Immune development in CD1-deficient mice

Y. H. Chen, B. Wang, L. Zhao, C. R. Wang

Research output: Contribution to journalArticle

Abstract

CD1 molecules are evolutionarilly conserved MHC class Ib molecules. Two CD1 genes in the mouse (mCD1.1 and mCD1.2) have been cloned and sequenced. To assess the function of the CD1 genes, we generated CD1.1 knockout (CD1.1 -/-) and CD1.1, 1.2-knockout (CD1 -/-) mice using gene targeting techniques. The CD1 -/- mice lack surface expression of CD1 in all organs, while CD1.1 -/- mice showed significant amounts of CD1.2 expression in thymus but very low levels in other organs. In both animal models, a subpopulation of NK1 + T cells, particularly those with a canonical gene rearrangement of Vα14-Jα281, is greatly diminished. Absence of this T cell population renders CD1-deficient mice unable to generate a rapid IL-4 response following systemic T cell activation. However, CD1-deficient mice can generate an effective antigen-specific Th2 response. Thus, CD1 is required for the development of NK1 + T cells, and the early IL-4 production from NK1 + T cells is not essential for Th2 differentiation. The expression of CD1.2 in the thymus can not compensate for CD1.1 in selecting a subset of NK1 + T cell populations. It has been suggested that NK1 + T cells participate in the innate immune response against L. monocytogenes. However, no significant differences in cytokine profiles and bacteria burden can be detected between listeria-infected CD1 -/- and control mice . This result suggests that although NK1 + T cells may be able to modulate some innate immune responses, other cell types in innate immunity may be sufficient for the early clearance of bacteria.

Original languageEnglish (US)
JournalFASEB Journal
Volume12
Issue number5
StatePublished - Mar 20 1998

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

Fingerprint Dive into the research topics of 'Immune development in CD1-deficient mice'. Together they form a unique fingerprint.

  • Cite this