedback loop controls Toxoplasma chronic differentiation.

Successful infection strategies must balance pathogen amplification and persistence. In the obligate intracellular parasite Toxoplasma gondii this is accomplished through differentiation into dedicated cyst-forming chronic stages that avoid clearance by the host immune system. The transcription factor BFD1 is both necessary and sufficient for stage conversion; however, its regulation is not understood.

IL-18BP mediates the balance between protective and pathological immune responses to Toxoplasma gondii.

Interleukin-18 (IL-18) promotes natural killer (NK) and T cell production of interferon (IFN)-γ, a key factor in resistance to Toxoplasma gondii, but previous work has shown a limited role for endogenous IL-18 in control of this parasite. Although infection with T. gondii results in release of IL-18, the production of IFN-γ induces high levels of the IL-18 binding protein (IL-18BP).

Toxoplasma gondii Dissemination in the Brain Is Facilitated by Infiltrating Peripheral Immune Cells.

Despite recent advances in our understanding of pathogenic access to the central nervous system (CNS), the mechanisms by which intracellular pathogens disseminate within the dense cellular network of neural tissue remain poorly understood. To address this issue, longitudinal analysis of Toxoplasma gondii dissemination in the brain was conducted using 2-photon imaging through a cranial window in living mice that transgenically express enhanced green fluorescent protein (eGFP)-claudin-5. Extracellular T.

T cell surveillance of Toxoplasma gondii: Basic insights into how T cells operate in the central nervous system.

The ability of T cells to operate in the central nervous system (CNS) is required for resistance to multiple pathogens that affect this tissue. The intracellular parasite Toxoplasma gondii has evolved to persist in the CNS and poses unique challenges to the immune system with the need to control parasite replication while balancing the adverse pathology associated with local inflammation. This article reviews the models used to study the response to T.

cDC1 coordinate innate and adaptive responses in the omentum required for T cell priming and memory.

In the peritoneal cavity, the omentum contains fat-associated lymphoid clusters (FALCs) whose role in response to infection is poorly understood. After intraperitoneal immunization with , conventional type 1 dendritic cells (cDC1s) were critical to induce innate sources of IFN-γ and cellular changes in the FALCs. Unexpectedly, infected peritoneal macrophages that migrated into the FALCs primed CD8 T cells.

Impact of secondary TCR engagement on the heterogeneity of pathogen-specific CD8+ T cell response during acute and chronic toxoplasmosis.

Initial TCR engagement (priming) of naive CD8+ T cells results in T cell expansion, and these early events influence the generation of diverse effector and memory populations. During infection, activated T cells can re-encounter cognate antigen, but how these events influence local effector responses or formation of memory populations is unclear. To address this issue, OT-I T cells which express the Nur77-GFP reporter of TCR activation were paired with the parasite Toxoplasma gondii that expresses OVA to assess how secondary encounter with antigen influences CD8+ T cell responses.

Long live the king: Toxoplasma gondii nucleomodulin inhibits necroptotic cell death.

Toxoplasma gondii is a parasite that results in chronic infection of the central nervous system, but the basis for its ability to persist is unknown. In this issue of Cell Host & Microbe, Rosenberg and Sibley (2021) identify a parasite effector produced by the latent bradyzoite stage that inhibits host cell necroptosis.