ArticleFrontiers in immunology2015
Gut-Associated Plasmacytoid Dendritic Cells Display an Immature Phenotype and Upregulated Granzyme B in Subjects with HIV/AIDS.
Article in Frontiers in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- The normal human lymph node cell classification and landscape defined by high-dimensional spatial proteomics.PloS one · 2026Article
- Mucosal Immunity and the Gut-Microbiota-Brain-Axis in Neuroimmune Disease.International journal of molecular sciences · 2022Review
- Gut Bacteria Induce Granzyme B Expression in Human Colonic ILC3s In Vitro in an IL-15-Dependent Manner.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Gut Innate Immunity and HIV Pathogenesis.Current HIV/AIDS reports · 2021Review
- Plasmacytoid Dendritic Cells as Cell-Based Therapeutics: A Novel Immunotherapy to Treat Human Immunodeficiency Virus Infection?Frontiers in cellular and infection microbiology · 2020Review
- Nutritional modulation of the intestinal microbiota; future opportunities for the prevention and treatment of neuroimmune and neuroinflammatory disease.The Journal of nutritional biochemistry · 2018Review
- Marked Enteropathy in an Accelerated Macaque Model of AIDS.The American journal of pathology · 2017Article
- Dendritic Cell Immune Responses in HIV-1 Controllers.Current HIV/AIDS reports · 2017Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plasmacytoid dendritic cells (pDCs) in the periphery of subjects with human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) decrease over time, and the fate of these cells has been the subject of ongoing investigation. Previous studies using animal models as well as studies with humans suggest that these cells may redistribute to the gut. Other studies using animal models propose that the periphery pDCs are depleted and gut is repopulated with naive pDCs from the bone marrow. In the present study, we utilized immunohistochemistry to survey duodenum biopsies of subjects with HIV/AIDS and controls. We observed that subjects with HIV/AIDS had increased infiltration of Ki-67(+)/CD303(+) pDCs, a phenotype consistent with bone marrow-derived pre-pDCs. In contrast, Ki-67(+)/CD303(+) pDCs were not observed in control biopsies. We additionally observed that gut-associated pDCs in HIV/AIDS cases upregulate the proapoptotic enzyme granzyme B; however, no granzyme B was observed in the pDCs of control biopsies. Our data are consistent with reports in animal models that suggest periphery pDCs are depleted by exhaustion and that naive pDCs egress from the bone marrow and ultimately infiltrate the gut mucosa. Additionally, our observation of granzyme B upregulation in naive pDCs may identify a contributing factor to the gut pathology associated with HIV infection.
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