Regular ArticleThe Role of CD40–CD40 Ligand (CD154) Interactions in Immunoglobulin Light Chain Repertoire Generation and Somatic Mutation
References (52)
- et al.
Regulation of B cell commitment to plasma cells or to memory cells
Semin. Immunol.
(1997) - et al.
The CD40 ligand, gp39, is defective in activated T cells from patients with X-linked hyper-IgM syndrome
Cell
(1993) - et al.
The immune responses in CD40 deficient mice: Impaired immunoglobulin class switching and germinal center formation
Immunity
(1994) - et al.
Mice deficient for CD40 ligand
Immunity
(1994) - et al.
Somatic hypermutagenesis in immunoglobulin genes. II. Influence of neighbouring base sequences on mutagenesis
Biochem. Biophys. Acta
(1992) Life and death in germinal centers
Immunity
(1996)- et al.
Immunoglobulin Genes
(1995) - et al.
The changing preference of T and B cells for partners as T-dependent antibody responses develop
Immunol. Rev.
(1997) - et al.
CD40–CD40 ligand: A multifunctional receptor–ligand pair
Adv. Immunol.
(1996) - et al.
CD40 ligand and appropriate cytokines induce switching to IgG, IgA, and IgE and coordinated germinal center and plasmacytoid phenotypic differentiation in a human monoclonal IgM+IgD+ B cell line
J. Immunol.
(1998)
Immunohistologic analyis of ineffective CD40–CD40 ligand interaction in lymphoid tissues from paitents with X-linked imunodeficiency with hyper-IgM. Abortive germinal center cell reaction and severe depletion of folicular dendritic cells
J. Immunol.
Bidirectional regulation of human B cell responses by CD40–CD40 ligand interactions
J. Immunol.
The role of CD40–CD40 ligand interaction in human T cell-B cell collaboration
J. Immunol.
Immune regulation by CD40 and its ligand gp39
Annu. Rev. Immunol.
Absence of IgD-CD27+ memory B cell population in X-linked hyper-IgM syndrome
J. Clin. Invest.
Memory B cells are biased towards terminal differentiation: A strategy that may prevent repertoire freezing
J. Exp. Med.
Cellular interaction in germinal centers. Roles of Cd40 ligand and B7-2 in established germinal centers
J. Immunol.
CD40 ligand gene defects responsible for X-linked hyper-IgM syndrome
Science
CD40 ligand mutations in X-linked immunodeficiency with hyper-IgM
Nature
The hyper-IgM (HIM) syndrome
Springer Semin. Immunopathol.
Humoral immune responses in CD40 ligand-deficient mice
J. Exp. Med.
The influence of CD40–CD154 interactions on the expressed human VH repertoire: Analysis of VH genes expressed by individual B cells of a patient with X-linked hyper-IgM syndrome
Int. Immunol.
Defects of T cell effector function and post-thymic maturation in X-linked hyper-IgM syndrome
J. Clin. Invest.
The CD40 ligand expressed by human B cells costimulates B cell responses
J. Immunol.
Molecular mechanisms and selection influence the generation of the human VlJl repertoire
J. Immunol.
Cited by (20)
Class Switch Recombination and Somatic Hypermutation in Early Mouse B Cells Are Mediated by B Cell and Toll-like Receptors
2007, ImmunityCitation Excerpt :AID is expressed upon activation of B lymphocytes, and it has been widely accepted that CSR and SHM occur during germinal center (GC) reactions after antigen activation of mature B cells with T cell help (Kelsoe, 1995; Muramatsu et al., 1999). However, some studies have indicated that SHM may occur outside of the GCs (Kato et al., 1998; Wang et al., 2000; William et al., 2002), that SHM can occur without T cell help (Monson et al., 2001; Toellner et al., 2002; Weller et al., 2001), and that SHM can occur even in the absence of an immune response (Reynaud et al., 1995; Weller et al., 2004). The exact mechanisms involved in T-independent SHM processes that occur outside of the GCs are not known.
Cerebrospinal fluid B cells from multiple sclerosis patients are subject to normal germinal center selection
2007, Journal of NeuroimmunologyIntrathymic differentiation of natural antibody-producing plasma cells in human neonates
2021, Nature Communications
- 1
To whom correspondence and reprint requests should be addressed at National Institute of Arthritis and Musculoskeletal and Skin Diseases, Building 10, Room 9N228, 10 Center Drive MSC 1820, Bethesda, MD 20892-1820. Fax: (301) 402-0012. E-mail: [email protected].