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Identifying the MAGUK protein Carma-1 as a central regulator of humoral immune responses and atopy by genome-wide mouse mutagenesis.

In a genome-wide ENU mouse mutagenesis screen a recessive mouse mutation, unmodulated, was isolated with profound defects in humoral immune responses, selective deficits in B cell activation by antigen receptors and T cell costimulation by CD28, and gradual development of atopic dermatitis with hyper-IgE. Mutant B cells are specifically defective in forming connections between antigen receptors and two key signaling pathways for immunogenic responses, NF-kappaB and JNK, but signal normally to calcium, NFAT, and ERK. The mutation alters a conserved leucine in the coiled-coil domain of CARMA-1/CARD11, a member of the MAGUK protein family implicated in organizing multimolecular signaling complexes. These results define Carma-1 as a key regulator of the plasticity in antigen receptor signaling that underpins opposing mechanisms of immunity and tolerance.

Pubmed ID: 12818157

Authors

  • Jun JE
  • Wilson LE
  • Vinuesa CG
  • Lesage S
  • Blery M
  • Miosge LA
  • Cook MC
  • Kucharska EM
  • Hara H
  • Penninger JM
  • Domashenz H
  • Hong NA
  • Glynne RJ
  • Nelms KA
  • Goodnow CC

Journal

Immunity

Publication Data

June 23, 2003

Associated Grants

None

Mesh Terms

  • Aging
  • Amino Acid Sequence
  • Animals
  • Antibody Formation
  • B-Lymphocytes
  • Dermatitis
  • Guanylate Kinase
  • JNK Mitogen-Activated Protein Kinases
  • Mice
  • Mitogen-Activated Protein Kinases
  • Molecular Sequence Data
  • Mutagenesis
  • NF-kappa B
  • Nucleoside-Phosphate Kinase
  • T-Lymphocytes