| Oral mucosal expression of HIV-1 receptors, co-receptors, and alpha-defensins: tableau of resistance or susceptibility to HIV infection? | |
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MedLine Citation:
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PMID: 16672549 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The basic premise of whether transmission of HIV-1 through the oral mucosa actually occurs, and through what route, is a topic of intense interest. Our work has focused on HIV-1 receptors/co-receptors and alpha-defensin-1 in situ in human gingiva. Regardless of HIV-1 infection, the role that C-type lectin receptors might play in periodontal pathogenesis is of great interest. We have shown that the gingival lamina propria, when inflamed, becomes increasingly infiltrated with DC-SIGN+MR+ dermal dendritic cells (DDCs), while the inflamed epithelium shows a decrease in Langerin+ Langerhans cells (LCs). Moreover, DDCs and LCs contribute to the mature CD83+ DC pool in situ, and form immune conjugates with CD4+ T-cells in the lamina propria (Jotwani and Cutler, 2003). This raises the intriguing possibility that oral mucosal DCs may be involved in HIV-1 transfer to T-cells in situ. However, this possibility is tendered by the challenges faced by the virus in gaining access to oral mucosal immune cells, including their ability to survive the salivary defenses, cross the mucosal barrier, resist inactivation by alpha-defensins, and overcome the paucity of co-receptor CCR5 in (healthy) oral mucosa (i.e., required for productive infection [Jotwani et al., 2004]). To date, there is little evidence of direct infection by HIV-1 of oral mucosal DCs/T cells and other cells in situ. Abbreviations used in this paper: CP, chronic periodontitis; CCR5, chemokine receptor 5; CXCR4, C-X-C receptor 4; DCs, dendritic cells; DC-SIGN, DC-specific ICAM-3 grabbing non-integrin; DDC, dermal dendritic cells; LCs, Langerhans cells; LP, lamina propria; MR, mannose receptor. |
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Authors:
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C W Cutler; R Jotwani |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review Date: 2006-04-01 |
Journal Detail:
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Title: Advances in dental research Volume: 19 ISSN: 1544-0737 ISO Abbreviation: Adv. Dent. Res. Publication Date: 2006 |
Date Detail:
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Created Date: 2006-05-04 Completed Date: 2006-07-18 Revised Date: 2011-06-10 |
Medline Journal Info:
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Nlm Unique ID: 8802131 Medline TA: Adv Dent Res Country: United States |
Other Details:
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Languages: eng Pagination: 49-51 Citation Subset: D |
Affiliation:
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Periodontal Molecular Immunology Laboratory, Department of Periodontics, School of Dental Medicine, J-110 Rockland Hall, Stony Brook University-SUNY, Stony Brook, NY 11794-8703, USA. christopher.cutler@sunysb.edu |
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| MeSH Terms | |
Descriptor/Qualifier:
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Cell Adhesion Molecules
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biosynthesis* Dendritic Cells / immunology Disease Susceptibility / immunology Gingiva / cytology, metabolism, virology HIV Infections / immunology*, transmission HIV-1 / physiology* Humans Lectins, C-Type / biosynthesis* Mouth Mucosa / cytology, metabolism, virology* Receptors, Cell Surface / biosynthesis* Receptors, HIV / biosynthesis* alpha-Defensins / biosynthesis* |
| Grant Support | |
ID/Acronym/Agency:
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R01 DE014328-07/DE/NIDCR NIH HHS; R01 DE14328/DE/NIDCR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Cell Adhesion Molecules; 0/DC-specific ICAM-3 grabbing nonintegrin; 0/Lectins, C-Type; 0/Receptors, Cell Surface; 0/Receptors, HIV; 0/alpha-Defensins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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