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Journal of Endotoxin Research
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Defective responsiveness of CD5+ B1 cells to lipopolysaccharide in cytokine production

Naoki Koide

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan, koide{at}aichi-med-u.ac.jp

Akiko Morikawa

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Hiroyasu Ito

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Tsuyoshi Sugiyama

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Ferdaus Hassan

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Shamima Islam

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Gantsetseg Tumurkhuu

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Isamu Mori

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Tomoaki Yoshida

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Takashi Yokochi

Department of Microbiology and Immunology, Aichi Medical University School of Medicine, Nagakute, Aichi, Japan

Previously, we found that mouse TH2.52 cells possess the characteristic of CD5+ B1 cells and proliferate in response to lipopolysaccharide (LPS). The effect of LPS on cytokine production by TH2.52 B1 cells was studied. TH2.52 cells constitutively produced a small amount of tumor necrosis factor (TNF)-{alpha} and interleukin (IL)-6, and TNF-{alpha} and IL-6 production was markedly enhanced by LPS stimulation. Although interferon (IFN)-{gamma} caused the production of various cytokines, such as IL-2, IL-4, IL-6 and TNF-{alpha} in TH2.52 cells, LPS did not cause the production of such cytokines. LPS did not induce IFN-ß production in TH2.52 cells and TH2.52 cells lacked the expression of several molecules participating in the MyD88-independent pathway in LPS signaling. Defective responsiveness of TH2.52 B1 cells to LPS in cytokine production might be responsible for the failure of IFN-ß production due to the lack of molecules participating in the MyD88-independent pathway.

Key Words: CD5+ B cell • B1 cell • LPS • IFN-{gamma} • TNF-{alpha}

Journal of Endotoxin Research, Vol. 12, No. 6, 346-351 (2006)
DOI: 10.1177/09680519060120060401


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