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Inverse Association between T‐Cell Immunoglobulin and Mucin Domain‐1 and T‐bet in a Mouse Model of Allergic Rhinitis
Author(s) -
Xu Geng,
Cheng Lei,
Wen Weiping,
Oh Yun,
Mou Zhonglin,
Shi Jianbo,
Xu Rui,
Li Huabin
Publication year - 2007
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1097/mlg.0b013e318041549c
Subject(s) - flow cytometry , ovalbumin , peripheral blood mononuclear cell , antibody , reverse transcription polymerase chain reaction , microbiology and biotechnology , immunoglobulin e , immunology , real time polymerase chain reaction , t cell , messenger rna , biology , antigen , immune system , gene , biochemistry , in vitro
Background : It has been suggested that human hepatitis A virus cellular receptor, also known as T‐cell immunoglobulin and mucin domain‐1 (TIM‐1), plays an important role in the development of allergic diseases on the basis of epidemiologic data, but the molecular mechanism has been unclear. In a murine model of ovalbumin (OVA)‐sensitized allergic rhinitis (AR), we examined the expression of TIM‐1 and its correlation with T helper1‐associated transcription factor, T‐bet, as a potential mediator of T‐cell immunoglobulin expression. Methods : Mice were challenged intranasally with OVA to elicit AR. The expression of TIM‐1 in nasal tissues was examined by real‐time reverse‐transcription polymerase chain reaction (RT‐PCR), and the surface expression of TIM‐1 in peripheral blood mononuclear cells was evaluated by means of flow cytometry. In addition, the expression of TIM‐1 as well as T‐bet in splenic lymphocytes was examined by Western blotting. Results : TIM‐1 mRNA was increased significantly in nasal tissues ( P < .05) as seen by real‐time RT‐PCR. Flow cytometry indicated a differential TIM‐1 expression of 135.5 ± 34.2 in the AR group versus 51.1 ± 10.9 in the control group ( P < .05). The mean values of normalized TIM‐1 were 0.43 ± 0.18 and 0.21 ± 0.10 in AR and control groups, respectively, whereas the mean values of normalized T‐bet were 0.22 ± 0.13 and 0.67 ± 0.17 in the AR and control groups, respectively. There was a significant difference in the production of TIM‐1 as well as T‐bet in AR mice versus control mice ( P < .05). The increased production of TIM‐1 correlated significantly with the decreased T‐bet in spleen tissue of AR mice ( r = −0.52, P < .05). Conclusion : Our experimental model recapitulates an increase in lymphocyte TIM‐1 expression seen in AR both locally and systemically. Our results also demonstrate an inverse relationship between lymphocyte TIM‐1 and T‐bet expression, suggesting a possible mechanism that TIM‐1 influences the development of AR.