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Mecanismos de escape a la respuesta inmune innata en cáncer cervicouterino asociado a VPH
Resumen
El cáncer cervicouterino (CaCU) se caracteriza por el establecimiento de una infección persistente causada por el virus del papiloma humano (VPH). Pero ¿por qué el sistema inmune ignora o al menos muestra fallas para detectar la infección por VPH? Esta ha sido una pregunta central que ha permanecido durante años y que aún sigue sin contestarse en su totalidad, aunque en la actualidad ya se sabe que el VPH emplea una variedad de estrategias para evadir o subvertir la vigilancia inmune, lo cual será crítico para definir si persiste o no la infección viral y, por consiguiente, el riesgo de progresión a cáncer. Por lo mismo, en esta revisión se abordarán algunos de los mecanismos más importantes que el VPH utiliza para escapar al ataque inicial impuesto por la respuesta inmune innata y que le permiten establecerse como una infección persistente, lo cual facilita la progresión de las lesiones cervicales hasta que se convierten en cáncer. Indudablemente, el entendimiento del equilibrio entre factores virales e inmunológicos proporcionará información determinante que deberá tomarse en cuenta en la planeación estratégica de vacunas profilácticas y terapéuticas contra el CaCU asociado a la infección por VPH.
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Referencias
Cuschieri KS, Cubie HA, Whitley MW, Gilkison G, Arends MJ, Graham C, et al. Persistent high risk HPV infection associated with development of cervical neoplasia in a prospective population study. J Clin Pathol. 2005;58:946-50.
Dalstein V, Riethmuller D, Pretet JL, Le Bail Carval K, Sautiere JL, Carbillet JP, et al. Persistence and load of high-risk HPV are predictors for development of high-grade cervical lesions: a longitudinal French cohort study. Int J Cancer. 2003;106:396-403.
Bosch FX, Lorincz A, Munoz N, Meijer CJ, Shah KV. The causal relation between human papillomavirus and cervical cancer. J Clin Pathol. 2002;55:244-65.
Kjellberg L, Hallmans G, Ahren AM, Johansson R, Bergman F, Wadell G, et al. Smoking, diet, pregnancy and oral contraceptive use as risk factors for cervical intra-epithelial neoplasia in relation to human papillomavirus infection. British Journal of Cancer. 2000;82:1332-8.
Frazer IH. Immunology of papillomavirus infection. Current Opinion in Immunology. 1996;8:484-91.
Dugue PA, Rebolj M, Garred P, Lynge E. Immunosuppression and risk of cervical cancer. Expert Rev Anticancer Ther. 2013;13:29-42.
Stanley MA. Immune responses to human papilloma viruses. Indian J Med Res. 2009;130:266-76.
Doorbar J. The papillomavirus life cycle. J Clin Virol. 2005;32 Suppl 1:S7-15.
Longworth MS, Laimins LA. Pathogenesis of human papillomaviruses in differentiating epithelia. Microbiol Mol Biol Rev. 2004;68:362-72.
Zheng ZM, Baker CC. Papillomavirus genome structure, expression, and post-transcriptional regulation. Front Biosci. 2006;11:2286-302.
De Jong EC, Smits HH, Kapsenberg ML. Dendritic cell-mediated T cell polarization. Springer Semin Immunopathol. 2005;26:289-307.
Granucci F, Zanoni I, Ricciardi-Castagnoli P. Central role of dendritic cells in the regulation and deregulation of immune responses. Cell Mol Life Sci. 2008;65:1683-97.
Hibma MH. The immune response to papillomavirus during infection persistence and regression. The Open Virology Journal. 2012;6:241-8.
Matthews K, Leong CM, Baxter L, Inglis E, Yun K, Backstrom BT, et al. Depletion of Langerhans cells in human papillomavirus type 16-infected skin is associated with E6-mediated down regulation of E-cadherin. J Virol. 2003;77:8378-85.
Zimmermmann JB, Gobbi H, Alves MJ, Quirino MG, Melo VH. Langerhans cell density in cervical intraepithelial neoplasia associated with human papillomavirus infection in HIV-infected and HIV-noninfected Brazilian women. Int J Gynecol Cancer. 2012;22:1291-6.
Hubert P, Caberg JH, Gilles C, Bousarghin L, Franzen-Detrooz E, Boniver J, et al. E-cadherin-dependent adhesion of dendritic and Langerhans cells to keratinocytes is defective in cervical human papillomavirus-associated (pre)neoplastic lesions. J Pathol. 2005;206:346-55.
Keating PJ, Cromme FV, Duggan-Keen M, Snijders PJ, Walboomers JM, Hunter RD, et al. Frequency of down-regulation of individual HLA-A and -B alleles in cervical carcinomas in relation to TAP-1 expression. British Journal of Cancer. 1995;72:405-11.
Rattis FM, Peguet-Navarro J, Staquet MJ, Dezutter-Dambuyant C, Courtellemont P, Redziniak G, et al. Expression and function of B7-1 (CD80) and B7-2 (CD86) on human epidermal Langerhans cells. Eur J Immunol. 1996;26:449-53.
Mota F, Rayment N, Chong S, Singer A, Chain B. The antigen-presenting environment in normal and human papillomavirus (HPV)-related premalignant cervical epithelium. Clin Exp Immunol. 1999;116:33-40.
Cassandri F, Tozetti IA, Fernandes CE, Almeida FG, Falcao GR, Scapulatempo ID, et al. S100, CD68, and MHC class II molecule expression in cervical high- and low-grade HPV-induced lesions. Rev Soc Bras Med Trop. 2012;45:3-8.
Ryu KS, Lee YS, Kim BK, Park YG, Kim YW, Hur SY, et al. Alterations of HLA class I and II antigen expression in preinvasive, invasive and metastatic cervical cancers. Exp Mol Med. 2001;33:136-44.
Glew SS, Duggan-Keen M, Cabrera T, Stern PL. HLA class II antigen expression in human papillomavirus-associated cervical cancer. Cancer Res. 1992;52:4009-16.
Disbrow GL, Hanover JA, Schlegel R. Endoplasmic reticulum-localized human papillomavirus type 16 E5 protein alters endosomal pH but not trans-Golgi pH. J Virol. 2005;79:5839-46.
Zhang B, Li P, Wang E, Brahmi Z, Dunn KW, Blum JS, et al. The E5 protein of human papillomavirus type 16 perturbs MHC class II antigen maturation in human foreskin keratinocytes treated with interferon-gamma. Virology. 2003;310:100-8.
Breitburd F, Ramoz N, Salmon J, Orth G. HLA control in the progression of human papillomavirus infections. Seminars in Cancer Biology. 1996;7:359-71.
Cromme FV, Airey J, Heemels MT, Ploegh HL, Keating PJ, Stern PL, et al. Loss of transporter protein, encoded by the TAP-1 gene, is highly correlated with loss of HLA expression in cervical carcinomas. The Journal of Experimental Medicine. 1994;179:335-40.
Abele R, Tampe R. Modulation of the antigen transport machinery TAP by friends and enemies. FEBS letters. 2006;580:1156-63.
Ljunggren HG, Karre K. In search of the 'missing self': MHC molecules and NK cell recognition. Immunology Today. 1990;11:237-44.
Moretta L, Bottino C, Pende D, Castriconi R, Mingari MC, Moretta A. Surface NK receptors and their ligands on tumor cells. Seminars in Immunology. 2006;18:151-8.
Arnheim L, Dillner J, Sanjeevi CB. A population-based cohort study of KIR genes and genotypes in relation to cervical intraepithelial neoplasia. Tissue antigens. 2005;65:252-9.
Satam MN, Suraiya JN, Nadkarni JJ. Natural killer and antibody-dependent cellular cytotoxicity in cervical carcinoma patients. Cancer Immunology, Immunotherapy: CII. 1986;23:56-9.
Fauriat C, Just-Landi S, Mallet F, Arnoulet C, Sainty D, Olive D, et al. Deficient expression of NCR in NK cells from acute myeloid leukemia: Evolution during leukemia treatment and impact of leukemia cells in NCRdull phenotype induction. Blood. 2007;109:323-30.
Garcia-Iglesias T, Del Toro-Arreola A, Albarran-Somoza B, Del Toro-Arreola S, Sanchez-Hernandez PE, Ramirez-Duenas MG, et al. Low NKp30, NKp46 and NKG2D expression and reduced cytotoxic activity on NK cells in cervical cancer and precursor lesions. BMC Cancer. 2009;9:186.
Kono K, Ressing ME, Brandt RM, Melief CJ, Potkul RK, Andersson B, et al. Decreased expression of signal-transducing zeta chain in peripheral T cells and natural killer cells in patients with cervical cancer. Clinical Cancer Research. 1996;2:1825-8.
Whiteside TL. Down-regulation of zeta-chain expression in T cells: a biomarker of prognosis in cancer? Cancer Immunology, Immunotherapy: CII. 2004;53:865-78.
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