Imary N. brasiliensis infection.Intestinal goblet cell hyperplasia was assessed by

Imary N. brasiliensis infection.Intestinal goblet cell hyperplasia was assessed by determining the total number of PAS-positive goblet cells per 5 villi in histological sections of the small intestine at day 7 and 10 PI (C). Total IgE production in the serum was measured by ELISA at day 7 and 10 PI (D). The data are representative of the results of two independent experiments with mean values+SEM and n = 4 or 5 mice per group. ND, not detected, ns = not significant. One-WayANOVA, *P,.05, **P,.01. (TIF)Figure 1676428 S3 N. brasiliensis infection is comparable between BALB/c and IL-4Ra2/lox mice. Five mice per group were infected with 750 N. brasiliensis L3 larvae. Faeces were collected from day 5 to 10 post infection (PI) and egg production was calculated using the modified McMaster order PD-1/PD-L1 inhibitor 1 technique (A). At days 7 and 10 PI the worm burden in the small intestine was assessed (B). Intestinal goblet cell hyperplasia was assessed by determining the total number of PAS-positive 15481974 goblet cells per 5 villi in histological sections of the small intestine at day 7 and 10 PI (C). Total IgE production in the serum was measured by ELISA at day 7 and 10 PI (D). Comparison of the response of infected BALB/c and IL-4Ra2/lox mice to acetylcholine is also shown for day 7 p.i. The data represents one (A-D) and two (E) independent experiment with n = 5 per group and mean values + SEM. ND, not detected. Unpaired two-tailed Student t test, ns = not significant. (TIF) Table S1 Summary of IL-4Ra surface expression on TSupporting InformationFigure S1 IL-4 responsive T cells are not needed for expulsion of N. brasiliensis. Duplicated worm burdens from figure 1B represented as individual counts at days 7 and 10 PI. As above, the data represents three independent experiments combined, with n = 4 or 5 per group, ns = not significant. OneWay-ANOVA, ***P,.001. (TIF) Figure S2 N. brasiliensis infection is comparable between iLckcreIL-4Ra2/lox and LckcreIL-4Ra2/lox mice. iLckcreIL-4Ra2/lox, LckcreIL-4Ra2/lox and control mice were infected with 750 N. brasiliensis L3 larvae. Faeces were collected from day 5 to 10 post infection (PI) and egg production was calculated using the modified McMaster technique (A). At days 7 and 10 PI the worm burden in the small intestine was assessed (B).cell subpopulations. Table S1 summarizes the surface expression of IL-4Ra on T cell Pluripotin Subpopulations determined by FACS as previously described [29,30]. Subpopulations include CD4+, CD8+, cd T cells and NK T cells. (DOC)AcknowledgmentsWe thank Lizette Fick, Wendy Green, Rayaana Fredericks for their technical assistance. Current Address of HM, Malaghan Institute of Medical Research, Wellington 6012, New Zealand and AJC, Histocompatibility and Immunogenetics Research group, NHS Blood and Transplant, Colindale, London, UK.Author ContributionsConceived and designed the experiments: SS JCH WGCH AJC FB. Performed the experiments: SS JCH HM. Analyzed the data: SS JCH TMB. Wrote the paper: SS JCH WGCH FB.
Caenorhabditis elegans is an extremely versatile and appropriate animal model for mimicking and recapitulating in vivo the key molecular mechanisms underlying the gene-and tissue-specific protein misfolding and toxicity related to the human pathogenesis [1]. Despite the evolutionary distance from vertebrates, human proteins substantially maintain their structure and function when they are expressed in C. elegans [1]. Many variant proteins associated to human diseases cause a pathological phenotype in worms and this c.Imary N. brasiliensis infection.Intestinal goblet cell hyperplasia was assessed by determining the total number of PAS-positive goblet cells per 5 villi in histological sections of the small intestine at day 7 and 10 PI (C). Total IgE production in the serum was measured by ELISA at day 7 and 10 PI (D). The data are representative of the results of two independent experiments with mean values+SEM and n = 4 or 5 mice per group. ND, not detected, ns = not significant. One-WayANOVA, *P,.05, **P,.01. (TIF)Figure 1676428 S3 N. brasiliensis infection is comparable between BALB/c and IL-4Ra2/lox mice. Five mice per group were infected with 750 N. brasiliensis L3 larvae. Faeces were collected from day 5 to 10 post infection (PI) and egg production was calculated using the modified McMaster technique (A). At days 7 and 10 PI the worm burden in the small intestine was assessed (B). Intestinal goblet cell hyperplasia was assessed by determining the total number of PAS-positive 15481974 goblet cells per 5 villi in histological sections of the small intestine at day 7 and 10 PI (C). Total IgE production in the serum was measured by ELISA at day 7 and 10 PI (D). Comparison of the response of infected BALB/c and IL-4Ra2/lox mice to acetylcholine is also shown for day 7 p.i. The data represents one (A-D) and two (E) independent experiment with n = 5 per group and mean values + SEM. ND, not detected. Unpaired two-tailed Student t test, ns = not significant. (TIF) Table S1 Summary of IL-4Ra surface expression on TSupporting InformationFigure S1 IL-4 responsive T cells are not needed for expulsion of N. brasiliensis. Duplicated worm burdens from figure 1B represented as individual counts at days 7 and 10 PI. As above, the data represents three independent experiments combined, with n = 4 or 5 per group, ns = not significant. OneWay-ANOVA, ***P,.001. (TIF) Figure S2 N. brasiliensis infection is comparable between iLckcreIL-4Ra2/lox and LckcreIL-4Ra2/lox mice. iLckcreIL-4Ra2/lox, LckcreIL-4Ra2/lox and control mice were infected with 750 N. brasiliensis L3 larvae. Faeces were collected from day 5 to 10 post infection (PI) and egg production was calculated using the modified McMaster technique (A). At days 7 and 10 PI the worm burden in the small intestine was assessed (B).cell subpopulations. Table S1 summarizes the surface expression of IL-4Ra on T cell subpopulations determined by FACS as previously described [29,30]. Subpopulations include CD4+, CD8+, cd T cells and NK T cells. (DOC)AcknowledgmentsWe thank Lizette Fick, Wendy Green, Rayaana Fredericks for their technical assistance. Current Address of HM, Malaghan Institute of Medical Research, Wellington 6012, New Zealand and AJC, Histocompatibility and Immunogenetics Research group, NHS Blood and Transplant, Colindale, London, UK.Author ContributionsConceived and designed the experiments: SS JCH WGCH AJC FB. Performed the experiments: SS JCH HM. Analyzed the data: SS JCH TMB. Wrote the paper: SS JCH WGCH FB.
Caenorhabditis elegans is an extremely versatile and appropriate animal model for mimicking and recapitulating in vivo the key molecular mechanisms underlying the gene-and tissue-specific protein misfolding and toxicity related to the human pathogenesis [1]. Despite the evolutionary distance from vertebrates, human proteins substantially maintain their structure and function when they are expressed in C. elegans [1]. Many variant proteins associated to human diseases cause a pathological phenotype in worms and this c.

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