Human immunodeficiency virus-1 infection protects against a Tc1-to-Tc2 shift in CD8+ T cells

Gulzar, Naveed; Diker, Bilge; Balasubramanian, Sowmya; Jiang, Jiefeng; Copeland, Karen F.T.

doi:10.1016/j.humimm.2011.08.012

Cited by 7 publications

(7 citation statements)

References 48 publications

(34 reference statements)

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“…HIV‐1 induces qualitative and quantitative changes in T‐cell subsets during disease progression. A Th1→Th2 switch hypothesis has been reported previously in HIV‐1 infection [Becker, ], while controversial findings were reported about whether a similar shift occurs in Tc1 and Tc2 [Maggi et al, ; Bogner et al, ; Gulzar et al, ]. Therefore, this study focused on the dynamic changes of Th1, Th2, Tc1, and Tc2 in HIV/AIDS patients before and after HAART, and their relationship with oral and systemic opportunistic infections.…”

Section: Introductionmentioning

confidence: 79%

“…Some have claimed that no Tc1/Tc2 shift was detected during early or late stages of HIV infection in their study [Bogner et al, ; Onlamoon et al, ]. Some researchers have even asserted that HIV‐1 infection protected against a Tc1‐to‐Tc2 shift and caused increased Tc1 differentiation in CD8 + T cells [Gulzar et al, ]. The discrepant results reported might be associated with gating strategies that were not completely equivalent.…”

Section: Discussionmentioning

confidence: 99%

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Dynamics of T-cell subsets and their relationship with oral and systemic opportunistic infections in HIV/AIDS patients during the first year of HAART in Guangxi, China

et al. 2015

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To analyze the dynamic changes in Th1, Th2, Tc1, and Tc2 of HIV/AIDS patients during the first year of highly active antiretroviral therapy (HAART) and to explore their relationship with oral and systemic opportunistic infections, a cohort study was carried out among HIV/AIDS patients in Guangxi, China. Ninety HIV/AIDS patients and 30 healthy controls (HC) were included. The enrolled HIV/AIDS patients were examined at baseline and after 3, 6, and 12 months of HAART. On each visit, oral and systemic opportunistic infections were recorded, oral Candida load and plasma viral load (VL) were counted, differential T-cell counts and flow cytometric analysis of T-cell subsets were performed. During the first year of HAART, the total number of opportunistic infections decreased steadily with the change in oral candidiasis (OC) most representatively. A significant Th1→Th2 switch (Th1/Th2 ratio 0.23 ± 0.12, HC 1.45 ± 0.38) and slight Tc1→Tc2 shift (Tc1/Tc2 ratio 0.93 ± 0.29, HC 1.13 ± 0.33) were found at baseline, and both received slow mitigation after HAART. LgCFU and clinical OC were correlated positively with both LgVL and clinical stage (P < 0.05) at baseline. LgCFU was also correlated positively with clinical stage at all four time points (P < 0.05). In multiple factor analysis, Th1 was confirmed to be correlated negatively with LgVL (Std.B = -0.295, P = 0.025) and LgCFU (Std.B = -0.227, P < 0.001) at baseline. After HAART, LgCFU and clinical stage were only correlated negatively with CD4 when all factors were included. These results suggest that oral candidiasis and oral Candida load could be useful clinical markers in the evaluation of HIV/AIDS patients. Th1 may play an important role against oral and systemic opportunistic infections. Tc1 and Tc2 both showed positive roles in the control of viremia without HAART. J. Med. Virol. 87:1158-1167, 2015. © 2015 Wiley Periodicals, Inc.

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Section: Introductionmentioning

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Dynamics of T-cell subsets and their relationship with oral and systemic opportunistic infections in HIV/AIDS patients during the first year of HAART in Guangxi, China

et al. 2015

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“…Summarizing, CD4 T cells can be divided into functionally polarized subsets based on the cytokines they produce: Th1 cells produce mainly type 1 cytokines, including interferon-gamma (IFN-γ) and interleukin-2 (IL-2), and promote cell-mediated immune responses, whereas Th2 cells secrete type 2 cytokines, including IL-4, IL-5, IL-6, IL-10, and IL-13, and enhance humoral immune responses [14], [15], [16]. Moreover, a similar cytokine secretion pattern has been observed for CD8 cytotoxic T cells that are designated Tc1 and Tc2 cells [14], [15], [17], [18]. In particular, CC chemokine receptor (CCR) 5 and CXC chemokine receptor (CXCR) 3 are usually associated with a Th1 phenotype, while Th2-associated chemokine receptor CCR2 and CCR4 have been reported [19].…”

Section: Introductionmentioning

confidence: 87%

Regulation of Inflammatory Chemokine Receptors on Blood T Cells Associated to the Circulating Versus Liver Chemokines in Dengue Fever

et al. 2012

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Little is known about the role of chemokines/chemokines receptors on T cells in natural DENV infection. Patients from DENV-2 and -3- outbreaks were studied prospectively during the acute or convalescent phases. Expression of chemokine receptor and activation markers on lymphocyte subpopulations were determined by flow cytometry analysis, plasma chemokine ligands concentrations were measured by ELISA and quantification of CCL5/RANTES + cells in liver tissues from fatal dengue cases was performed by immunochemistry. In the acute DENV-infection, T-helper/T-cytotoxic type-1 cell (Th1/Tc1)-related CCR5 is significantly higher expressed on both CD4 and CD8 T cells. The Th1-related CXCR3 is up-regulated among CD4 T cells and Tc2-related CCR4 is up-regulated among CD8 T cells. In the convalescent phase, all chemokine receptor or chemokine ligand expression tends to reestablish control healthy levels. Increased CCL2/MCP-1 and CCL4/MIP-1β but decreased CCL5/RANTES levels were observed in DENV-patients during acute infection. Moreover, we showed an increased CD107a expression on CCR5 or CXCR3-expressing T cells and higher expression of CD29, CD44 HIGH and CD127 LOW markers on CCR4-expressing CD8 T cells in DENV-patients when compared to controls. Finally, liver from dengue fatal patients showed increased number of cells expressing CCL5/RANTES in three out of four cases compared to three death from a non-dengue patient. In conclusion, both Th1-related CCR5 and CXCR3 among CD4 T cells have a potential ability to exert cytotoxicity function. Moreover, Tc1-related CCR5 and Tc2-related CCR4 among CD8 T cells have a potential ability to exert effector function and migration based on cell markers evaluated. The CCR5 expression would be promoting an enhanced T cell recruitment into liver, a hypothesis that is corroborated by the CCL5/RANTES increase detected in hepatic tissue from dengue fatal cases. The balance between protective and pathogenic immune response mediated by chemokines during dengue fever will be discussed.

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“…However, Th1 cytokines, such as interferon-gamma (IFN-γ), IL-2, and tumor necrosis factors (TNFs), can be elicited in certain circumstances, such as with cytomegalovirus (CMV) infection or BCG vaccine [17], or in certain cytokine milieus [18–21]. Both HIV and pregnancy are characterized by alterations in Th1, Th2, and Th17 cytokines [22,23], and HIV infection may cause a Tc2-to-Tc1 bias [24] that may alter neonatal antigen responses in exposed, uninfected neonates [25]. …”

Section: Introductionmentioning

confidence: 99%

In-utero exposure to maternal HIV infection alters T-cell immune responses to vaccination in HIV-uninfected infants

Kidzeru

Hesseling

Passmore

et al. 2014

Aids

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Objective In sub-Saharan Africa, HIV-exposed uninfected (HEU) infants have higher morbidity and mortality than HIV-unexposed infants. To evaluate whether immune dysfunction contributes to this vulnerability of HEU infants, we conducted a longitudinal, observational cohort study to assess T-cell immune responses to infant vaccines (Mycobacterium bovis BCG and acellular pertussis) and staphylococcal enterotoxin B (SEB). In total, 46 HEU and 46 HIV-unexposed infants were recruited from Khayelitsha, Cape Town. Methods Vaccine-specific T-cell proliferation (Ki67 expression) and intracellular expression of four cytokines [interferon-γ, interleukin (IL)-2, IL-13 and IL-17] were measured after whole blood stimulation with antigens at 6 and 14 weeks of age. Results HEU infants demonstrated elevated BCG-specific CD4+ and CD8+ T-cell proliferative responses at 14 weeks (P = 0.041 and 0.002, respectively). These responses were significantly increased even after adjusting for birth weight, feeding mode and gestational age. Similar to BCG, increased CD4+ and CD8+ T-cell proliferation was evident in response to SEB stimulation (P = 0.004 and 0.002, respectively), although pertussis-specific T cells proliferated comparably between the two groups. Within HEU infants, maternal CD4+ cell count and length of antenatal antiretroviral exposure had no effect on T-cell proliferation to BCG or SEB. HIV exposure significantly diminished measurable cytokine polyfunctionality in response to BCG, Bordetella pertussis and SEB stimulation. Conclusion These data show for the first time, when adjusting for confounders, that exposure to HIV in utero is associated with significant alterations to CD4+ and CD8+T-cell immune responses in infants to vaccines and nonspecific antigens.

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Human immunodeficiency virus-1 infection protects against a Tc1-to-Tc2 shift in CD8+ T cells

Cited by 7 publications

References 48 publications

Dynamics of T-cell subsets and their relationship with oral and systemic opportunistic infections in HIV/AIDS patients during the first year of HAART in Guangxi, China

Dynamics of T-cell subsets and their relationship with oral and systemic opportunistic infections in HIV/AIDS patients during the first year of HAART in Guangxi, China

Regulation of Inflammatory Chemokine Receptors on Blood T Cells Associated to the Circulating Versus Liver Chemokines in Dengue Fever

In-utero exposure to maternal HIV infection alters T-cell immune responses to vaccination in HIV-uninfected infants

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