title: IgG1 cytoplasmic tail is essential for cell surface expression in Igβ down-regulated cells.
abstract: It has been shown that cytoplasmic tail of the IgG1 B cell receptors (BCRs) are essential for the induction of T-dependent immune responses. Also it has been revealed that unique tyrosine residue in the cytoplasmic tail of IgG2a has the potential of being phosphorylated at tyrosine and that this phosphorylation modulates BCR signaling. However, it still remains unclear whether such phosphorylation of IgG cytoplasmic tail is involved in the regulation of BCR surface expression. In order to approach the issue, we established and analyzed the cell lines which express wild-type or mutated forms of IgG1 BCR. As the result, we found that IgG1 BCR expressed normally on the surface of A20 B cell line independent of the cytoplasmic tail. In contrast, IgG1 BCR whose cytoplasmic tyrosine was replaced with glutamic acid which mimics phosphorylated tyrosine, was expressed most efficiently on the surface of non-B lineage cells and Igβ-down-regulated B cell lines. These results suggest that tyrosine residue in IgG cytoplasmic tail is playing a essential role for the efficient expression of IgG BCR on the cell surface when BCR associated signaling molecules, including Igβ, are down-regulated.
authors.affiliation: Center for Innovation in Immunoregulative Technology and Therapeutics, Graduate School of Medicine, Kyoto University, Yoshidakonoecho, Sakyoku, Kyoto 606-8501, Japan.
authors.forename: Kagefumi
authors.initials: K
authors.lastname: Todo
authors.affiliation: Center for Innovation in Immunoregulative Technology and Therapeutics, Graduate School of Medicine, Kyoto University, Yoshidakonoecho, Sakyoku, Kyoto 606-8501, Japan.
authors.forename: Orie
authors.initials: O
authors.lastname: Koga
authors.affiliation: Center for Innovation in Immunoregulative Technology and Therapeutics, Graduate School of Medicine, Kyoto University, Yoshidakonoecho, Sakyoku, Kyoto 606-8501, Japan.
authors.forename: Miwako
authors.initials: M
authors.lastname: Nishikawa
authors.affiliation: Center for Innovation in Immunoregulative Technology and Therapeutics, Graduate School of Medicine, Kyoto University, Yoshidakonoecho, Sakyoku, Kyoto 606-8501, Japan. Electronic address: hikida@ak.med.kyoto-u.ac.jp.
authors.forename: Masaki
authors.initials: M
authors.lastname: Hikida
mesh_terms: D020816:Amino Acid Motifs; D000595:Amino Acid Sequence; D019943:Amino Acid Substitution; D000818:Animals; D001402:B-Lymphocytes / Q000378:metabolism*; D051925:CD79 Antigens / Q000235:genetics*; D002460:Cell Line; D045744:Cell Line, Tumor; D015536:Down-Regulation; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007074:Immunoglobulin G / Q000737:chemistry / Q000235:genetics*; D016393:Lymphoma, B-Cell / Q000235:genetics*; D051379:Mice; D008969:Molecular Sequence Data; D011947:Receptors, Antigen, B-Cell / Q000737:chemistry / Q000235:genetics*; D017452:Receptors, IgG / Q000737:chemistry / Q000235:genetics*
chemical_list: D051925:CD79 Antigens; D007074:Immunoglobulin G; D011947:Receptors, Antigen, B-Cell; D017452:Receptors, IgG
keywords: B cell; Germinal center; ITT motif; IgG; Igβ