Abstract: Zeng Yu, Zhang Yue, Cheng Yanfeng, Zhang Duo, Yang Fan, Li Lin, Han Xiuping. Department of Dermatology, Affiliated Shengjing Hospital, China Medical University, Shenyang 110004, China Corresponding author: Han Xiuping, Email: hanxiuping66@126.com 【Abstract】 Objective To evaluate the roles of Toll-like receptor 2 （TLR2）, TLR4 and myeloid differentiation factor 88 （MyD88） in immune recognition and immune mediation in sporotrichosis by detecting their expressions in skin lesions of sporotrichosis. Methods Biopsy specimens were obtained from the skin lesions of 19 patients with sporotrichosis and normal skin of 12 healthy human controls. Immunohistochemistry was performed to observe the expressions of TLR4 and MyD88, and real-time fluorescence-based quantitative PCR to quantify the expressions of TLR2 and MyD88 mRNAs. Data were expressed as mean ± standard error. Statistical analysis was done with the SPSS17.0 software. Independent samples t-test was conducted to compare the parameters between the lesional and control specimens. A p-value of less than 0.05 was considered to be statistically significant. Results TLR4 and MyD88 were mainly observed in the whole epidermis except the stratum corneum as well as plasma cells and lymphocytes in the dermis and subcutaneous tissue in lesional skin. However, TLR4 was nearly absent and MyD88 was weakly expressed in the dermis and subcutaneous tissue in normal skin. The expression levels of TLR4 and MyD88 were significantly higher in the lesional skin than in the control skin （TLR4, 63.767 ± 3.829 vs. 5.167 ± 3.246, t = 4.82, P ＜ 0.05; MyD88, 57.236 ± 4.744 vs. 10.588 ± 1.640, t = 3.30, P ＜ 0.05）. Similarly, the lesional skin showed significantly stronger expressions of TLR2 and MyD88 mRNAs compared with the normal skin（TLR2, 1.974 ± 1.452 vs. 1.430 ± 1.073, P < 0.05; MyD88, 2.028 ± 2.061 vs. 0.688 ± 0.422, P < 0.05）. Conclusion Sporothrix may induce the development of sporotrichosis by interacting with host immune system via TLR signaling pathways.

Key words: Sporotrichosis, Toll-like receptor 2, Toll-like receptor 4, Myeloid differentiation factor 88