scholarly journals Mucosal Th17 Cell Function Is Altered during HIV Infection and Is an Independent Predictor of Systemic Immune Activation

2013 ◽  
Vol 191 (5) ◽  
pp. 2164-2173 ◽  
Author(s):  
Connie J. Kim ◽  
Lyle R. McKinnon ◽  
Colin Kovacs ◽  
Gabor Kandel ◽  
Sanja Huibner ◽  
...  
Keyword(s):  
Hiv Infection ◽  
Immune Activation ◽  
Th17 Cell ◽  
Cell Function ◽  
Independent Predictor ◽  
Systemic Immune Activation

scholarly journals Gut Leakage of Fungal‐Related Products: Turning Up the Heat for HIV Infection

2021 ◽  
Vol 12 ◽  
Author(s):  
Stéphane Isnard ◽  
John Lin ◽  
Simeng Bu ◽  
Brandon Fombuena ◽  
Léna Royston ◽  
...  
Keyword(s):  
Hiv Infection ◽  
Immune Activation ◽  
Cell Function ◽  
Experimental Treatment ◽  
Intestinal Epithelial ◽  
Barrier Dysfunction ◽  
Gut Leakage ◽  
Microbial Products ◽  
Treatment Responses

The intestinal epithelial layer serves as a physical and functional barrier between the microbiota in the lumen and immunologically active submucosa. Th17 T-cell function protects the gut epithelium from aggression from microbes and their by-products. Loss of barrier function has been associated with enhanced translocation of microbial products which act as endotoxins, leading to local and systemic immune activation. Whereas the inflammatory role of LPS produced by Gram-negative bacteria has been extensively studied, the role of fungal products such as β-D-glucan remains only partially understood. As HIV infection is characterized by impaired gut Th17 function and increased gut permeability, we critically review mechanisms of immune activation related to fungal translocation in this viral infection. Additionally, we discuss markers of fungal translocation for diagnosis and monitoring of experimental treatment responses. Targeting gut barrier dysfunction and reducing fungal translocation are emerging strategies for the prevention and treatment of HIV-associated inflammation and may prove useful in other inflammatory chronic diseases.

scholarly journals Systemic Immune Activation in HIV Infection Is Associated with Decreased MDC Responsiveness to TLR Ligand and Inability to Activate Naive CD4 T-Cells

PLoS ONE ◽  
2011 ◽  
Vol 6 (9) ◽  
pp. e23884 ◽  
Author(s):  
Nicole L. Yonkers ◽  
Benigno Rodriguez ◽  
Robert Asaad ◽  
Michael M. Lederman ◽  
Donald D. Anthony
Keyword(s):  
T Cells ◽  
Hiv Infection ◽  
Immune Activation ◽  
Cd4 T Cells ◽  
Systemic Immune Activation

scholarly journals Elevated Autotaxin and LPA Levels during Chronic Viral Hepatitis and Hepatocellular Carcinoma Associate with Systemic Immune Activation

Cancers ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 1867 ◽  
Author(s):  
Lenche Kostadinova ◽  
Carey L Shive ◽  
Donald D Anthony
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Disease ◽  
Hiv Infection ◽  
Immune Activation ◽  
Chronic Viral Hepatitis ◽  
Data Set ◽  
Fibrotic Liver ◽  
Direct Acting Antiviral ◽  
Systemic Immune Activation ◽  
Fibrotic Liver Disease

Circulating autotaxin (ATX) is elevated in persons with liver disease, particularly in the setting of chronic hepatitis C virus (HCV) and HCV/HIV infection. It is thought that plasma ATX levels are, in part, attributable to impaired liver clearance that is secondary to fibrotic liver disease. In a discovery data set, we identified plasma ATX to be associated with parameters of systemic immune activation during chronic HCV and HCV/HIV infection. We and others have observed a partial normalization of ATX levels within months of starting interferon-free direct-acting antiviral (DAA) HCV therapy, consistent with a non-fibrotic liver disease contribution to elevated ATX levels, or HCV-mediated hepatocyte activation. Relationships between ATX, lysophosphatidic acid (LPA) and parameters of systemic immune activation will be discussed in the context of HCV infection, age, immune health, liver health, and hepatocellular carcinoma (HCC).

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