The comparison of Th1, Th2, Th9, Th17 and Th22 cytokine profiles in acute and chronic HIV-1 infection

Gorenec, Lana; Lepej, Snježana Židovec; Grgic, Ivana; Planinić, Ana; Bes, Janja Iscic; Vince, Adriana; Begovać, Josip

doi:10.1016/j.micpath.2016.06.008

Cited by 39 publications

(35 citation statements)

References 33 publications

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“…The study demonstrated statistically significant increase in the production of IL-6 and IL-17A which have been demonstrated in other studies to cause renal and vascular dysfunction and lead to blood pressure elevation [28]. Hypertension comorbidity may present as a primary complication of inflammatory process on endothelial linings of cardio vasculature or secondary to metabolic syndrome.…”

Section: Discussionsupporting

confidence: 71%

Cytokine Expression and Hypertension Comorbidity in HIV/AIDS Patients at Kenyatta National Hospital HIV Care Centre, Nairobi, Kenya

Chepchirchir¹,

Nyagol²,

Jaoko³

2018

Int J Cardiovasc Res

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Chronic inflammation in HIV disease is sustained by immune reconstitution that results from use of combination therapy by patients and manifested by increased expression of inflammatory cytokines. Chronic inflammation in HIV disease is associated with endothelial dysfunction of the cardio vasculature giving rise to reduced elasticity resulting in high blood pressure. This state is marked by increased IL-6 cytokine expression as manifested in patients with type 2 diabetes and hypertension. This study sought to establish cytokine expression in HIV seropositive patients with hypertension comorbidity and correlate with HIV/AIDS progression. We hypothesized that chronic inflammation and presence of hypertension comorbidity presents higher levels of expression of selected interleukins namely IL-6, IL-8 and IL-17A. This study demonstrated that the IL-6 cytokine expression have a positive correlation with the release of IL-8 cytokine as patients with higher IL-6 cytokine values were more likely to have higher IL-8 cytokine levels. This shows that a synergistic effect from both cytokines may accelerate the development of atherosclerosis on blood vessels. Therefore routine measurement of these cytokines may increase prediction of risk of development of hypertension in patients on HIV care.

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Section: Discussionsupporting

confidence: 71%

Cytokine Expression and Hypertension Comorbidity in HIV/AIDS Patients at Kenyatta National Hospital HIV Care Centre, Nairobi, Kenya

Chepchirchir¹,

Nyagol²,

Jaoko³

2018

Int J Cardiovasc Res

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“…In URMC-099-treated humanized mice, LC3B puncta in CD68 + macrophages were also readily apparent ( Figure 7C). These results suggest that URMC-099 modulates HIV-1-induced cytokine responses in vivo through autophagy (6,47). …”

mentioning

confidence: 78%

Autophagy facilitates macrophage depots of sustained-release nanoformulated antiretroviral drugs

Gnanadhas¹,

Dash²,

Sillman³

et al. 2017

Journal of Clinical Investigation

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Long-acting anti-HIV products can substantively change the standard of care for patients with HIV/AIDS. To this end, hydrophobic antiretroviral drugs (ARVs) were recently developed for parenteral administration at monthly or longer intervals. While shorter-acting hydrophilic drugs can be made into nanocarrier-encased prodrugs, the nanocarrier encasement must be boosted to establish long-acting ARV depots. The mixed-lineage kinase 3 (MLK-3) inhibitor URMC-099 provides this function by affecting autophagy. Here, we have shown that URMC-099 facilitates ARV sequestration and its antiretroviral responses by promoting the nuclear translocation of the transcription factor EB (TFEB). In monocyte-derived macrophages, URMC-099 induction of autophagy led to retention of nanoparticles containing the antiretroviral protease inhibitor atazanavir. These nanoparticles were localized within macrophage autophagosomes, leading to a 4-fold enhancement of mitochondrial and cell vitality. In rodents, URMC-099 activation of autophagy led to 50-fold increases in the plasma drug concentration of the viral integrase inhibitor dolutegravir. These data paralleled URMC-099-mediated induction of autophagy and the previously reported antiretroviral responses in HIV-1-infected humanized mice. We conclude that pharmacologic induction of autophagy provides a means to extend the action of a long-acting, slow, effective release of antiretroviral therapy. Center for Neural Development and Disease, University of Rochester Medical Center (URMC), Rochester, New York, USA. Conflict of interest:H.A. Gelbard and H.E. Gendelman are members of the scientific advisory board for WavoDyne Therapeutics Inc., which is developing URMC-099 as a firstin-class MLK-3 inhibitor for clinical trials. URMC-099 is owned by URMC (patent nos. US 8,846,909 B2;8,877,772;and 9,181,247 and associated international patents). tion of TFEB mRNA by approximately 4-to 8-fold under different treatment conditions ( Figure 2F). With HIV-1 infection, TFEB mRNA levels were reduced by 2-to 3-fold compared with levels in uninfected controls, and URMC-099 could recover the phenotype. Increased TFEB translocation was delayed and did not reach significant levels until day 7 after URMC-099 treatment (Supplemental Figure 2B). These data confirm that URMC-099 regulates TFEB nuclear translocation in an mTORC1-dependent manner. URMC-099 stimulates autophagy in human MDMs. On the basis of the preceding data sets, we theorized that nuclear translocation of TFEB induces autophagy and lysosomal biogenesis. TFEB serves as the master regulator of both autophagy and lysosomal biogenesis (26), and such regulation could have a profound role in nanoART intracellular sequestration in MDMs. Thus, we examined the autophagosome markers microtubule-associated protein 1 light chain 3 β (LC3B, also known as MAP1LC3B) and beclin 1 (BECN1). Using Western blot assays, we found that each marker was significantly upregulated by URMC-099 ( Figure 3, A-C and Supplemental Figure 3A). URMC-099 increased the expression ...

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“…In the early stage of HIV infection, gut Th17 cells are largely depleted . In chronic HIV infection, depletion of gut‐derived Th17 cells is also significant, contributing to the loss of mucosal barrier function, increased microbial translocation and systemic immune hyperactivation . HIV‐specific Th17 cells were detected during early infection but not in chronic infection .…”

Section: Treg and Th17 Cells In Hiv Infectionmentioning

confidence: 99%

Regulatory T cells and T helper 17 cells in viral infection

et al. 2020

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CD4 + T cells are the central element of the adaptive immune responses and protect the body from a variety of pathogens. Starting from naive cells, CD4 + T cells can differentiate into various effector cell subsets with specialized functions including T helper (Th) 1, Th2, Th17, regulatory T (Treg) and T follicular helper (Tfh) cells. Among them, Tregs and Th17 cells show a strong plasticity allowing the functional adaptation to various physiological and pathological environments during immune responses. Although they are derived from the same precursor cells and their differentiation pathways are interrelated, the terminally differentiated cells have totally opposite functions. Studies have shown that Tregs and Th17 cells have rather complex interplays in viral infection: Th17 cells may contribute to immune activation and disease progression while Tregs may inhibit this process and play a key role in the maintenance of immune homoeostasis, possibly at the cost of compromised viral control. In this review, we take respiratory syncytial virus (RSV), hepatitis B virus (HBV)/hepatitis C virus (HCV) and human immunodeficiency virus (HIV) infections as examples to discuss these interplays and their impacts on disease progression in viral infection. How to cite this article: Wan Z, Zhou Z, Liu Y, et al. Regulatory T cells and T helper 17 cells in viral infection. Scand J Immunol. 2020;91:e12873.

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The comparison of Th1, Th2, Th9, Th17 and Th22 cytokine profiles in acute and chronic HIV-1 infection

Cited by 39 publications

References 33 publications

Cytokine Expression and Hypertension Comorbidity in HIV/AIDS Patients at Kenyatta National Hospital HIV Care Centre, Nairobi, Kenya

Cytokine Expression and Hypertension Comorbidity in HIV/AIDS Patients at Kenyatta National Hospital HIV Care Centre, Nairobi, Kenya

Autophagy facilitates macrophage depots of sustained-release nanoformulated antiretroviral drugs

Regulatory T cells and T helper 17 cells in viral infection

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