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. 1983 Feb;48(2):343–350.

Genetic control of immunity to Trichinella spiralis: influence of H-2-linked genes on immunity to the intestinal phase of infection

D Wakelin, Anne M Donachie
PMCID: PMC1453913  PMID: 6401687

Abstract

The time course of expulsion of adult Trichinella spiralis from the intestine was determined in B10 background, H-2 congenic and recombinant mice. Non-H-2 genes exerted the major influence on worm expulsion (i.e. determined rapid or slow response phenotype) but marked time course differences were seen among the slow responder B10 background strains, implying that H-2-linked genes also influence this parameter of immunity. Independent H-2q haplotype mice showed the most rapid expulsion, H-2k and H-2b the slowest. Data from H-2 recombinant mice carrying the q allele suggested that alleles at H-2K loci have a strong influence in immunity, but showed also that H-2D alleles exert a significant modulating effect. The q allele in otherwise susceptible k haplotype mice (B10.AKM) gave increased resistance; the d allele at H-2D in mice carrying the q resistance allele elsewhere [B10.T(6R)] gave decreased resistance. Adoptive transfers using immune mesenteric node lymphocytes (IMLNC) from a series of donors were used to identify how the modulating influence of H-2Dd was expressed in B10.T(6R) mice. IMLNC from this strain transferred immunity to recipients of other (histocompatible) strains, but IMLNC from such strains failed to accelerate expulsion in B10.T(6R) recipients as did homologous B10.T(6R) cells. Two alternative models are proposed to explain these results: either that H-2Dd influences the response of myeloid precursors to lymphocyte-derived factors, and thus the generation of intestinal inflammatory changes necessary for expulsion, or, on the assumption that the generation of intestinal inflammation requires initial cooperation between helper and effector lymphocytes, that H-2Dd is associated with a restricted ability of effector cells to respond to the helpers present in IMLNC.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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