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      Impact of smoking on dendritic cells in patients with oral squamous cell carcinoma

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          Abstract

          Abstract Smoking has been shown to alter innate and adaptive immune responses and is directly associated with the onset of oral squamous cell carcinoma (OSCC). The purpose of this study was to evaluate the effect of cigarette smoke exposure on dendritic cells (DCs) from OSCC patients. CD1a and CD83 antibodies were used to identify immature and mature DCs, respectively, by immunohistochemistry in OSCC samples of 24 smokers and 24 non-smokers. Density of DCs was calculated in intra and peritumoral areas. Clinical and microscopic findings were reviewed and analyzed for all patients. Smokers with OSCC had a lower density of intra and peritumoral DCs when compared to non-smokers. Tumors classified as moderately/poorly differentiated had lower peritumoral CD1a+ DCs than well-differentiated tumors (p < 0.001). Smoking contributed to a depletion of immature and mature DCs in the OSCC.

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          Most cited references40

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          Lipid accumulation and dendritic cell dysfunction in cancer

          Professional antigen presenting cells, dendritic cells (DC) are responsible for initiation and maintenance of immune responses. Here, we report that a substantial proportion of DCs in tumor-bearing mice and cancer patients have increased levels of triglycerides. Lipid accumulation in DCs was caused by increased uptake of extracellular lipids due to up-regulation of scavenger receptor A. DCs with high lipid content were not able to effectively stimulate allogeneic T cells or present tumor-associated antigens. DCs with high and normal lipid levels did not differ in expression of MHC and co-stimulatory molecules. However, lipid-laden DCs had reduced capacity to process antigens. Pharmacological normalization of lipid levels in DCs with an inhibitor of acetyl-CoA carboxylase restored the functional activity of DCs and substantially enhanced the effects of a cancer vaccine. These findings support the regulation of immune responses in cancer by manipulation of lipid levels in DCs.
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            Tobacco Smoke Induces and Alters Immune Responses in the Lung Triggering Inflammation, Allergy, Asthma and Other Lung Diseases: A Mechanistic Review

            Many studies have been undertaken to reveal how tobacco smoke skews immune responses contributing to the development of chronic obstructive pulmonary disease (COPD) and other lung diseases. Recently, environmental tobacco smoke (ETS) has been linked with asthma and allergic diseases in children. This review presents the most actual knowledge on exact molecular mechanisms responsible for the skewed inflammatory profile that aggravates inflammation, promotes infections, induces tissue damage, and may promote the development of allergy in individuals exposed to ETS. We demonstrate how the imbalance between oxidants and antioxidants resulting from exposure to tobacco smoke leads to oxidative stress, increased mucosal inflammation, and increased expression of inflammatory cytokines (such as interleukin (IL)-8, IL-6 and tumor necrosis factor α ([TNF]-α). Direct cellular effects of ETS on epithelial cells results in increased permeability, mucus overproduction, impaired mucociliary clearance, increased release of proinflammatory cytokines and chemokines, enhanced recruitment of macrophages and neutrophils and disturbed lymphocyte balance towards Th2. The plethora of presented phenomena fully justifies a restrictive policy aiming at limiting the domestic and public exposure to ETS.
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              Antigen-Specific Inhibition of CD8+ T Cell Response by Immature Myeloid Cells in Cancer Is Mediated by Reactive Oxygen Species

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                Author and article information

                Journal
                bor
                Brazilian Oral Research
                Braz. oral res.
                Sociedade Brasileira de Pesquisa Odontológica - SBPqO (São Paulo, SP, Brazil )
                1806-8324
                1807-3107
                2021
                : 35
                : e075
                Affiliations
                [3] Campinas São Paulo orgnameUniversidade Estadual de Campinas orgdiv1School of Medical Sciences orgdiv2Department of Pathology Brazil
                [1] Florianópolis Santa Catarina orgnameUniversidade Federal de Santa Catarina orgdiv1Department of Dentistry Brazil
                [4] Florianópolis Santa Catarina orgnameUniversidade Federal de Santa Catarina orgdiv1Department of Pathology Brazil
                [2] São Paulo SP orgnameAC Camargo Cancer Center orgdiv2Department of Head & Neck Brazil
                Article
                S1806-83242021000100276 S1806-8324(21)03500000276
                10.1590/1807-3107bor-2021.vol35.0075
                7f697791-9c44-432f-bd83-33d0db2a22a3

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                : 12 December 2020
                : 02 August 2020
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 40, Pages: 0
                Product

                SciELO Brazil

                Categories
                Original Research

                Mouth Neoplasms,Immunity,Cigarette Smoking
                Mouth Neoplasms, Immunity, Cigarette Smoking

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