Dynamics and functions of CD4+CD25high regulatory T lymphocytes in Chinese rhesus macaques during the early stage of infection with SIVmac239

Li, Shaoyou; Xia, Houjun; Dai, Zheng-Xi; Zhang, Gao-Hong; Fan, Bo; Li, Minghua; Wang, Ruirui; Zheng, Yong‐Tang

doi:10.1007/s00705-012-1252-8

Cited by 5 publications

(3 citation statements)

References 28 publications

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“…Similar to HIV infection, the exact mechanism of regulatory T cells function as well as its frequency during Simian Immunodeficiency Virus (SIV) infection is unclear. Li et al [ 51 ] observed a higher absolute and relative number of Treg cells in Chinese Rhesus macaques in the early stages after SIV infection. No alteration on Treg cells suppressive capacity after infection was described.…”

Section: The Role Of Treg Cells On Hiv Infectionmentioning

confidence: 99%

New Insights about Treg and Th17 Cells in HIV Infection and Disease Progression

Valverde-Villegas

Matte

Medeiros

et al. 2015

Journal of Immunology Research

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Treg and Th17 cell subsets are characterized by the expression of specific transcriptional factors and chemokine receptor as well as by secretion of specific cytokine and chemokines. These subsets are important to the differentiation, expansion, homing capacity, and recruitment of several different immune cell populations to the site of infection. Whereas Treg cells maintain self-tolerance and control the activation and expansion of autoreactive CD4+ T effector cells through an anti-inflammatory response, Th17 cells, in an exacerbated unregulated proinflammatory response, can promote autoimmunity. Despite such apparently opposite functions, Th17 and Treg cells share common characteristics, and their differentiation pathways are interconnected. Recent studies have revealed quite intricate relations between Treg and Th17 cells in HIV infection and progression to AIDS. Considering Treg cells, different subsets were already investigated in the context of HIV infection, indicating a fluctuation in the total number and frequency throughout the disease course. This review focuses on the recent findings regarding the role of regulatory T and Th17 cells in the context of HIV infection, highlighting the importance of the balance between these two subsets on disease progression.

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Section: The Role Of Treg Cells On Hiv Infectionmentioning

confidence: 99%

New Insights about Treg and Th17 Cells in HIV Infection and Disease Progression

Valverde-Villegas

Matte

Medeiros

et al. 2015

Journal of Immunology Research

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“…T cells associate with both non-progression and durable control of HIV replication and that virus controllers have high levels of HIV-1-specific CD8 ? T cells producing IL-2 alone or in combination with TNF-a [11,24,42,44], these results further suggest that the protective function of T cells was destroyed in the ID group monkeys. Although it is not known whether the cells that secrete a single cytokine or several cytokines have other functions, these results suggest that abnormality of these functional subsets may be associated with the death of infected monkeys.…”

Section: Discussionmentioning

confidence: 74%

“…SHIV89.6 provirus was quantified by measuring SHIV89.6 gag levels in 500 ng of total DNA using Premix Ex Taq (Takara, Dalian, China). Plasmid pGEM-4Z-SIV gag357, described by Li et al, was used as standard template [24], diluted in nuclease-free water, ranging from 0.01 to 10 9 10 6 copies/vial/10 ll. The limit of detection by PCR was 0.1 copy/well/10 ll.…”

Section: Quantitative Pcr For Plasma Viral Load and Proviral Loadmentioning

confidence: 99%

High immune activation and abnormal expression of cytokines contribute to death of SHIV89.6-infected Chinese rhesus macaques

Tian

Zhang

et al. 2015

Arch Virol

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Chinese rhesus macaques (CRMs) are ideal experimental animals for studying the pathogenesis of human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) and for vaccine research. SHIV89.6 has been reported to be an attenuated virus because, in most cases, SHIV89.6 infection only causes limited alteration of immune cells and tissues, and it has been used commonly for vaccine research. After two serial passages in vivo, SHIV (SHIV-89.6P) induces CD4 lymphopenia and an AIDS-like disease with wasting and opportunistic infections. However, the pathogenic ability of SHIV89.6 is not well understood. In this study, we found that 6 of 14 SHIV89.6-infected CRMs died within 127 weeks after infection. We found especially high immune activation, low IFN-α expression, and distinctive cytokine expression profiles in the infected and dead (ID) group of monkeys, while there was only few change in the CD4(+) T counts and distribution of T cell subsets in the ID group monkeys. Also, there was a similar dynamic of viral load between infected and surviving (IS) and ID group monkeys. Furthermore, we found various correlations among immune activation, IFN-α expression, and frequencies of cytokine-secreting cells. These results suggest that SHIV89.6 infections have pathogenic potential in CRMs and that high immune activation and abnormal expression of cytokines contribute to death of SHIV89.6-infected CRMs. This also implies that high immune activation may be relevant to dysfunction of immune cells. It is proposed that high immune activation and dysfunction of immune cells may be good predictors for disease progression and markers for therapy.

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Development and Function of Human CD4+CD25+FOXP3+ Regulatory T Cells in Humanized Mouse and HIV-1 Infection

Nunoya

2014

Humanized Mice for HIV Research

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Dynamics and functions of CD4+CD25high regulatory T lymphocytes in Chinese rhesus macaques during the early stage of infection with SIVmac239

Cited by 5 publications

References 28 publications

New Insights about Treg and Th17 Cells in HIV Infection and Disease Progression

New Insights about Treg and Th17 Cells in HIV Infection and Disease Progression

High immune activation and abnormal expression of cytokines contribute to death of SHIV89.6-infected Chinese rhesus macaques

Development and Function of Human CD4+CD25+FOXP3+ Regulatory T Cells in Humanized Mouse and HIV-1 Infection

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