Brain ingress of regulatory T cells in a murine model of HIV-1 encephalitis☆

Gong, Ni; Liu, Jianuo; Reynolds, Ashley D.; Gorantla, Santhi; Mosley, R. Lee; Gendelman, Howard E.

doi:10.1016/j.jneuroim.2010.08.014

Cited by 26 publications

(22 citation statements)

References 61 publications

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“…Dopamine can not only inhibit T reg function, but may also inhibit CCL22-mediated migration of T regs to inflammatory sites, which may contribute further to an immunostimulatory effect of dopamine in the CNS. In a murine model of HIV encephalitis, T regs exhibited anti-inflammatory and neuroprotective functions (Liu et al 2009; Gong et al 2011). Dopamine mediated inhibition of T reg function in the CNS may reduce this protective role, contributing to an increase in neuroinflammation and neurotoxicity in HIV infected drug abusers.…”

Section: Dopamine and Hiv In T Cellsmentioning

confidence: 99%

Drug Induced Increases in CNS Dopamine Alter Monocyte, Macrophage and T Cell Functions: Implications for HAND

Gaskill

Calderon

Coley

et al. 2013

J Neuroimmune Pharmacol

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Central nervous system (CNS) complications resulting from HIV infection remain a major public health problem as individuals live longer due to the success of combined antiretroviral therapy (cART). As many as 70% of HIV infected people have HIV associated neurocognitive disorders (HAND). Many HIV infected individuals abuse drugs, such as cocaine, heroin or methamphetamine, that may be important cofactors in the development of HIV CNS disease. Despite different mechanisms of action, all drugs of abuse increase extracellular dopamine in the CNS. The effects of dopamine on HIV neuropathogenesis are not well understood, and drug induced increases in CNS dopamine may be a common mechanism by which different types of drugs of abuse impact the development of HAND. Monocytes and macrophages are central to HIV infection of the CNS and to HAND. While T cells have not been shown to be a major factor in HIV-associated neuropathogenesis, studies indicate that T cells may play a larger role in the development of HAND in HIV infected drug abusers. Drug induced increases in CNS dopamine may dysregulate functions of, or increase HIV infection in, monocytes, macrophages and T cells in the brain. Thus, characterizing the effects of dopamine on these cells is important for understanding the mechanisms that mediate the development of HAND in drug abusers.

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Section: Dopamine and Hiv In T Cellsmentioning

confidence: 99%

Drug Induced Increases in CNS Dopamine Alter Monocyte, Macrophage and T Cell Functions: Implications for HAND

Gaskill

Calderon

Coley

et al. 2013

J Neuroimmune Pharmacol

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“…In parallel, Treg effects the up-regulation of neurotrophins and leads to neuroprotection [61]. Tregs readily migrate across the BBB, are retained within virus-induced neuroinflammatory sites and modulate microglial responses [62]. …”

Section: Rodent Models Of Hiv Diseasementioning

confidence: 99%

“…The major characteristics of chimeric animals are the higher rate of HSC acceptance with low doses of irradiation [96]; stable population of human cells in mouse bone marrow [97]; occupancy of murine thymus with human thymocytes and their maturation into T cell subsets [62, 98, 99]; complete reconstitution of residual murine lymph nodes with human T, B and dendritic cells [59, 100]; formation of splenic white pulp [94]; and the distribution of human cells of macrophage lineage throughout brain, the meninges and perivascular spaces [100]. The degree of reconstitution of mouse bone marrow by human cells determines the amount of human cells of macrophage lineage accumulation with age in CD34+ cell transplanted NSG animals.…”

Section: Rodent Models Of Hiv Diseasementioning

confidence: 99%

Rodent models for HIV-associated neurocognitive disorders

Gorantla

Poluektova

Gendelman

2012

Trends in Neurosciences

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Human immunodeficiency virus (HIV)-associated neurocognitive disorders (HAND) reflect the spectrum of neural impairments seen during chronic viral infection. Current research efforts focus on improving antiretroviral and adjunctive therapies, defining disease onset and progression, facilitating drug delivery, and halting neurodegeneration and viral resistance. As HIV is species-specific, generating disease in small animal models has proved challenging. After two decades of research, rodent HAND models now include those containing a human immune system. Antiviral responses, neuroinflammation and immunocyte blood-brain barrier (BBB) trafficking follow HIV infection in these rodent models. Here, we review these and other rodent models of HAND and discuss their unmet potential in reflecting human pathobiology and in facilitating disease monitoring and therapeutic discoveries.

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“…66 These findings suggest that the virus-induced alteration of DCs is a likely cause of the immunosuppression mediated by Tregs. The neuronal protection by Tregs was found to be mediated in several viral-encephalitis such as human HIV-1 encephalitis 67 and Japanese encephalitis. 10 In Japanese encephalitis, the infection of DCs with JEV P3 expanded the population of CD4 + Foxp3 + regulatory T cell (Treg) with immunosuppressive potential, suggesting that the virus-induced alteration of DCs in JEV infection is likely cause of the immunosuppression by iTregs.…”

Section: -65mentioning

confidence: 99%

Interactions of Host’s Innate and Adaptive Immune Components in the Pathogenesis of Viral Encephalitis: a Review

Rahman¹

2014

MOJPB

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Viral encephalitis has attracted the attention of researchers and physicians for millennia. In almost all cases, specific causes of central nervous system (CNS) syndromes of viral origin have been difficult and sometime impossible to identify. Immunological mechanisms involved in viral encephalitis are also diverse and complex which greatly limit the advent of modern antiviral therapies against viral encephalitis. This review will focus on the immunopathogenesis of viral encephalitis. Although a considerable emphasis will be placed on Japanese encephalitis, other viral infections of the CNS will be discussed. Role of Treg and Th17 cells, their plasticity and balance in viral encephalitis will be discussed with great details.

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Brain ingress of regulatory T cells in a murine model of HIV-1 encephalitis☆

Cited by 26 publications

References 61 publications

Drug Induced Increases in CNS Dopamine Alter Monocyte, Macrophage and T Cell Functions: Implications for HAND

Drug Induced Increases in CNS Dopamine Alter Monocyte, Macrophage and T Cell Functions: Implications for HAND

Rodent models for HIV-associated neurocognitive disorders

Interactions of Host’s Innate and Adaptive Immune Components in the Pathogenesis of Viral Encephalitis: a Review

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