Nooshin Sohrabi - Mycology Research Centre, Faculty of Veterinary Medicine, Tehran University, Tehran, Iran
Ali Reza Khosravi - Mycology Research Centre, Faculty of Veterinary Medicine, Tehran University, Tehran, Iran
Zuhair Mohammad Hassan - Immunology Department, School of Medicine, Tarbiat Modares University, Tehran, Iran
Mehdi Mahdavi - Immunology Department, School of Medicine, Tarbiat Modares University, Tehran, Iran
Abbas Ali Amini - Immunology Department, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Majid Tebianian - Immunology Department, School of Medicine, Tarbiat Modares University, Tehran, Iran

Objective(s) Using a cancer murine model of invasive aspergillosis (IA), we investigated the expression of TLR-۲, Dectin-۱ and the level of cytokine production by CD۴+ T helper cells in different groups of mice (with or without cancer), also, the effect of invasive aspergillosis on the immune response pattern of cancer mice. Materials and Methods Patterns of susceptibility and resistance to infection obtained with different groups of mice injected with Aspergillus fumigatusconidia. TLR-۲ and Dectin-۱ analyzed applying flowcytometry and cytokine production of cultured splenocytes by ELISA method. Results Cancer mice that challenged with A. fumigatus conidia showed significant increase in TLR-۲ and Dectin-۱ levels compared with the two other control groups (normal mice challenged with A. fumigatus and                 non-infected cancer mice). Moreover, it showed insignificant decrease in IFN-γ and IL-۱۰ levels and insignificant increase in TNF-α level. The data demonstrated remarkable rise in IL-۴ level and the mortality of cancer mice that intravenously infected with A. fumigatus. Conclusion Probably IA causes stimulation in innate immunity and Th۲ cells, also some disorganization in cytokine production in CD۴+ T helper cells. We hypothesize that concomitance of IA and cancer may change the microenvironment for local or systemic immune responses. Other complementary studies could help supporting our hypothesis.

Aspergillosis, Cancer, Cytokines, Dectin ۱, Toll-like receptor ۲