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* Division of Host Defense and
Division of Molecular and Clinical Genetics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan;
Department of Pathology, Faculty of Veterinary Medicine, Kasetsart University, Nakhonpathom, Thailand; and
Department of Microbiology and Immunology, University of Miami, Miami, FL 33101
A CD30 ligand (CD30L, CD153) is a type II membrane-associated glycoprotein belonging to the TNF family. To illustrate the potential role of CD30L in CD4+ Th1 cell responses, we investigated the fate of Ag-specific CD4+ T cells in CD30L-deficient (CD30L–/–) mice after Mycobacterium bovis bacillus Calmette-Guérin (BCG) infection. The number of bacteria was significantly higher in organs of CD30L–/– mice than in wild-type (WT) mice 4 wk postinfection. The numbers of purified protein derivative- or Ag85B-specific-IFN-
-producing-CD4+ T cells in spleen, lung, or peritoneal exudate cells were significantly fewer in CD30L–/– mice than in WT mice. During the infection, CD30L was expressed mainly by CD44+CD3+CD4+ T cells but not by CD3+CD8+ T cells, B cells, dendritic cells, or macrophages. Costimulation with agonistic anti-CD30 mAb or coculturing with CD30L-transfected P815 cells restored IFN- production by CD4+ T cells from BCG-infected CD30L–/– mice. Coculturing with CD30L+/+CD4+ T cells from BCG-infected WT mice also restored the number of IFN-+CD30L–/–CD4+ T cells. When transferred into the CD30L+/+ mice, Ag-specific donor CD30L–/– CD4+ T cells capable of producing IFN- were restored to the compared level seen in CD30L+/+ CD4+ T cells on day 10 after BCG infection. When naive CD30L+/+ T cells were transferred into CD30L–/– mice, IFN--producing-CD4+ Th1 cells of donor origin were normally generated following BCG infection, and IFN--producing-CD30L–/–CD4+ Th1 cells of host origin were partly restored. These results suggest that CD30L/CD30 signaling executed by CD30+ T-CD30L+ T cell interaction partly play a critical role in augmentation of Th1 response capable of producing IFN- against BCG infection.
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1 This work was supported by the Program of Founding Research Centers for Emerging and Reemerging Infectious Diseases and was launched as a project commissioned by the Ministry of Education, Culture, Sports, Science and Technology, Japan by a Grant-in-Aid from the Japan Society for the Promotion of Science and by grants from the Japanese Ministry of Education, Science and Culture (to Y.Y.).
2 Address correspondence and reprint requests to Dr. Yasunobu Yoshikai, Division of Host Defense, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan. E-mail address: yoshikai{at}bioreg.kyushu-u.ac.jp
3 Abbreviations used in this paper: TNFRSF, TNFR superfamily; TNFSF, TNF superfamily; BCG, Mycobacterium bovis bacillus Calmette-Guérin; DC, dendritic cell; rBCG-Ag85B, recombinant BCG secreting Ag85B; i.t., intratracheal(ly); PPD, purified protein derivative; MNC, mononuclear cell; PEC, peritoneal exudate cell; CD30L, CD30 ligand; CD62L, CD62 ligand; MMC, mitomycin C; TRAF, TNF receptor-associated factor.
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