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Reduced CD4 type 1 cytokine response by HIV-1 transgenic rat may be correlated with increased SOCS-1 expression from dendritic cells

Suppressor of cytokine signaling-1 (SOCS-1) is an inducible negative regulator of the JAK/STAT signal pathway; SOCS-1 is expressed in dendritic cells (DCs) and negatively regulates activation and type 1 regulatory cytokine production. Infection with human immunodeficiency virus type 1 (HIV-1) results in cytokine dysregulation by DCs. Since effector/memory formation depends upon clonal expansion of naïve T cells following the initial encounter with antigen and since cytokines play a critical role in the initiation and regulation of immune responses by DCs, events that negatively affect antigen presentation, co-stimulation and cytokine production by DCs can also negatively affect T cell immune responses. We have earlier reported that HIV-1 transgenic rats have defects in type 1 cytokine production, type 1 cytokine responses and generation of effector/memory CD4 T cell subsets. Here we show that BMDC from HIV-1 transgenic rats express significantly elevated levels of IL10 and reduced levels of IL-12 proteins in addition to elevated SOCS-1 mRNA following stimulation with lipolysaccharide (LPS) compared to age matched controls. These results suggest that elevated levels of SOCS-1 in DCs may negatively regulate type 1 cytokine production leading to dysregulation of T helper 1 responses reported in the HIV-1 transgenic rat.

Acknowledgements

NIH-NIAID R01-A163171.

Author information

Correspondence to William C Reid.

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Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution 2.0 International License (https://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Keywords

  • Human Immunodeficiency Virus
  • Dendritic Cell
  • Cytokine Production
  • Antigen Presentation
  • Cell Subset