| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5654835 | Clinical Immunology | 2017 | 34 Pages |
Abstract
The present study suggests that defects in Pyk2 suppress KD-like experimental vasculitis, presumably through CXCL9- and CXCL10-dependent interference with neo-angiogenesis. Since Pyk2-KO mice show no life-threatening phenotype, Pyk2 may be a promising therapeutic molecular target for KD.
Keywords
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Immunology
Authors
Chinatsu Suzuki, Akihiro Nakamura, Noriko Miura, Kuniyoshi Fukai, Naohito Ohno, Tomoyo Yahata, Akiko Okamoto-Hamaoka, Maiko Fujii, Ayako Yoshioka, Yuki Kuchitsu, Kazuyuki Ikeda, Kenji Hamaoka,