Genetic manipulation of CD74 in mouse strains of different backgrounds can result in opposite responses to central nervous system injury

J Immunol. 2007 Jan 1;178(1):163-71. doi: 10.4049/jimmunol.178.1.163.

Abstract

The ability to recover from CNS injuries is strain dependent. Transgenic mice that weakly express the p41 CD74 isoform (an integral membrane protein functioning as a MHC class II chaperone) on an I-A(b) genetic background have normal CD4(+) T cell populations and normal surface expression of MHC class II, but their B cell development is arrested while the cells are still immature. After a CNS injury, these mice recover better than their matched wild-type controls. We generated p41-transgenic mice on an I-A(d) background (p41-I-A(d) mice), and found that their recovery from CNS injuries was worse than that of controls. A correlative inverse effect was seen with respect to the kinetics of T cell and B cell recruitment to the injured CNS and the expression of insulin-like growth factor at the lesion site. These results, besides verifying previous findings that B cells function in the damaged CNS, demonstrate that the outcome of a particular genetic manipulation may be strain dependent.

MeSH terms

  • Animals
  • Antigens, Differentiation, B-Lymphocyte / genetics*
  • B-Lymphocytes / immunology*
  • Central Nervous System / injuries*
  • Central Nervous System / pathology
  • Central Nervous System Diseases / genetics*
  • Central Nervous System Diseases / immunology*
  • Central Nervous System Diseases / pathology
  • Haplotypes
  • Histocompatibility Antigens Class II / genetics*
  • Histocompatibility Antigens Class II / immunology
  • Mice
  • Mice, Transgenic
  • Protein Isoforms / genetics
  • T-Lymphocytes / immunology

Substances

  • Antigens, Differentiation, B-Lymphocyte
  • Histocompatibility Antigens Class II
  • I-A(b) antigen, mouse
  • I-Ad antigen
  • Protein Isoforms
  • invariant chain