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Author Topic: CD8 cells LTNP longterm nonprogrssrs Chinese prove new therapeutic option  (Read 7300 times)

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Offline bimazek

  • Member
  • Posts: 781
I just read thru 500 of the 5280 new articles that have HIV in the title... published in 2007

found many interesting things...

Chinese in Bejing building on harvard breakthrough prove that LTNP is because of the CD8 cells...
have special quality to their CD8 killer cells...

Blocking PD-1/PD-L1 pathway may represent a new therapeutic option for this disease.
looks like they just proved that CD8 cells in LTNP long-term non-progressors  are somehow , well they do not have this immunoreceptor PD-1 upregulated on CD8(+) T cells so their CD8 cells do not become exhausted

LTNP exhibited functional HIV-specific memory CD8(+) T cells with lower PD-1 expression.

Progressors showed up-regulated PD-1 expression correlated with a reduction in CD4 T-cell number and an elevation in plasma viral load.

Importantly, PD-1 upregulation was also associated with reduced perforin and IFN-gamma production, as well as decreased HIV-specific effector memory CD8(+) T-cell proliferation in TP but not LTNP individuals.

Blocking PD-1/PD-L1 interactions efficiently restored HIV-specific CD8(+) T-cell effector function and proliferation. Taken together, these findings confirm the hypothesis that high PD-1 upregulation mediates HIV-specific CD8(+) T-cell exhaustion. Blocking PD-1/PD-L1 pathway may represent a new therapeutic option for this disease, and provide more insight into immune pathogenesis in LTNP individuals

Chinese in Bejing... have you seen asian arab new buildings.... makes USA look like a slum

1: Blood. 2007 Feb 1; [Epu
    PD-1 upregulation is correlated with HIV-specific memory CD8+ T-cell exhaustion in typical progressors, but not in long-term non-progressors.

        * Zhang JY,
        * Zhang Z,
        * Wang X,
        * Fu JL,
        * Yao J,
        * Jiao Y,
        * Chen L,
        * Zhang H,
        * Wei J,
        * Jin L,
        * Shi M,
        * Gao GF,
        * Wu H,
        * Wang FS.

    Institute of Microbiology, Chinese Academy of Sciences (CAS), Beijing, China.

    The immunoreceptor PD-1 is significantly upregulated on exhausted CD8(+) T cells during chronic viral infections like HIV-1. However, it remains unknown whether PD-1 expression on CD8(+) T cells differs between typical progressors (TP) and long-term non-progressors (LTNP). In this report, we examined PD-1 expression on HIV-specific CD8(+) T cells from 63 adults with chronic HIV infection. We found that LTNP exhibited functional HIV-specific memory CD8(+) T cells with markedly lower PD-1 expression. TP, in contrast, showed significantly up-regulated PD-1 expression that was closely correlated with a reduction in CD4 T-cell number and an elevation in plasma viral load. Importantly, PD-1 upregulation was also associated with reduced perforin and IFN-gamma production, as well as decreased HIV-specific effector memory CD8(+) T-cell proliferation in TP but not LTNP individuals. Blocking PD-1/PD-L1 interactions efficiently restored HIV-specific CD8(+) T-cell effector function and proliferation. Taken together, these findings confirm the hypothesis that high PD-1 upregulation mediates HIV-specific CD8(+) T-cell exhaustion. Blocking PD-1/PD-L1 pathway may represent a new therapeutic option for this disease, and provide more insight into immune pathogenesis in LTNP individuals


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17272504&dopt=Citation

Offline bimazek

  • Member
  • Posts: 781
this is important because if they can coax the CD8 cells to turn back on... then the body can naturally fight off the hiv and supress it completely

Offline Customer

  • Member
  • Posts: 98
I think you're right bimazek. They key in eradicating HIV from the body is in boosting the body's own autoimmune system.
It is practically impossible to kill out all the millions of viruses in thye gut through means of HAART, and if bodys own autoimmunen system remains vulnerable to the virus attack, re-infection will be persistent.





Offline LPinUK

  • Member
  • Posts: 58
Re: CD8 cells LTNP longterm nonprogrssrs Chinese prove new therapeutic option
« Reply #3 on: September 01, 2007, 11:54:52 am »
You read through 500 articles?  wow, i dont know how you have the time !!
Diagnosed Poz September 2003, Current Regimen Truvada & Sustiva.

Offline Miss Philicia

  • Member
  • Posts: 24,793
  • celebrity poster, faker & poser
Re: CD8 cells LTNP longterm nonprogrssrs Chinese prove new therapeutic option
« Reply #4 on: September 01, 2007, 12:05:31 pm »
You read through 500 articles?  wow, i dont know how you have the time !!

Thanks for pointing this out.  I think I will have to put this thread in a special notation file marked "bim".
"I’ve slept with enough men to know that I’m not gay"

Offline thunter34

  • Member
  • Posts: 7,374
  • His name is Carl.
Re: CD8 cells LTNP longterm nonprogrssrs Chinese prove new therapeutic option
« Reply #5 on: September 01, 2007, 12:26:04 pm »
I just read thru 500 of the 5280 new articles that have HIV in the title... published in 2007

found many interesting things...

Chinese in Bejing building on harvard breakthrough prove that LTNP is because of the CD8 cells...
have special quality to their CD8 killer cells...

Blocking PD-1/PD-L1 pathway may represent a new therapeutic option for this disease.
looks like they just proved that CD8 cells in LTNP long-term non-progressors  are somehow , well they do not have this immunoreceptor PD-1 upregulated on CD8(+) T cells so their CD8 cells do not become exhausted

LTNP exhibited functional HIV-specific memory CD8(+) T cells with lower PD-1 expression.

Progressors showed up-regulated PD-1 expression correlated with a reduction in CD4 T-cell number and an elevation in plasma viral load.

Importantly, PD-1 upregulation was also associated with reduced perforin and IFN-gamma production, as well as decreased HIV-specific effector memory CD8(+) T-cell proliferation in TP but not LTNP individuals.

Blocking PD-1/PD-L1 interactions efficiently restored HIV-specific CD8(+) T-cell effector function and proliferation. Taken together, these findings confirm the hypothesis that high PD-1 upregulation mediates HIV-specific CD8(+) T-cell exhaustion. Blocking PD-1/PD-L1 pathway may represent a new therapeutic option for this disease, and provide more insight into immune pathogenesis in LTNP individuals

    The immunoreceptor PD-1 is significantly upregulated on exhausted CD8(+) T cells during chronic viral infections like HIV-1. However, it remains unknown whether PD-1 expression on CD8(+) T cells differs between typical progressors (TP) and long-term non-progressors (LTNP). In this report, we examined PD-1 expression on HIV-specific CD8(+) T cells from 63 adults with chronic HIV infection. We found that LTNP exhibited functional HIV-specific memory CD8(+) T cells with markedly lower PD-1 expression. TP, in contrast, showed significantly up-regulated PD-1 expression that was closely correlated with a reduction in CD4 T-cell number and an elevation in plasma viral load. Importantly, PD-1 upregulation was also associated with reduced perforin and IFN-gamma production, as well as decreased HIV-specific effector memory CD8(+) T-cell proliferation in TP but not LTNP individuals. Blocking PD-1/PD-L1 interactions efficiently restored HIV-specific CD8(+) T-cell effector function and proliferation. Taken together, these findings confirm the hypothesis that high PD-1 upregulation mediates HIV-specific CD8(+) T-cell exhaustion. Blocking PD-1/PD-L1 pathway may represent a new therapeutic option for this disease, and provide more insight into immune pathogenesis in LTNP individuals



And knick-knack paddy-whack give a dog a bone.   

What the heck does all this mean??  I must be REALLY stupid.


And philly, like I said....that ''500" must be a mistake.   I'm sure he just forgot to add the last "0".
« Last Edit: September 01, 2007, 12:30:06 pm by thunter34 »
AIDS isn't for sissies.

Offline Cerrid

  • Member
  • Posts: 500
  • only as good as your last haircut
Re: CD8 cells LTNP longterm nonprogrssrs Chinese prove new therapeutic option
« Reply #6 on: September 01, 2007, 12:58:43 pm »
That's what I understand: HIV switches off the immune T killer cells which would otherwise destroy it. The switch is called 'programmed death-1" (PD-1), for some reason. By masking this switch with a drug, it's possible to get the killer cells back alive and kicking, so they can attack the virus themselves. It works in the test tube. However, activating killer cells in the body might cause other problems like autoimmune reactions, but it's still something worth investigating.

As for the 500 studies... that was already on March 30th. We're way beyond now.

"Boredom is always counterrevolutionary. Always." (Guy Debord)

Offline sunzidog

  • Member
  • Posts: 19
Re: CD8 cells LTNP longterm nonprogrssrs Chinese prove new therapeutic option
« Reply #7 on: September 01, 2007, 10:35:59 pm »
Thanks, Bimazek for the great info!
Infected 01/02/07
03/07: VL<3800 CD4s 506 (Started Atripla)
04/07: VL<500 CD4s 585
05/07: VL<500 CD4s 606
07/07: VL<50 CD4s 1000

Offline bimazek

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  • Posts: 781
Re: CD8 cells LTNP longterm nonprogrssrs Chinese prove new therapeutic option
« Reply #8 on: September 05, 2007, 01:54:53 pm »
the receptor is called 'programmed death-1" (PD-1), because when they first noticed it they found it in cells that were in the process of self distruction, later after they named it they realized that it is more of a high med low switch that just happens to be more visible when a cell is going thru programmed death or self distruction -- cells do this all the time

at first they thought it was the self distruct switch but now they know it is not

many receptors have many different names


Offline bimazek

  • Member
  • Posts: 781
Re: CD8 cells LTNP longterm nonprogrssrs Chinese prove new therapeutic option
« Reply #9 on: September 05, 2007, 02:00:33 pm »

in the last two weeks so new science disputes have errupted between some scientists that say they have proven that it is only when the CD4 cell is infected by two variants (i wont even say strains - that is too broad, and we are not talking about co infection) but two slight varients of the same strain that the real disasterous fall of CD4 cells happens.  for exmaple when the cd4s drop from 300 to 200 then rapidly from 200 down to much lower, the end phase, some science says it is 

only when the CD4 cell is infected by two variants

other science says that other factors, basically they are not sure

and these are scientists that are also not studying pd-1 so in the end it could be a new theory or new model of why the cliff of cd4s happens

we do know that there are still tons of cd4s left but

cd8s are disfunctional





 


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