Human CD4<sup>-</sup> CD8<sup>-</sup> Invariant Natural Killer T Cells Promote IgG Secretion from B Cells Stimulated by Cross-Linking of Their Antigen Receptors — Oak Academic Publishing
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Human CD4<sup>-</sup> CD8<sup>-</sup> Invariant Natural Killer T Cells Promote IgG Secretion from B Cells Stimulated by Cross-Linking of Their Antigen Receptors
Department of Medical Microbiology, Mycology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan
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Department of Medical Microbiology, Mycology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan
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Department of Medical Microbiology, Mycology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan
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Department of Medical Microbiology, Mycology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan
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Department of Medical Microbiology, Mycology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan
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Department of Chemotherapy and Mycoses, National Institute of Infectious Diseases, Tokyo, Japan
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Department of Chemotherapy and Mycoses, National Institute of Infectious Diseases, Tokyo, Japan
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Division of Immunology, Aichi Cancer Center Research Institute (ACCRI), Nagoya, Japan
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Key Laboratory of Cancer Center, Chinese PLA General Hospital, Beijing, China
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Division of Immunology, Aichi Cancer Center Research Institute (ACCRI), Nagoya, Japan
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Division of Cancer Immunotherapy, Exploratory Oncology Research & Clinical Trial Center, National Cancer Center (NCC), Kashiwa, Japan
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Department of Medical Microbiology, Mycology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan
1 Department of Medical Microbiology, Mycology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan
2 Department of Medical Microbiology, Mycology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan
3 Department of Medical Microbiology, Mycology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan
4 Department of Medical Microbiology, Mycology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan
5 Department of Medical Microbiology, Mycology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan
6 Department of Chemotherapy and Mycoses, National Institute of Infectious Diseases, Tokyo, Japan
7 Department of Chemotherapy and Mycoses, National Institute of Infectious Diseases, Tokyo, Japan
8 Division of Immunology, Aichi Cancer Center Research Institute (ACCRI), Nagoya, Japan
9 Key Laboratory of Cancer Center, Chinese PLA General Hospital, Beijing, China
10 Division of Immunology, Aichi Cancer Center Research Institute (ACCRI), Nagoya, Japan
11 Division of Cancer Immunotherapy, Exploratory Oncology Research & Clinical Trial Center, National Cancer Center (NCC), Kashiwa, Japan
12 Department of Medical Microbiology, Mycology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan
Immunoglobulin (Ig) M production can be induced by the interaction of thymus-independent type-2 (TI-2) antigen (Ag) with B cell Ag receptors (BCRs) without the involvement of conventional T cells; for IgG production through the same process, however, a second signal is required. Previous studies have reported that invariant natural killer T (iNKT) cells may be responsible for the second signal involved in IgG production. In the present study, we addressed whether human iNKT cells could participate in the production of Ig against TI-2 Ag in vitro. Two major distinct subsets of human iNKT cells, CD4 + CD8β - (CD4) and CD4 - CD8β - [double negative (DN)] cells, were generated from peripheral blood monocytes from a healthy volunteer. BCR engagement, triggered by anti-IgM antibody stimulation, examined here as a model of BCR engagement triggered by TI-2 Ag, induced abundant IgM production by B cells. Both CD4 and DN iNKT cells reduced IgM production and conversely enhanced IgG production in a dose-dependent manner. In addition, IgG production by CD19 + CD27 - (naïve) and CD19 + CD27 + (memory) B cells was predominantly promoted by DNiNKT cells rather than CD4 iNKT cells; nevertheless, IgM production by both B cell subsets was similarly reduced by either subset of iNKT cells. These results suggest that the DN iNKT subsets may preferentially promote Ig class switching by B cells upon stimulation with TI-2 Ag.
KeywordsInvariant Natural Killer T CellsTI-2 AntigenB CellsIgMIgG
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