Mice deficient for the CD40 ligand

Immunity. 1994 Aug;1(5):423-31. doi: 10.1016/1074-7613(94)90073-6.


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.

MeSH terms

  • Animals
  • Antibody Formation
  • B-Lymphocytes / immunology
  • CD40 Ligand
  • Disease Models, Animal
  • Female
  • Gene Targeting
  • Hypergammaglobulinemia / immunology
  • Immunoglobulin A / biosynthesis
  • Immunoglobulin A / genetics
  • Immunoglobulin G / blood
  • Immunoglobulin G / genetics
  • Immunoglobulin M / blood
  • Immunoglobulin M / genetics
  • Immunologic Memory
  • Male
  • Membrane Glycoproteins / genetics*
  • Membrane Glycoproteins / physiology
  • Mice
  • Mice, Mutant Strains
  • Phenotype
  • Thymus Gland / immunology


  • Immunoglobulin A
  • Immunoglobulin G
  • Immunoglobulin M
  • Membrane Glycoproteins
  • CD40 Ligand