Genetic‐linked variation in susceptibility of mice to <i>Schistosomiasis mansoni</i>

Fanning, Mary M.; Kazura, James W.

doi:10.1111/j.1365-3024.1984.tb00784.x

Cited by 21 publications

(9 citation statements)

References 19 publications

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“…It was of interest to examine the susceptibility of 129/J mice bred al the Walter and Eliza Hall Institute (WEHI) to S. mansoni. Fanning and Kazura (1984) did not find any peculiarities in 129/J mice exposed to S. mansoni. In this paper we report that WEHI 129/J mice are resistant to S. mansoni (Puerto Rico) and that antibody specificities exist in sera from S. mansoni-expoxd 129/J mice that are nol apparent in sera from S. mansoni-infecled BALB/c mice.…”

Section: Introductionmentioning

confidence: 67%

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RESISTANCE OF 129/J MICE TO SCHISTOSOMA MANSONI INFECTION

A²,

Jc³

et al. 1986

Aust J Exp Biol Med

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Summary. Mice of the strain 129/J bred at this Institute (WEHI 129/J) were exposed once or repeatedly to cercariae of Schistosoma mansoni and worm burdens determined. In keeping with reports of S. japonicum infection in these mice, a high level of resistance was recorded. Radio-labelled extracted antigens of S. mansoni adult worms were reacted with sera from exposed 129/J mice and infected BALB/c mice. Immunoprecipitated antigens preferentially recognized by antibodies in 129/J mice include proteins of Mr 99,000 and 21,000. Whether responses to these antigens are a cause or a consequence of resistance remains to be established.

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Section: Introductionmentioning

confidence: 67%

“…A protein that did not appear to be recognized differentially by sera from the two types of mice was a dominant antigen of Mr 27.000. The relationship of this molecule to the Mr 28,000 .n f I ; ; PP "-" "'"^'^ ^^P°"'='^ ">' F^""i"g and Kazura (1984) usin. a different ou ce of 129/J m,ce.…”

Section: Discussionmentioning

confidence: 96%

RESISTANCE OF 129/J MICE TO SCHISTOSOMA MANSONI INFECTION

A²,

Jc³

et al. 1986

Aust J Exp Biol Med

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“…These include the high susceptibility of 129/J mice to infection with Sendai and CMV viruses and the induction of systemic lupus erythematosus as well as differences in their susceptibility to experimental autoimmune encephalomyelitis (25,26,29,30). 129/J mice are also more susceptible to infection with Schistosoma mansoni than are B6, and when infected with the intraerythrocytic Babesia-like organism, WA-1, 129/J mice exhibit higher levels of peak parasitemia and a 5-fold higher mortality rate (43,44). The role for NK cells in general, or DAP12-coupled receptors specifically, in these processes is poorly defined.…”

Section: Discussionmentioning

confidence: 99%

Aberrant DAP12 Signaling in the 129 Strain of Mice: Implications for the Analysis of Gene-Targeted Mice

McVicar

Winkler‐Pickett

Taylor

et al. 2002

The Journal of Immunology

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NK cells are implicated in antiviral responses, bone marrow transplantation and tumor immunosurveillance. Their function is controlled, in part, through the Ly49 family of class I binding receptors. Inhibitory Ly49s suppress signaling, while activating Ly49s (i.e., Ly49D) activate NK cells via the DAP12 signaling chain. Activating Ly49 signaling has been studied primarily in C57BL/6 mice, however, 129 substrains are commonly used in gene-targeting experiments. In this study, we show that in contrast to C57BL/6 NK cells, cross-linking of DAP12-coupled receptors in 129/J mice induces phosphorylation of DAP12 but not calcium mobilization or cytokine production. Consistent with poor-activating Ly49 function, 129/J mice reject bone marrow less efficiently than C57BL/6 mice. Sequence analysis of receptors and DAP12 suggests no structural basis for inactivity, and both the 129/J and C57BL/6 receptors demonstrate normal function in a reconstituted receptor system. Most importantly, reconstitution of Ly49D in 129/J NK cells demonstrated that the signaling deficit is within the NK cells themselves. These unexpected findings bring into question any NK analysis of 129/J, 129Sv, or gene-targeted mice derived from these strains before complete backcrossing, and provide a possible explanation for the differences observed in the immune response of 129 mice in a variety of models.

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“…In mice exposed to Schistosoma mansoni, the host response to the parasite appears to be subject to genetic control. This is seen as the variation between inbred mouse strains in the establishment of adult worm burdens (Bickle et al 1980;Colley & Freeman 1980;Dean 1983;Fanning & Kazura 1984), the resistance to challenge infections of mice previously vaccinated with irradiated cercariae (Sher et al 1984) and the late modulation of hepatosplenomegaly, portal venous pressure and granuloma size in chronically infected mice (Fanning & Kazura 1981). Attempts to correlate such variation with the genetic constitution of the mouse strains have yielded equivocal results but suggest that genes both within and outside the major histocompatibility complex are involved (Sher et al 1984, Fanning & Kazura 1985.…”

Section: Introductionmentioning

confidence: 99%

Genetic influence on the antibody response to antigens of Schistosoma mansoni in chronically infected mice

Kee

Taylor

Cordingley

et al. 1986

Parasite Immunology

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Immunoprecipitations of in vitro translation products of mRNA from adult Schistosoma mansoni worms with sera from chronically infected mice of 12 inbred strains reveal a strain-dependent heterogeneity in the antibody responses to schistosome antigens. Of the strains tested the response to the 86K antigen was restricted to mice of haplotypes H-2d H-2k, and H-2a while the 14K antigen was only recognized by H-2k mice. Responses to other antigens revealed the influence of non-H-2 genes on the antibody response although no clear correlation was apparent between the antigens recognized and the non-H-2 genes of the strains. Both dominant and recessive responses towards individual antigens were seen in F1 animals. Some of these results support the cross tolerance model of Ir gene function.

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Genetic‐linked variation in susceptibility of mice to Schistosomiasis mansoni

Cited by 21 publications

References 19 publications

RESISTANCE OF 129/J MICE TO SCHISTOSOMA MANSONI INFECTION

RESISTANCE OF 129/J MICE TO SCHISTOSOMA MANSONI INFECTION

Aberrant DAP12 Signaling in the 129 Strain of Mice: Implications for the Analysis of Gene-Targeted Mice

Genetic influence on the antibody response to antigens of Schistosoma mansoni in chronically infected mice

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