Immunological relationships during primary infection with Heligmosomoides polygyrus. Regulation of fast response phenotype by H-2 and non-H-2 genes

Parasitology. 1993 Sep:107 ( Pt 3):343-50. doi: 10.1017/s0031182000079312.

Abstract

The inheritance of response phenotype to Heligmosomoides polygyrus was investigated in F1 hybrid progeny of fast and slow responder mouse strains. The fast responses of SJL(H-2s) and SWR(H-2q) mice were mediated by dominant genes complementing each other in F1 hybrids which lost worms earlier and produced faster parasite-specific IgG1 antibody responses than either parent. However, the response of F1 hybrids from crosses of C57BL/10 (B10, H-2b) mice with either SJL or SWR differed from that of the parental strains and from each other: (B10 x SWR)F1 lost worms earlier than SWR whilst (B10 x SJL)F1 lost worms later than SJL mice. The F1 progeny of SJL mice with congenic strains B10.G (H-2q) and B10.S (H-2s) lost worms as quickly as SJL. Therefore, the response phenotype mediated by the genome of SJL mice was unaffected by H-2 heterozygosity (with H-2q) or homozygosity (H-2s) despite heterozygosity with B10 background genes, but was slowed significantly by heterozygosity with H-2b. All hybrids involving heterozygosity with B10, irrespective of MHC haplotype or background, failed to clear worms completely, in each case a proportion of mice harbouring residual worm burdens after loss of worms from parental strains.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Helminth / biosynthesis
  • Enzyme-Linked Immunosorbent Assay
  • Gene Expression Regulation / immunology
  • H-2 Antigens / genetics
  • H-2 Antigens / immunology*
  • Immunity, Innate / genetics
  • Immunoglobulin G / biosynthesis
  • Mice
  • Mice, Inbred C57BL
  • Nematospiroides dubius / genetics
  • Nematospiroides dubius / immunology*
  • Phenotype
  • Strongylida Infections / immunology*
  • Time Factors

Substances

  • Antibodies, Helminth
  • H-2 Antigens
  • Immunoglobulin G