Journal of Research in Medical Sciences (Jan 2014)

Comparison of immune regulatory factors in acute and chronic lesions of cutaneous leishmaniasis due to Leishmania major

  • Shervin Ghaffari Hoseini,
  • Shaghayegh Haghjooy Javanmard,
  • Seyed Hossein Hejazi,
  • Laleh Rafiei,
  • Sayyed Hamid Zarkesh,
  • Khadije Karbalaii,
  • Ali Khamesipour

Journal volume & issue
Vol. 19, no. 13
pp. 36 – 40

Abstract

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Background: Adaptive immune response is an important factor in the healing process and development of protection in cutaneous leishmaniasis (CL). Little information is available in human CL about the importance of the balance between effector and regulatory immune responses. Therefore, the aim of this study was to asses messenger ribonucleic acid (mRNA) expression of interleukin-10 (IL-10), IL-4, transforming growth factor-β1 (TGF-β1), interferon-g (IFN-g), and forkhead box P3 (Foxp3) (as a marker of regulatory T cells) in acute and chronic CL lesions caused by Leishmania major compared with normal skin samples. Materials and Methods: Thirty biopsies were obtained from CL patients with acute lesions (AL, n = 13), chronic lesions (CH, n = 11) and healthy volunteers (n = 6). Relative expressions of target genes were determined by means of reverse transcription real time polymerase chain reaction and were compared with the controls. Results: Expression of Foxp3, IL-4, and IFN-g were significantly more in CH than AL group of patients (Foxp3: Median 0.48, inter-quartile range 0.32-0.76 [arbitrary units] for AL, and 0.97 (0.75-1.30) for CH, P = 0.006; IFN-g: 45.98 (33.39-173.48) for AL, and 200.53 (97.49-361.76) for CH, P = 0.023; IL-4: 0.49 (0.34-2.16) for AL, and 2.14 (1.30-7.11) for CH, P = 0.021). Expression of TGF-β was not significantly different between groups. Conclusion: The results indicate that IL-4 secretion at the site of L. major infection rather than low IFN-g production might have a role in prolongation of disease. Despite a moderate increase of Foxp3 expression in chronic lesions, function of Tregs in persistent infection is not clear.

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