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Mice deficient for the CD40 ligand.

Abstract
To study the potential roles of CD40L in immune responses, we generated CD40L-deficient mice by gene targeting. Similar to the effects of CD40L mutations in humans (hyper-IgM syndrome), CD40L-deficient mice have a decreased IgM response to thymus-dependent antigens, fail altogether to produce an antigen-specific IgG1 response following immunization, yet respond normally to a T-independent antigen, TNP-Ficoll. Moreover, these mice do not develop germinal centers in response to thymus-dependent antigens, suggesting an inability to develop memory B cell responses. Although CD40L-deficient mice have low levels of most circulating immunoglobulin isotypes, they do not exhibit the spontaneous hyper-IgM syndrome seen in humans, at least up to 12 weeks of age. In summary, our study confirms the important role of CD40-CD40L interactions in thymus-dependent humoral immune responses and germinal center formation.
AuthorsJ Xu, T M Foy, J D Laman, E A Elliott, J J Dunn, T J Waldschmidt, J Elsemore, R J Noelle, R A Flavell
JournalImmunity (Immunity) Vol. 1 Issue 5 Pg. 423-31 (Aug 1994) ISSN: 1074-7613 [Print] United States
PMID7882172 (Publication Type: Journal Article)
Chemical References
  • Immunoglobulin A
  • Immunoglobulin G
  • Immunoglobulin M
  • Membrane Glycoproteins
  • CD40 Ligand
Topics
  • Animals
  • Antibody Formation
  • B-Lymphocytes (immunology)
  • CD40 Ligand
  • Disease Models, Animal
  • Female
  • Gene Targeting
  • Hypergammaglobulinemia (immunology)
  • Immunoglobulin A (biosynthesis, genetics)
  • Immunoglobulin G (blood, genetics)
  • Immunoglobulin M (blood, genetics)
  • Immunologic Memory
  • Male
  • Membrane Glycoproteins (genetics, physiology)
  • Mice
  • Mice, Mutant Strains
  • Phenotype
  • Thymus Gland (immunology)

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