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 HIV-1 infection of IFN-α expression was inhibited

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yoxi5236



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Join date : 2012-03-30

PostSubject: HIV-1 infection of IFN-α expression was inhibited    Wed May 23, 2012 3:07 am

Although interferon alpha (IFN-alpha) incremental generation phenomenon was found in HIV-1 infected individuals, circulating plasma cells, dendritic cells (PDC), the ligand of the Toll-like receptor activation reaction is essentially damaged. The researchers found that DPP7 HIV-1 infected individuals CD4 + T cells less than 500/μl, but the reason for this lack of functional PDC is still uncertain. Recently, the German national retroviral Barbara Schmidt and his colleagues study: chronic immune activation in the HIC-1 infection, at least in part, by increased CD40 and CD40L interaction to weaken the innate immune response of peripheral PDC. The research is published in DPP8 the March 21 Public Library of Science • Comprehensive "(Consolidation) of the Public Library of Science.


Interferon (IFN) is a broad-spectrum antiviral agents, are not directly kill or inhibit the virus, but mainly through cell surface receptors causes cells to produce anti-viral proteins, thus inhibiting the replication of the hepatitis B virus; but can also enhance the natural killer cells (NK cells), macrophages and T lymphocytes, vitality, and thus play an DPP9 immunomodulatory role and enhance the antiviral activity of interferon is a group activity of the protein has multiple functions (mainly glycoproteins) is a cytokines produced by monocytes and lymphocytes. In the same cell has a broad-spectrum antiviral, cell growth and differentiation, immune function and a variety of biological activity.

The researchers provided evidence that, around the HIV-1 infection of IFN-α generated by the interaction of CD40 ligand (CD40L) enhanced active suppression, and CD40L receptor CD40 by immune activation has been raised. Did not receive any treatment of DR1 HIV-1 infected individuals Soluble CD40L plasma levels significantly higher than the long-term individuals receiving antiretroviral therapy (n = 62, p <0.03), while the level in the uninfected control group ( n = 16, p <0.001). The same time, in the HIV-1 infected persons, the cell-associated CD40L and the expression of the receptor CD40 on the PDC significant increase (p <0.05). Soluble and cell associated CD40L CpG polynucleotide dose dependent inhibition of DRAP1 IFN-α. Individual peripheral blood mononuclear cells (PBMC) in HIV-1 infection, compared with control group CD40L concentration (p <0.05), this inhibition was found lower. CpG induced IFN-α produced in HIV-1 infected PBMC directly with the PDC and CD4 + T cell count, and RP on the viral load (p <0.001). HIV-1 infection of CD4 + T cells less than 500/μl in patients, the percentage of CpG-induced IFN-alpha expression levels of CD40 expression PDC, as well as the level of CD40 expression in these cells (p <0.05) one correspondence.However, plasma levels of CD40L in this process is unimportant.

In addition, in contrast to the control group, low dose of CD40L promotes IL-6 and IL-8 in HIV-1 infection of PBMC enhanced expression. The data support this conclusion: chronic immune activation in the HIC-1 infection, at least in part, through the enhancement of CD40 and CD40L interaction to weaken the innate immune response of peripheral PDC

article sourceDPP7,DR1 ,DRAP1
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