In early HIV infection, host expression of the protective HLA-B*81 allele was associated with lower RC (<i>P</i> = 0.05), as was expression of HLA-B*07 (<i>P</i> = 0.02), suggesting early immune-driven attenuation of RT-integrase by these alleles.
A similar scenario is observed in humans where the expression of HLA-B*27 or HLA-B*57 has been linked to slow or no progression to AIDS after HIV infection.
The reduction in LPS-induced IL-12 p40 protein and mRNA following acute in vitro HIV infection of THP-1 cells and monocytes was not attributed to IL-10 or TGF-beta activity and was not restored by priming with IL-4, IL-13, or IFN-gamma.
Aberrant antigen presentation by antigen-presenting cells (APCs) that exhibit increased B7-H1 expression and IL-10 production in HIV infection could be responsible for T-lymphocyte unresponsiveness and loss of protective immunity.
Similarly, the CCR2b ligands MCP-1 and MCP-3 inhibit productive infection of PBMCs by both CCR5- and CXCR4-dependent strains of HIV-1, suggesting that expression of the MCP-1 chemokine may affect HIV infection via signaling through the CCR2 receptor and subsequent desensitization of the CCR5 and/or CXCR4 signaling pathway.
Genetic polymorphisms in the IL-10 gene promoter that lead to decreased IL-10 expression have been associated with more rapid disease progression in late stages of HIV infection, suggesting that the anti-inflammatory effects of IL-10 may be protective in the setting of chronic immune activation.
Gamma interferon and interleukin-10 (IL-10) mRNA expression in tuberculosis patients with or without human immunodeficiency virus infection was high, whereas IL-4 expression in the same patients was low.
We therefore cannot recommend at this time the use of plasma MBL levels or MBL2 genetic variants as a prognostic marker in HIV infection, disease progression, and survival in this adult population in Africa.
As a result, CD4+ T cells generally lack effector functions in LNs, including cytolytic capacity and IFNγ and β-chemokine expression, even in HIV elite controllers and during acute/early HIV infection.
Within individuals, CD8 T cells showed the highest IFN-gamma expression regardless of HIV status, which suggests that HIV infection enhances the IFN-gamma gene expression in CD8 T cells rather than inducing a shift to and/or increasing expression of IFN-gamma mRNA in other cell types.
In addition, because human immunodeficiency virus (HIV) infection in vivo and in vitro has been shown to dysregulate the production of and/or the response to cytokines, PBMCs from both healthy uninfected and HIV-infected individuals were studied for their constitutive and IL-6-induced expression of MCP-1.
Increased IL-10 levels have been observed during HIV infection and IL-10 blockade has been shown to enhance T-cell function in some HIV-infected subjects.
We suggest that dysfunctional naive CD8(low) T cells are generated as a result of IFNα-mediated up-regulation of MHC-I on stromal cells in the thymus and antigen-presenting cells in the periphery, and that dysfunction in this naive compartment contributes to the immunodeficiency of HIV disease.
Increased expression of IFN-gamma genes in CD4 T cells, however, indicates that these cells may be responsible for substantial amounts of circulating IFN-gamma that occur in HIV infection.
Increased levels of interferon-gamma (IFN-gamma), IL-4 and transforming growth factor-beta (TGF-beta) mRNA expressing blood mononuclear cells in human HIV infection.
Therefore, we analysed the regulation of B7 expression by cytokines, namely IL-10 and tumour necrosis factor-alpha (TNF-alpha), the production of which is enhanced in HIV infection and have similar inhibitory effects on B7 expression.
SDF-1 activates two G protein-coupled receptors, CXCR4 and CXCR7; these are expressed in both developing and mature CNSs and participate in multiple physiological and pathological events, e.g., inflammatory response, neurogenesis, angiogenesis, hematopoiesis, cancer metastasis, and HIV infection.
This review highlights these results and explores the ways in which HLA-C surface expression could affect immune system function in the setting of HIV disease.
In the CD4 T cells, on a per-cell basis, the mean mRNA levels of IFN-gamma, IL-10, and TNF-alpha were increased substantially (p < 0.001) in HIV infection.
Although polymorphisms of chemokine genes (SDF1, stromal cell-derived factor-1 and RANTES, regulated on activation, normal T cell expressed and secreted) and chemokine-receptor genes (CCR5, CCR2, CX(3)CR1) were shown to be associated with sensitivity to HIV infection and untreated HIV disease progression, their association with the response to highly active antiretroviral therapy (HAART) remains unclear.