Soluble membrane attack complex in the blood and cerebrospinal fluid of HIV-infected individuals, relationship to HIV RNA, and comparison with HIV negatives

Anderson, Albert M.; Schein, Theresa N.; Kalapila, Aley G.; Lai, Lillin; Waldrop‐Valverde, Drenna; Moore, Raeanne C.; Franklin, Donald; Letendre, Scott; Barnum, Scott R.

doi:10.1016/j.jneuroim.2017.07.014

Cited by 5 publications

(3 citation statements)

References 26 publications

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“…It may be speculated that subjects susceptible to VTE exhibit a certain pathophysiological milieu in the valvular sinuses, which makes them prone to complement activation and thereby development of VTE. Alternatively, other inflammatory conditions associated with increased plasma levels of TCC may be differentially distributed between subjects who will and will not develop VTE. However, because the inflammatory response, in our study assessed by plasma CRP levels, secondary to such conditions would be in the causal pathway between plasma TCC and VTE risk, it would be methodological incorrect to adjust for plasma CRP levels in the statistical analyses.…”

Section: Discussionmentioning

confidence: 99%

Complement activation assessed by the plasma terminal complement complex and future risk of venous thromboembolism

Høiland

Liang

Brækkan

et al. 2019

Journal of Thrombosis and Haemostasis

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Background: It remains uncertain whether activation of the complement system, assessed by the soluble terminal C5b-9 complement complex (plasma TCC), is associated with future risk of incident venous thromboembolism (VTE). Objectives:To investigate the association between plasma levels of TCC and future risk of incident VTE in a nested case-control study, and to explore genetic variants associated with TCC using protein quantitative trait loci analysis of exome sequencing data. Methods:We sampled 415 VTE cases and 848 age-and sex-matched controls from a population-based cohort, the Tromsø study. Logistic regression models were used to calculate odds ratios with 95% confidence intervals for VTE across quartiles of plasma levels of TCC. Whole exome sequencing was conducted using the Agilent SureSelect 50 Mb capture kit.Results: The risk of VTE increased across increasing quartiles of plasma TCC, particularly for unprovoked VTE. Participants with TCC in the highest quartile (>1.40 complement arbitrary units/mL) had an odds ratio for unprovoked VTE of 1.74 (95% confidence interval: 1.10-2.78) compared with those with TCC in the lowest quartile (≤0.80 complement arbitrary units/mL) in analyses adjusted for age, sex, and body mass index. A substantially higher risk for VTE was observed in samples taken shortly before VTE event. We found no association between genome-wide or complementrelated gene variants and plasma levels of TCC. Conclusions:We found that high levels of plasma TCC were associated with VTE risk, and unprovoked events in particular. There was no genome-wide association between gene variants and plasma levels of TCC. K E Y W O R D S complement system, protein quantitative trait loci analysis, terminal complement complex, venous thromboembolism, whole exome sequencing | 935 HØILAND et AL. S U PP O RTI N G I N FO R M ATI O N Additional supporting information may be found online in the Supporting Information section at the end of the article. How to cite this article: Høiland II, Liang RA, Braekkan SK, Pettersen K, Ludviksen JK, Latysheva N, et al. Complement activation assessed by the plasma terminal complement complex and future risk of venous thromboembolism. J Thromb Haemost. 2019;17:934-943. https ://doi.

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Section: Discussionmentioning

confidence: 99%

Complement activation assessed by the plasma terminal complement complex and future risk of venous thromboembolism

Høiland

Liang

Brækkan

et al. 2019

Journal of Thrombosis and Haemostasis

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“…As a result, normal levels of sMAC in CSF have frequently been derived from cohorts with “other neurological diseases” or from patients who underwent lumbar puncture as a part of standard clinical care and had negative bacterial cultures. In most studies using the Quidel sC5b-9 ELISA, CSF sMAC levels range from undetectable to the low nanogram/ml range (10–20 ng/ml) ( 130 , 142 , 144 , 172 , 173 ). Studies analyzing the sMAC CSF/serum quotient using Reiber–Felgenhauer nomograms of IgM suggest that sMAC is intrathecally produced rather than diffusing across the blood brain barrier (BBB) as has been shown for C9 ( 173 , 174 ).…”

Section: Introductionmentioning

confidence: 99%

Soluble Membrane Attack Complex: Biochemistry and Immunobiology

2020

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“…HIV-infected cells provide almost all resources and environments for HIV survival and generation, such as the storage of viral genes, expression of viral proteins, and packaging of viral particles. − Killing HIV-infected cells has been a crucial means for decreasing HIV production and inhibiting disease progress . Immune attacks from cytotoxic lymphocytes (CTLs), natural killer cells, and complement membrane attack complex play important roles in clearing HIV-infected cells in vivo. − Strikingly, HIV-specific CTLs can produce tumor necrosis factor alpha (TNF-α) to effectively induce the death of HIV-infected cells. − Given such an important role of CTLs-derived TNF-α, we hypothesize that developing a nanomaterial to facilitate CTL-derived TNF-α will significantly promote the death of HIV-infected cells.…”

mentioning

confidence: 99%

Amantadine Surface-Modified Silver Nanorods Improves Immunotherapy of HIV Vaccine Against HIV-Infected Cells

Balachandran

Hao

et al. 2018

ACS Appl. Mater. Interfaces

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Surface modifications can endow nanomaterials with presupposed immunoregulatory functions to optimize vaccine-induced immune responses. In this work, we modified an immunoregulatory molecule, amantadine (Ada), on the outermost layer of PVP-PEG-coated silver nanorods (Ada-PVP-PEG silver nanorods). Such Ada surface-modified silver nanorods promote HIV vaccine-triggered cytotoxic lymphocytes (CTLs) to produce around eightfold stronger tumor necrosis factor alpha (TNF-α) in vivo. The enhancement of HIV-specific CTL-derived TNF-α significantly facilitates the death of HIV-infected cells (from 28.86 to 84.19%) and reduces HIV production (around sixfold). This work supports the critical role of surface modifications of nanomaterials in fundamentally improving the immunotherapy of HIV vaccine against HIV-infected cells.

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Soluble membrane attack complex in the blood and cerebrospinal fluid of HIV-infected individuals, relationship to HIV RNA, and comparison with HIV negatives

Cited by 5 publications

References 26 publications

Complement activation assessed by the plasma terminal complement complex and future risk of venous thromboembolism

Complement activation assessed by the plasma terminal complement complex and future risk of venous thromboembolism

Soluble Membrane Attack Complex: Biochemistry and Immunobiology

Amantadine Surface-Modified Silver Nanorods Improves Immunotherapy of HIV Vaccine Against HIV-Infected Cells

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