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measure of immune system on interferon or gcmaf - il21 or trl7

this one is very very interesting since measure of interleuckin 21 is not complicated, maybe available at redlabs or europeanlaboratory

http://www.jci.org/articles/view/44198

this is also interesting but measuring trl7 is not something easy and available, but we may start to look for trl7 agonists even on natural substances or already available drugs

http://www.ihlpress.com/pdf%20files/bridging_presentations/Locarnini_aj_060906.pdf

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Avatar universal

another positive effect of maf 314 or frequent injections of gcmaf is nk cells rise/cd4 rise
a rise in nk cells has probably the effect of lowering il10, increase of interferon gamma which stops hbv replication and increase of il21 too

i will try if i can check this ipoteis on myself

it is also so stupid all research on hbv, we do know all cytokines and interferon to silence hbv abd we are still stuck with stupid interferon alpha/lambda which have marginal effects on hbv
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Avatar universal

another measure of immune suppression, IL-10, this can also be used to monitor gcmaf effect
CFS patients on gcmaf monitor cytokines at redlabs, i havent found IL21, probably not useful on CFS infection, but IL10 is monitored by them too because it is a general immune suppressive cytokine
i will see if i can have these measured at pisa research center free of charge otherwise i ll see if i can monitor at ELN holland

NK cells are enriched in the liver, constituting around a third of intrahepatic lymphocytes. We have previously demonstrated that they upregulate the death ligand TRAIL in patients with chronic hepatitis B virus infection (CHB), allowing them to kill hepatocytes bearing TRAIL receptors. In this study we investigated whether, in addition to their pathogenic role, NK cells have antiviral potential in CHB. We characterised NK cell subsets and effector function in 64 patients with CHB compared to 31 healthy controls. We found that, in contrast to their upregulated TRAIL expression and maintenance of cytolytic function, NK cells had a markedly impaired capacity to produce IFN-γ in CHB. This functional dichotomy of NK cells could be recapitulated in vitro by exposure to the immunosuppressive cytokine IL-10, which was induced in patients with active CHB. IL-10 selectively suppressed NK cell IFN-γ production without altering cytotoxicity or death ligand expression. Potent antiviral therapy reduced TRAIL-expressing CD56bright NK cells, consistent with the reduction in liver inflammation it induced; however, it was not able to normalise IL-10 levels or the capacity of NK cells to produce the antiviral cytokine IFN-γ. Blockade of IL-10 +/− TGF-β restored the capacity of NK cells from both the periphery and liver of patients with CHB to produce IFN-γ, thereby enhancing their non-cytolytic antiviral capacity. In conclusion, NK cells may be driven to a state of partial functional tolerance by the immunosuppressive cytokine environment in CHB. Their defective capacity to produce the antiviral cytokine IFN-γ persists in patients on antiviral therapy but can be corrected in vitro by IL-10+/− TGF-β blockade.
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Avatar universal

my guess is infected cells produces nagalase this blocks macrophages to detect cccdna inside them and repair human dna from cccdna or finish to destroy all infected cells
the resolving hbv is made by no rise of alt during hbvdna decrease, interferon gamma and others make the job without killing infected cells.once there is no hbvdna starts the alt rise a lot and hbsag goes down too
in cronic hbv it is not working this way there is a lot of cells killing but no decrease in hbsag

as you can see it menthions catechins in a slide, catechines are produced by vit d3
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Avatar universal
Intersting slides from Stephan Locarnini, wish we can have  the accompanying text as well. Too hard to understand for me. One thing that bothers me is:

Why our immune system seems to stop clearing infected liver cells when hbvdna decreases (as indicated by accompanying decrease in ALT)?
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these articles are from 2000 periods, i wounder why they are trying interlekin 7 if we know i-21 works
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC136645/

Interleukin-18 Inhibits Hepatitis B Virus Replication in the Livers of Transgenic Mice†
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Avatar universal
The induced IL-21 levels in CD4(+) T cells of peripheral blood from the different clinical types of patients infected with hepatitis B virus].
[Article in Chinese]
Ding YR, Zhang Y, Lian JQ, Li XH, Wang LX, Huang CX.
Source
Center of Infectious Diseases, Tangdu Hospital, Fourth Military Medical University, Xi'an 710038, China. ***@****
Abstract
AIM:
To investigate the levels of interleukin (IL)-21 in CD4(+);T cells of peripheral blood from the different types of patients infected with hepatitis B virus (HBV) and elucidate its role in the hepatitis B pathogenesis.

METHODS:
Peripheral blood mononuclear cells (PBMCs) from the patients infected with HBV and healthy individuals were stimulated with or without PMA coupled with ionomycin. The levels of IL-21 in CD4(+) T cells and Th17 cells were analyzed by flow cytometry.

RESULTS:
PMA and ionomycin induced the expression of IL-21, and IL-21 was mainly produced by CD4(+); T cells, but IL-17A(+) IL-21(+) CD4(+) T cells were not detected. The frequencies of IL-21(+) CD4(+) T cells in the patients of acute hepatitis B and chronic asymptomatic HBV carriers were higher than in healthy controls and severe chronic hepatitis B patients; there were no remarkable differences in the proportion of Th17 cells among the different groups of patients. Furthermore, the proportion of IL-21(+) CD4(+) T cells correlated with Th17 cells in all groups except for the acute hepatitis B patients.

CONCLUSION:
IL-21 levels, which correlated with Th17 cells, were different in CD4(+);T cells from the different types of patients infected with hepatitis B virus (HBV). The results showed that IL-21 may play a role in the hepatitis B pathogenesis.
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