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 Blood, 1 February 2005, Vol. 105, No. 3, pp. 1016-1020.
Prepublished online as a Blood First Edition Paper on September 30, 2004; DOI 10.1182/blood-2004-07-2811.

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HEMATOPOIESIS

Involvement of connective tissue–type mast cells in Th1 immune responses via Stat4 expression

Tatsuki R. Kataoka, Nobuyasu Komazawa, Eiichi Morii, Keisuke Oboki, and Toru Nakano

From the Department of Pathology, Medical School/Graduate School of Frontier Bioscience, the Department of Social and Environmental Medicine, Graduate School of Medicine, and the Department of Molecular Cell Biology, Research Institute for Microbial Disease, Osaka University, Japan; and the Department of Pathology, Osaka Medical Center for Cancer and Cardiovascular Diseases, Japan.

Mast cells are the sentinels of immune systems and, like other immuno-competent cells, they are produced by hematopoietic stem cells. We analyzed the expression of signal transducer and activator of transcription 4 (Stat4), and investigated its role in mast cells. Murine mast cells are usually divided into 2 distinct populations by their distribution and contents of their granules: mucosal mast cells (MMCs) and connective tissue–type mast cells (CTMCs). Stat4 protein was detected in CTMCs but not in MMCs. The absence of Stat4 expression in cultured mast cells was due to the presence of Stat6. In T-helper (Th) cells, Stat4 plays an important role in Th1 shift by inducing a set of genes, such as interferon gamma (IFN-{gamma}) and interleukin-18 receptor {alpha} subunit (IL-18R{alpha}). As in Th1 shift, we found that Stat4 trans-activated these genes in the Stat4-expressing cultured mast cells, namely, microphthalmia transcription factor (MITF)–deficient cultured MMCs, Stat6-deficient cultured MMCs, and cultured CTMCs. Stat4 also enhanced expression of nitric oxide synthase 2 (NOS2) in CTMCs, which brought about increased levels of NO-dependent cytotoxic activity. These data indicate that expression of Stat4 in CTMCs plays an important role on Th1 immune responses.


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