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Infection and Immunity, August 2005, p. 5144-5151, Vol. 73, No. 8
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.8.5144-5151.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

4-1BB (CD137) Is Required for Rapid Clearance of Listeria monocytogenes Infection

Sang-C. Lee,1 Seong-A. Ju,1 Ha-N. Pack,1 Sook-K. Heo,1 Jae-H. Suh,2 Sang-M. Park,1 Boem-K. Choi,1 Byoung S. Kwon,1,3* and Byung S. Kim1*

Immunomodulation Research Center, University of Ulsan, Ulsan, Korea, 680-749,1 Department of Pathology, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea, 682-060,2 LSU Eye Center, Louisiana State University Health Sciences Center School of Medicine, New Orleans, Louisiana 701123

Received 27 August 2004/ Returned for modification 11 October 2004/ Accepted 17 March 2005

4-1BB (CD137), a member of the tumor necrosis factor receptor superfamily, is a T-cell-costimulatory receptor that is expressed on activated T cells, dendritic cells, and NK cells. Little has been reported about its role in early host defense against bacterial infection. In this study, we report that 4-1BB-deficient (4-1BB–/–) mice are much more susceptible to Listeria monocytogenes (intracellular bacteria) infections than wild-type mice. Upon L. monocytogenes infection, 4-1BB–/– mice showed a lower survival rate, a higher bacterial burden in organs, and larger hepatic microabscesses than 4-1BB+/+ mice. 4-1BB–/– mice also had impairment in clearance of bacteria from the bloodstream. Neutrophils from 4-1BB+/+ mice constitutively expressed 4-1BB, which could be activated to induce intracellular Ca2+ influx by ligation with anti-4-1BB antibody. On the other hand, neutrophils from 4-1BB–/– mice were defective in reactive oxygen species generation, phagocytic activities, and intracellular Ca2+ mobilization. In addition, mice pretreated with anti-4-1BB monoclonal antibody were much more resistant to L. monocytogenes infection than control antibody-treated mice. Our results support the notion that 4-1BB may play a major role in host defense against intracellular pathogens through neutrophil activation.

* Corresponding author. Mailing address: Immunomodulation Research Center, University of Ulsan, San 29, Mukeo-dong, Nam-ku, Ulsan, Republic of Korea, 680-749. Phone for Byoung S. Kwon: 82-52-259-2875. Fax: 82-52-259-2740. E-mail: bskwon{at}mail.ulsan.ac.kr. Phone for Byung S. Kim: 82-52-259-1541. Fax: 82-52-259-2740. E-mail: sjc513{at}mail.ulsan.ac.kr.

Editor: F. C. Fang

Infection and Immunity, August 2005, p. 5144-5151, Vol. 73, No. 8
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.8.5144-5151.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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