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2015, Number S2

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Rev Med Inst Mex Seguro Soc 2015; 53 (S2)

Escape mechanisms to the innate immune response in HPV-associated cervical cancer

del Toro-Arreola S, García-Chagollán M, Jave-Suárez LF

Language: Spanish
References: 35
Page: 194-199
PDF size: 289.61 Kb.


ABSTRACT

Cervical cancer is characterized by persistent human papilloma virus (HPV) infection. But, why, in some cases, is the immune system unable to reliably detect the HPV infection? For years, this has been a central question, which has yet to be fully answered. At present, it is well known that HPV has evolved a variety of mechanisms to evade the immune attack, and it is the success of these, which will be critical to determine whether the infection will be cleared or remain as a persistent infection. This review will be particularly focused on addressing some of the mechanisms used by HPV to avoid early recognition by the host innate immune system, which will then facilitate viral persistence with the consequent risk of eventual progression towards cervical cancer. Undoubtedly, an understanding of the balance between viral and immunological factors will provide crucial information that must to be taken into account for the design of prophylactic and therapeutic vaccines against HPVassociated cervical cancer


REFERENCES

  1. 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.

  2. 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.

  3. 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.

  4. 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.

  5. Frazer IH. Immunology of papillomavirus infection. Current Opinion in Immunology. 1996;8:484-91.

  6. Dugue PA, Rebolj M, Garred P, Lynge E. Immunosuppression and risk of cervical cancer. Expert Rev Anticancer Ther. 2013;13:29-42.

  7. Stanley MA. Immune responses to human papilloma viruses. Indian J Med Res. 2009;130:266-76.

  8. Doorbar J. The papillomavirus life cycle. J Clin Virol. 2005;32 Suppl 1:S7-15.

  9. Longworth MS, Laimins LA. Pathogenesis of human papillomaviruses in differentiating epithelia. Microbiol Mol Biol Rev. 2004;68:362-72.

  10. Zheng ZM, Baker CC. Papillomavirus genome structure, expression, and post-transcriptional regulation. Front Biosci. 2006;11:2286-302.

  11. De Jong EC, Smits HH, Kapsenberg ML. Dendritic cell-mediated T cell polarization. Springer Semin Immunopathol. 2005;26:289-307.

  12. 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.

  13. Hibma MH. The immune response to papillomavirus during infection persistence and regression. The Open Virology Journal. 2012;6:241-8.

  14. 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.

  15. 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 HIVnoninfected Brazilian women. Int J Gynecol Cancer. 2012;22:1291-6.

  16. Hubert P, Caberg JH, Gilles C, Bousarghin L, Franzen-Detrooz E, Boniver J, et al. E-cadherindependent adhesion of dendritic and Langerhans cells to keratinocytes is defective in cervical human papillomavirus-associated (pre)neoplastic lesions. J Pathol. 2005;206:346-55.

  17. 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.

  18. 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.

  19. 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.

  20. Cassandri F, Tozetti IA, Fernandes CE, Almeida FG, Falcao GR, Scapulatempo ID, et al. S100, CD68, and MHC class II molecule expression in cervical highand low-grade HPV-induced lesions. Rev Soc Bras Med Trop. 2012;45:3-8.

  21. 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.

  22. 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.

  23. 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.

  24. 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.

  25. 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.

  26. 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.

  27. Abele R, Tampe R. Modulation of the antigen transport machinery TAP by friends and enemies. FEBS letters. 2006;580:1156-63.

  28. Ljunggren HG, Karre K. In search of the 'missing self': MHC molecules and NK cell recognition. Immunology Today. 1990;11:237-44.

  29. 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.

  30. Arnheim L, Dillner J, Sanjeevi CB. A populationbased cohort study of KIR genes and genotypes in relation to cervical intraepithelial neoplasia. Tissue antigens. 2005;65:252-9.

  31. 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.

  32. 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.

  33. 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.

  34. 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.

  35. 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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