چکیده (انگلیسی):

Background: T cell immunoglobulin domain and mucin domain-containing molecule 3 (TIM-3), which is
preferentially expressed on Th1 cells rather than Th2 cells, is considered to be a negative regulator of Th1
cell function. This suggests that TIM-3 indirectly enhances Th2-type immune responses by suppressing
Th1 cell function.
Methods: To investigate TIM-3's possible involvement in Th2-type acute and chronic airway inflammation,
wild-type and TIM-3-deficient (TIM-3
/
) mice were sensitized and challenged with a house dust
mite (HDM) extract. Airway inflammation and the number of inflammatory cells in bronchoalveolar
lavage fluids (BALFs) in the mice were determined by histological analysis and with a hemocytometer,
respectively. Expression of mRNA in the lungs was determined by quantitative PCR, while the levels of
cytokines in the BALFs and IgE in sera were determined by ELISA.
Results: Despite constitutive expression of TIM-3 mRNA in the lungs, the number of eosinophils in
bronchoalveolar lavage fluids (BALFs) and the score of pulmonary inflammation were comparable between
wild-type and TIM-3
/
mice during both acute and chronic HDM-induced airway inflammation.
On the other hand, the number of lymphocytes in the BALFs of TIM-3
/
mice was significantly increased
compared with wild-type mice during HDM-induced chronic, but not acute, airway inflammation, while
the levels of Th2 cytokines in the BALFs and HDM-specific IgG1 and IgG2a and total IgE in the sera were
comparable in both groups.
Conclusions: Our findings indicate that, in mice, TIM-3 is not essential for development of HDM-induced
acute or chronic allergic airway inflammation, although it appears to be involved in reduced lymphocyte
recruitment during HDM-induced chronic allergic airway inflammation.