Journal of the American Academy of Dermatology · 2008
Immunosuppression may be present within condyloma acuminata.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАПоддержка правительства СШАНазвание и аннотация: Перевод в очереди
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Le Poole Caroline, Denman Cecele J, Arbiser Jack L
Аннотация
BACKGROUND: Condyloma acuminatum are common lesions caused by human papillomavirus (HPV). HPV is associated with many human cancers, and a vaccine now prevents infection with high-risk HPV. However, eradication of established disease is difficult, indicating that these lesions are capable of local immunosuppression.
OBJECTIVE: This study examines the immunohistochemical staining characteristics of condyloma acuminatum lesions for markers of cellular immunity, including T-lymphocyte subsets, dendritic cells, and infected keratinocytes and markers of antigen presentation in condyloma tissue.
METHODS: Five snap-frozen, optimal cutting temperature-embedded condyloma lesions were immunostained for T-lymphocyte markers Fox P3, CD8, CD25 and molecules involved in antigen presentation.
RESULTS: Condylomas demonstrated hallmarks of immunosuppression, such as increased cellular interleukin-10 production, decreased expression of transporter associated with antigen presentation, CD40, and carbonic anhydrase IX, decreased dendritic cell counts, and increased T-regulatory cell infiltration.
LIMITATIONS: This study was performed with lesions from a single center, and control tissue from the same patients was not available because of lack of patient consent.
CONCLUSION: These results demonstrate that condylomas induce a local immunosuppressive environment, with deficits in antigen presentation and enhancement of immunosuppressive T-regulatory cell populations. Strategies to block this immunosuppression are required to elicit effective immune responses to HPV infection.
OBJECTIVE: This study examines the immunohistochemical staining characteristics of condyloma acuminatum lesions for markers of cellular immunity, including T-lymphocyte subsets, dendritic cells, and infected keratinocytes and markers of antigen presentation in condyloma tissue.
METHODS: Five snap-frozen, optimal cutting temperature-embedded condyloma lesions were immunostained for T-lymphocyte markers Fox P3, CD8, CD25 and molecules involved in antigen presentation.
RESULTS: Condylomas demonstrated hallmarks of immunosuppression, such as increased cellular interleukin-10 production, decreased expression of transporter associated with antigen presentation, CD40, and carbonic anhydrase IX, decreased dendritic cell counts, and increased T-regulatory cell infiltration.
LIMITATIONS: This study was performed with lesions from a single center, and control tissue from the same patients was not available because of lack of patient consent.
CONCLUSION: These results demonstrate that condylomas induce a local immunosuppressive environment, with deficits in antigen presentation and enhancement of immunosuppressive T-regulatory cell populations. Strategies to block this immunosuppression are required to elicit effective immune responses to HPV infection.