Jundishapur Journal of Microbiology

Published by: Kowsar

The Cytotoxic T Lymphocyte Antigen-4 +49A/G Single Nucleotide Polymorphism Association With Visceral Leishmaniasis

Mehrdad Hajilooi 1 , Pegah Lotfi 2 , Farhad Seif 3 , Ahad Bazmani 4 , Mohammad Momeni 5 , Ali Ravary 6 , Mohammad Kazemi Arababadi 5 and Ali Reza Khalilian 7 , *
Authors Information
1 Department of Immunology, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan, IR Iran
2 Department of Microbiology, Faculty of Medicine, Hamadan University of Medical Sciences, Hamadan, IR Iran
3 Department of Immunology and Microbiology, Faculty of Medicine, Shahrekord University of Medical Sciences, Shahrekord, IR Iran
4 Infectious and Tropical Diseases Research Center, Tabriz University of Medical Sciences, Tabriz, IR Iran
5 Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, IR Iran
6 Occupational Environment Research Center, Rafsanjan University of Medical Sciences, Rafsanjan, IR Iran
7 Faculty of Medicine, Shahid Beheshti Hospital, Hamadan University of Medical Sciences, Hamadan, IR Iran
Article information
  • Jundishapur Journal of Microbiology: October 01, 2014, 7 (10); e12143
  • Published Online: October 1, 2014
  • Article Type: Research Article
  • Received: June 10, 2013
  • Revised: August 4, 2013
  • Accepted: September 10, 2013
  • DOI: 10.5812/jjm.12143

To Cite: Hajilooi M, Lotfi P, Seif F, Bazmani A, Momeni M, et al. The Cytotoxic T Lymphocyte Antigen-4 +49A/G Single Nucleotide Polymorphism Association With Visceral Leishmaniasis, Jundishapur J Microbiol. 2014 ; 7(10):e12143. doi: 10.5812/jjm.12143.

Abstract
Copyright © 2014, Ahvaz Jundishapur University of Medical Sciences. This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/) which permits copy and redistribute the material just in noncommercial usages, provided the original work is properly cited.
1. Background
2. Objectives
3. Materials and Methods
4. Results
5. Discussion
Acknowledgements
Footnotes
References
  • 1. Hartemink N, Vanwambeke SO, Heesterbeek H, Rogers D, Morley D, Pesson B, et al. Integrated mapping of establishment risk for emerging vector-borne infections: a case study of canine leishmaniasis in southwest France. PLoS One. 2011; 6(8)[DOI][PubMed]
  • 2. Wiwanitkit V. Bone marrow leishmaniasis: a review of situation in Thailand. Asian Pac J Trop Med. 2011; 4(10): 757-9[DOI][PubMed]
  • 3. Herwaldt BL, Juranek DD. Laboratory-acquired malaria, leishmaniasis, trypanosomiasis, and toxoplasmosis. Am J Trop Med Hyg. 1993; 48(3): 313-23[PubMed]
  • 4. Meinecke CK, Schottelius J, Oskam L, Fleischer B. Congenital transmission of visceral leishmaniasis (Kala Azar) from an asymptomatic mother to her child. Pediatrics. 1999; 104(5)[PubMed]
  • 5. Newlove T, Robinson M, Meehan SA, Pomerantz R. Old World cutaneous leishmaniasis. Dermatol Online J. 2012; 18(12): 32[PubMed]
  • 6. Wilson ME, Jeronimo SM, Pearson RD. Immunopathogenesis of infection with the visceralizing Leishmania species. Microb Pathog. 2005; 38(4): 147-60[DOI][PubMed]
  • 7. Ali N, Mekuria AH, Requena JM, Engwerda C. Immunity to visceral leishmaniasis. J Trop Med. 2012; 2012: 780809[DOI][PubMed]
  • 8. Santos Cda S, Boaventura V, Ribeiro Cardoso C, Tavares N, Lordelo MJ, Noronha A, et al. CD8(+) granzyme B(+)-mediated tissue injury vs. CD4(+)IFNgamma(+)-mediated parasite killing in human cutaneous leishmaniasis. J Invest Dermatol. 2013; 133(6): 1533-40[DOI][PubMed]
  • 9. Linsley PS, Brady W, Urnes M, Grosmaire LS, Damle NK, Ledbetter JA. CTLA-4 is a second receptor for the B cell activation antigen B7. J Exp Med. 1991; 174(3): 561-9[PubMed]
  • 10. Uzer E, Dilmec F, Akkafa F, Boduroglu O, van Kuilenburg AB. Investigation of CTLA-4 and CD28 gene polymorphisms in patients with diabetes mellitus type 2 using PCR-RFLP in a Turkish population. West Indian Med J. 2010; 59(3): 235-40[PubMed]
  • 11. Anjos S, Nguyen A, Ounissi-Benkalha H, Tessier MC, Polychronakos C. A common autoimmunity predisposing signal peptide variant of the cytotoxic T-lymphocyte antigen 4 results in inefficient glycosylation of the susceptibility allele. J Biol Chem. 2002; 277(48): 46478-86[DOI][PubMed]
  • 12. Wang XB, Pirskanen R, Giscombe R, Lefvert AK. Two SNPs in the promoter region of the CTLA-4 gene affect binding of transcription factors and are associated with human myasthenia gravis. J Intern Med. 2008; 263(1): 61-9[DOI][PubMed]
  • 13. Oshaghi MA, Ravasan NM, Javadian EA, Mohebali M, Hajjaran H, Zare Z, et al. Vector incrimination of sand flies in the most important visceral leishmaniasis focus in Iran. Am J Trop Med Hyg. 2009; 81(4): 572-7[DOI][PubMed]
  • 14. Oshaghi MA, Ravasan NM, Hide M, Javadian EA, Rassi Y, Sadraei J, et al. Phlebotomus perfiliewi transcaucasicus is circulating both Leishmania donovani and L. infantum in northwest Iran. Exp Parasitol. 2009; 123(3): 218-25[DOI][PubMed]
  • 15. Mohebali M, Javadian E, Yaghoobi-Ershadi MR, Akhavan AA, Hajjaran H, Abaei MR. Characterization of Leishmania infection in rodents from endemic areas of the Islamic Republic of Iran. East Mediterr Health J. 2004; 10(4-5): 591-9[PubMed]
  • 16. Bachmann MF, Gallimore A, Jones E, Ecabert B, Acha-Orbea H, Kopf M. Normal pathogen-specific immune responses mounted by CTLA-4-deficient T cells: a paradigm reconsidered. Eur J Immunol. 2001; 31(2): 450-8[DOI][PubMed]
  • 17. Raitala A, Karjalainen J, Oja SS, Kosunen TU, Hurme M. Helicobacter pylori-induced indoleamine 2,3-dioxygenase activity in vivo is regulated by TGFB1 and CTLA4 polymorphisms. Mol Immunol. 2007; 44(5): 1011-4[DOI][PubMed]
  • 18. Gomes NA, Gattass CR, Barreto-De-Souza V, Wilson ME, DosReis GA. TGF-beta mediates CTLA-4 suppression of cellular immunity in murine kalaazar. J Immunol. 2000; 164(4): 2001-8[PubMed]
  • 19. Katara GK, Ansari NA, Verma S, Ramesh V, Salotra P. Foxp3 and IL-10 expression correlates with parasite burden in lesional tissues of post kala azar dermal leishmaniasis (PKDL) patients. PLoS Negl Trop Dis. 2011; 5(5)[DOI][PubMed]
  • 20. Goto H, Lindoso JA. Immunity and immunosuppression in experimental visceral leishmaniasis. Braz J Med Biol Res. 2004; 37(4): 615-23[PubMed]
  • 21. Murphy ML, Cotterell SE, Gorak PM, Engwerda CR, Kaye PM. Blockade of CTLA-4 enhances host resistance to the intracellular pathogen, Leishmania donovani. J Immunol. 1998; 161(8): 4153-60[PubMed]
  • 22. Murray HW, Lu CM, Brooks EB, Fichtl RE, DeVecchio JL, Heinzel FP. Modulation of T-cell costimulation as immunotherapy or immunochemotherapy in experimental visceral leishmaniasis. Infect Immun. 2003; 71(11): 6453-62[PubMed]
  • 23. Saha B, Chattopadhyay S, Germond R, Harlan DM, Perrin PJ. CTLA4 (CD152) modulates the Th subset response and alters the course of experimental Leishmania major infection. Eur J Immunol. 1998; 28(12): 4213-20[DOI][PubMed]
  • 24. Zubairi S, Sanos SL, Hill S, Kaye PM. Immunotherapy with OX40L-Fc or anti-CTLA-4 enhances local tissue responses and killing of Leishmania donovani. Eur J Immunol. 2004; 34(5): 1433-40[DOI][PubMed]
  • 25. Danilovic DL, Mendes-Correa MC, Lima EU, Zambrini H, K. Barros R , Marui S. Correlations of CTLA-4 gene polymorphisms and hepatitis C chronic infection. Liver Int. 2012; 32(5): 803-8[DOI][PubMed]
  • 26. Duan S, Zhang G, Han Q, Li Z, Liu Z, Chen J, et al. CTLA-4 exon 1 +49 polymorphism alone and in a haplotype with -318 promoter polymorphism may confer susceptibility to chronic HBV infection in Chinese Han patients. Mol Biol Rep. 2011; 38(8): 5125-32[DOI][PubMed]
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