27 During long-term exposure to the antigen, leading to a chroni

27. During long-term exposure to the antigen, leading to a chronic lung inflammation, the number of eosinophils and monocytes were significantly upregulated. The lack of Thy-1 resulted in decreased infiltration of eosinophils and monocytes into the lung during acute as well as chronic

inflammation, indicating a key role of Thy-1 Ipatasertib price in airway inflammation induced by OVA. Thus, investigating different inflammation models in Thy-1−/− mice, we could prove the physiological relevance of Thy-1 in the control of the recruitment of leukocytes at sites of inflammation in vivo. Due to strong expression of Thy-1 on TCs in mice, Thy-1 was investigated previously in mouse models with respect to the role of Thy-1 for development and function of TCs 14, 28, 29. Beissert et al. showed that Thy-1 deficiency in mice led to reduced contact hypersensitivity responses and a decreased irritant dermatitis, which were suggested to be due to a defective fine tuning of TC functions 14. In the light of our data, the impaired cutaneous immune responses in Thy-1−/− mice might, in addition to affected TC responses, also be caused by the lack of Thy-1 as an adhesion receptor on EC, mediating

the extravasation of leukocytes during inflammation. Considering the high expression of Thy-1 on murine TCs 29, 14 and the pathogenic role of TCs in OVA-induced lung inflammation 21, we excluded that the reduced lung inflammation in Thy-1−/− mice was dependent of the

different Thy-1 expression levels on TCs. In Thy-1 BM chimera, the Thy-1-expression was detectable on 70% of TCs. Although Thy-1−/− BM learn more chimera expressed Thy-1 on TCs and Thy-1−/− mice did not, airway inflammation was similarly reduced in both. In addition, BM transfer did not result in the incorporation of Thy-1-positive EC progenitor cells into the vessels, as Thy-1 staining of lungs revealed that PIK3C2G vessels did not express Thy-1 in the BM chimeras. Thus, we can conclude that reduced extravasation of eosinophils and monocytes during airway inflammation in Thy-1-deficient mice is independent of Thy-1 expression on TCs and relies on the Thy-1 expression on activated ECs. Gerwin et al. used the approach of generating BM chimera to exclude effects of TCs in an inflammation model in ICAM-2−/− mice. Accordingly, they also showed that the lack of ICAM-2 on ECs was responsible for the decreased eosinophil emigration during lung inflammation 30. As expected, the infiltration of leukocytes to the BAL fluid or into the peritoneal cavity was not completely inhibited in Thy-1−/− mice, suggesting a functional impact of further adhesion molecules. For example, ICAM-1−/− mice showed strongly decreased leukocyte infiltration in an OVA-induced inflammation model 31, as well as in a murine model of toluene diisocyanate-induced lung inflammation 32.

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