Quantification of Complement C5b-9 Binding to Cells by Flow Cytometry

Moskovich, Oren; Fishelson, Zvi

doi:10.1007/978-1-62703-724-2_8

Cited by 9 publications

(5 citation statements)

References 29 publications

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“…Of note, surface-attached C5b-9 complexes are sensitive to trypsin. 37 Thus, after trypsinization, EA.hy926 cells were recovered in cell culture medium at 37°C for 30 minutes 38 and then treated with PIPLC (0.4 U/mL) for 30 minutes at 37°C.…”

Section: Flow Cytometry Analysis Of C5b-9 Depositionmentioning

confidence: 99%

Modified Ham test for atypical hemolytic uremic syndrome

Gavriilaki¹,

Yuan²,

Ye³

et al. 2015

Blood

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Section: Flow Cytometry Analysis Of C5b-9 Depositionmentioning

confidence: 99%

Modified Ham test for atypical hemolytic uremic syndrome

Gavriilaki¹,

Yuan²,

Ye³

et al. 2015

Blood

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“…Reverse genetics A/X-31 (PR8-HK4 and 6) were used as model viruses. Reverse genetics derived chimeric PR8 containing the segment 4 from A/Hong Kong/1/1968, seg4-HK68 (PR8-HK4), or the segment 6 (PR8-HK6) were produced as previously described 54 – 56 . pDual plasmids were a kind gift from Dr. Ron Fouchier (Erasmus MC, Netherlands).…”

Section: Methodsmentioning

confidence: 99%

CD8+ tissue-resident memory T-cell development depends on infection-matching regulatory T-cell types

Barros,

Piontkivska,

Figueiredo-Campos

et al. 2023

Nat Commun

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Immunological memory is critical for immune protection, particularly at epithelial sites, which are under constant risk of pathogen invasions. To counter invading pathogens, CD8+ memory T cells develop at the location of infection: tissue-resident memory T cells (TRM). CD8+ T-cell responses are associated with type-1 infections and type-1 regulatory T cells (TREG) are important for CD8+ T-cell development, however, if CD8+ TRM cells develop under other infection types and require immune type-specific TREG cells is unknown. We used three distinct lung infection models, to show that type-2 helminth infection does not establish CD8+ TRM cells. Intracellular (type-1) and extracellular (type-3) infections do and rely on the recruitment of response type-matching TREG population contributing transforming growth factor-β. Nevertheless, type-1 TREG cells remain the most important population for TRM cell development. Once established, TRM cells maintain their immune type profile. These results may have implications in the development of vaccines inducing CD8+ TRM cells.

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“…C5b-9 deposition measurement was adapted from (103). Lentivirus encoding NA-GFP WT/E229A was added to A549 cells.…”

Section: Methodsmentioning

confidence: 99%

Complement Decay-Accelerating Factor is a modulator of influenza A virus lung immunopathology

Santos

Silva

Gomes

et al. 2021

Preprint

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Clearance of viral infections, such as SARS-CoV-2 and influenza A virus (IAV), must be fine-tuned to eliminate the pathogen without causing immunopathology. As such, an aggressive initial innate immune response favors the host in contrast to a detrimental prolonged inflammation. The complement pathway bridges innate and adaptive immune system and contributes to the response by directly clearing pathogens or infected cells, as well as recruiting proinflammatory immune cells and regulating inflammation. However, the impact of modulating complement activation in viral infections is still unclear. In this work, we targeted the complement decay-accelerating factor (DAF/CD55), a surface protein that protects cells from non-specific complement attack, and analyzed its role in IAV infections. We found that DAF modulates IAV infection in vivo, via an interplay with the antigenic viral proteins hemagglutinin (HA) and neuraminidase (NA), in a strain specific manner. Our results reveal that, contrary to what could be expected, DAF potentiates complement activation, increasing the recruitment of neutrophils, monocytes and T cells. We also show that viral NA acts on the heavily sialylated DAF and propose that it exacerbates complement activation, leading to lung immunopathology. Remarkably, this mechanism has no impact on viral loads but rather on the host resilience to infection and may have direct implications in zoonotic influenza transmissions.

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Quantification of Complement C5b-9 Binding to Cells by Flow Cytometry

Cited by 9 publications

References 29 publications

Modified Ham test for atypical hemolytic uremic syndrome

Modified Ham test for atypical hemolytic uremic syndrome

CD8+ tissue-resident memory T-cell development depends on infection-matching regulatory T-cell types

Complement Decay-Accelerating Factor is a modulator of influenza A virus lung immunopathology

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