Immunomodulation by ultraviolet light: clinical studies and biological effects

Pamphilon, Derwood; Alnaqdy, AA; Wallington, T. B.

doi:10.1016/0167-5699(91)90095-b

Cited by 60 publications

(29 citation statements)

References 32 publications

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“…Our study shows that multiple HPV types were more common in individuals who are frequently exposed to the sun (P50.073). One explanation for this could be immune suppression induced by increased exposure to UV radiation (Pamphilon et al, 1991;Parrish et al, 1983). However, a more thorough understanding of the cutaneous HPV transmission pathway and virus-host interactions would be needed in order to identify the mechanisms of HPV persistence in human skin.…”

Section: Discussionmentioning

confidence: 99%

Human papillomavirus type spectrum in normal skin of individuals with or without a history of frequent sun exposure

Chen

McMillan

Antonsson

2008

Journal of General Virology

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Cutaneous human papillomavirus (HPV) has been widely detected in healthy skin. Previous studies have found that UV radiation can activate several HPV types, and a possible role for cutaneous HPV in the development of non-melanoma skin cancer has been suggested. This study investigated the prevalence and type-spectrum of cutaneous HPV in relation to UV radiation by studying forehead skin swab samples from 50 healthy males frequently exposed to the sun and 50 healthy males who were not frequently exposed to the sun. A questionnaire including ethnic background of the participants, history of cancers and a self-assessment of sun-exposure was also conducted and analysed. PCR with the FAP primer pair was carried out to detect HPV DNA in samples. HPV prevalence was higher in individuals who spent more time outdoors and in individuals with a history of skin cancers (P50.044 and P50.04, respectively). Furthermore, individuals wearing sunglasses as a means of sun protection had a lower prevalence of HPV (P50.018). Interestingly, HPV-76 was only detected in the group without frequent sun-exposure (P50.001). These results suggest that increased UV radiation exposure may be a factor leading to a difference in prevalence of cutaneous HPV types. INTRODUCTIONHuman papillomaviruses (HPVs) infect cutaneous and mucosal epithelia and are recognized as the causative agents of warts. It has recently become apparent that clinically normal skin harbours many different HPV types, and many of these HPV types have not been described previously (Antonsson et al., 2000(Antonsson et al., , 2003a Astori et al., 1998). Furthermore, it has been shown that asymptomatic HPV infections are acquired very early in infancy with a broad spectrum of HPV types (Antonsson et al., 2003b), and that the prevalence of HPV DNA in healthy skin increases with age (Antonsson et al., 2000). Moreover, cutaneous HPV infections on healthy skin have often been found to persist over time (Hazard et al., 2006). Many studies have also suggested a role for HPV in the carcinogenesis of non-melanoma skin cancer (NMSC). Squamous cell carcinoma (SCC) can metastasize, and is known as the unfavourable form of NMSC compared with basal cell carcinoma (BCC). Interestingly, BCCs are found approximately three times more frequently in immunocompetent individuals; however, in immunosuppressed organ-transplant recipients, SCCs are more prevalent (Pfister, 2003). It has been reported that more HPV types have been found in actinic keratosis and SCC skin lesions than in normal skin (Alotaibi et al., 2006), and a greater variety of HPV types have also been found in immunosuppressed individuals than in immunocompetent individuals (Harwood et al., 2004). Both SCC and BCC develop mostly on sun-exposed sites (Frost & Green, 1994), and some specific types of HPV, including HPV-5, HPV-8, HPV-20 and HPV-77, have been shown to be activated by UV radiation (Akgül et al., 2005;Massimi et al., 2008;Michel et al., 2006;Purdie et al., 1999;Storey et al., 1998). Evidence of UV-induced E6/E7 oncogenici...

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Section: Discussionmentioning

confidence: 99%

Human papillomavirus type spectrum in normal skin of individuals with or without a history of frequent sun exposure

Chen

McMillan

Antonsson

2008

Journal of General Virology

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“…However, in the case of melanoma, not only is there a genetic susceptibility (fair skinned, freckles, ginger hair, moles) but also a history of recurrent severe sunburn, a phenomenon associated with Th1 immune suppression and angiogenesis (Pamphilon et al, 1991). Renal cell cancer may represent a stochastic genetic evolution on the susceptible gene pool not requiring immune activation or systemic immunosuppression.…”

Section: Exceptions That Prove the Rule?mentioning

confidence: 99%

“…It therefore behoves us to ask the question 'what tumours do not appear to be relevant to this model?'. Ironically the two immunologically associated tumours, melanoma and renal cell cancer as well as the endocrinologically sensitive tumours (breast and prostate) do not readily fit and neither do germ cell tumours and those which are clearly associated with inherited genetic defects.However, in the case of melanoma, not only is there a genetic susceptibility (fair skinned, freckles, ginger hair, moles) but also a history of recurrent severe sunburn, a phenomenon associated with Th1 immune suppression and angiogenesis (Pamphilon et al, 1991). Renal cell cancer may represent a stochastic genetic evolution on the susceptible gene pool not requiring immune activation or systemic immunosuppression.…”

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confidence: 99%

Chronic immune activation and inflammation as the cause of malignancy

2001

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Summary Several chronic infections known to be associated with malignancy have established oncogenic properties. However the existence of chronic inflammatory conditions that do not have an established infective cause and are associated with the development of tumours strongly suggests that the inflammatory process itself provides the prerequisite environment for the development of malignancy. This environment includes upregulation of mediators of the inflammatory response such as cyclo-oxygenase (COX)-2 leading to the production of inflammatory cytokines and prostaglandins which themselves may suppress cell mediated immune responses and promote angiogenesis. These factors may also impact on cell growth and survival signalling pathways resulting in induction of cell proliferation and inhibition of apoptosis. Furthermore, chronic inflammation may lead to the production of reactive oxygen species and metabolites such as malondialdehyde within the affected cells that may in turn induce DNA damage and mutations and, as a result, be carcinogenic. Here it is proposed that the conditions provided by a chronic inflammatory environment are so essential for the progression of the neoplastic process that therapeutic intervention aimed at inhibiting inflammation, reducing angiogenesis and stimulating cell mediated immune responses may have a major role in reducing the incidence of common cancers. 473-483 © 2001 Cancer Research Campaign doi: 10.1054/ bjoc.2001.1943, available online at http://www.idealibrary.com on http://www.bjcancer.com (Kirk and Clements, 1999;Lewis et al, 1999). Furthermore, in the majority of colorectal tumours not associated with inflammatory bowel disease, histology shows that the precursor lesions, whether adenomas or polyps, are often inflammatory in nature (Higaki et al, 1999). THE INFLAMMATORY ENVIRONMENT ASSOCIATED WITH THE SUBSEQUENT DEVELOPMENT OF CANCERWhereas the association between chronic immune activation and the development of cancer has been recognized for some years, only recently have we begun to understand the mechanisms underlying this phenomenon. The first concerns the nature of the local and systemic immune response seen in patients with chronic inflammatory conditions known to be associated with the development of malignant disease. Immune responses may be broadly divided into two categories -cell mediated immunity and humoral immunity. Cell mediated immunity (CMI) is associated with CD4 + T-lymphocytes which characteristically produce the cytokines interleukin(IL)-2, interferon-γ and tumour necrosis factor(TNF)-α (Thl-lymphocytes). Humoral immunity (HI) is associated with CD4+ T-lymphocytes which characteristically produce IL-4, IL-6 and IL-10 (Th2) (Mosmann and Coffman, 1989).Recent experimental evidence suggests that exposure to a foreign antigen results in upregulation of the non-specific pro-inflammatory cytokines IL-1α and -β and the Th1 cytokines in inflammatory cells. Cyclooxygenase (COX)-1 and COX-2 are among the most important enzymes involved in the regulation of th...

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“…Kripke showed effects of UV-B on the immune response [1] that led to the basic notion of applying UV-B irradiation to prevent side effects of transfusion [2]. Then UV-B irradiation to antigenpresenting cells (APC) has been reported as effective in prevention of alloimmunization in animal models [3,4].…”

Section: Introductionmentioning

confidence: 99%

Effects of ultraviolet B irradiation on cell–cell interaction; implication of morphological changes and actin filaments in irradiated cells

Maekawa

Takahashi

Fujihara

et al. 1996

Clinical and Experimental Immunology

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SUMMARYWe studied the effects of ultraviolet B (UV-B) irradiation on cell-cell interactions using mouse lymphoma RMA cells and T cell hybridoma HTB-176.10 cells. RMA cells act as stimulators by presenting H-2K b surface antigens to HTB-176.10 cells, inducing IL-2 production in HTB-176.10 cells. Irradiating RMA cells with 1000 J/m 2 UV-B suppressed cell cluster formation between RMA and HTB-176.10 cells and reduced the level of IL-2 production in HTB-176.10 cells, although H-2K b surface antigens of RMA cells were still expressed. Electron microscopic observations of irradiated RMA cells revealed that UV-B irradiation damaged cell structures, resulting in the disappearance of microvilli on the cell surface, destruction of mitochondria, vacuolation of cytoplasm and swelling of the perinuclear cisterna space. We found that these alterations were accompanied by polymerization of filamentous actin quantified by flow cytometry after NBD-phallacidin staining. Our results suggest that a target of UV-B-induced alterations is actin filaments, which support the cell morphology as the cytoskeleton, and that modification of filamentous actin inhibits interaction between RMA and HTB-176.10 cells. This underlying mechanism may account for the impaired interaction between antigen-presenting cells and T cells after transfusion with UV-B-irradiated allogeneic blood components.

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Immunomodulation by ultraviolet light: clinical studies and biological effects

Cited by 60 publications

References 32 publications

Human papillomavirus type spectrum in normal skin of individuals with or without a history of frequent sun exposure

Human papillomavirus type spectrum in normal skin of individuals with or without a history of frequent sun exposure

Chronic immune activation and inflammation as the cause of malignancy

Effects of ultraviolet B irradiation on cell–cell interaction; implication of morphological changes and actin filaments in irradiated cells

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