4a). Given these results, and the delay in B-cell maturation selleck products suggested by flow cytometric analysis of the bone marrow, we next considered the possibility that over-expression of the dnRAG1 transgene might render V(D)J recombination inefficient, resulting in a restricted B-cell repertoire. To test this possibility, we examined

the immunoglobulin heavy chain repertoire by amplifying VH-D-JH junctions from genomic DNA isolated from WT and dnRAG1 mouse spleens, and analysing nested runoff PCR products by sequencing gel electrophoresis as illustrated in Fig. 4(b).24 Three different VH gene families (J558, 7183, and Q52) were evaluated using this approach. In this assay, small differences in fragment length among amplicons from a given gene family reflect junctional diversification of CDR3 that occurs during V(D)J recombination: the pattern of the CDR3 length distribution is proportional to the fractional abundance of each rearrangement in the original sample. We found that the profile CHIR-99021 cell line of runoff products from several WT animals shows a largely Gaussian distribution for all three VH families

tested, indicative of a highly diverse repertoire. In contrast, the CDR3 length distributions of all three VH gene families from three different dnRAG1 mice are clearly skewed toward a smaller number of fragment lengths (Fig. 4c,d). These data suggest that while splenic B cells in dnRAG1 mice are clonally diverse, the CDR3 repertoire among these cells is more restricted than in their normal counterparts. Dimethyl sulfoxide Because B220lo CD19+

B cells in 12-week-old dnRAG1 mice account for about 20% of splenic B cells at this age, we considered the possibility that the molecular features of the B220hi CD19+ B cells may partly mask those of the B220lo CD19+ B-cell population in a bulk splenic B-cell preparation. To address this issue, we sorted the two populations (Fig. 5a), and isolated genomic DNA or total RNA to compare immunoglobulin gene rearrangement patterns and immunoglobulin light chain gene sequences (Fig. 5b,c). Consistent with results obtained with bulk splenocytes, B220hi CD19+ B cells from WT and dnRAG1 mice showed fairly similar patterns of VH-to-DJH and Vκ-to-Jκ rearrangements (Fig. 5b). Interestingly, however, skewing was clearly evident in the rearrangement patterns detected from B220lo CD19+ B cells, particularly in the Igκ locus, where Jκ1 segment usage predominates over other Jκ rearrangements (Fig. 5b). This finding is confirmed by the preponderance of light chain genes containing the Jκ1 segment cloned from B220lo CD19+ B cells (11/15 clones sequenced), whereas Jκ usage is more evenly distributed between Jκ1, Jκ2 and Jκ5 segments among clones sequenced from B220hi CD19+ B cells sorted from WT and dnRAG1 mice (Fig. 5c, lower left panel).

In the most literal sense, granulomatosis indicates a condition characterized by multiple granulomas. Sarcoidosis is an archetype granulomatosis, although the term granulomatosis is rarely used in discussing or writing about sarcoidosis. In fact, the term granulomatosis is most often used Rapamycin supplier in the medical literature in the context of GPA (WG). Especially in the acute lesions of GPA

(WG), the predominant pattern of inflammation is not granulomatous, but purulent. Thus, the inflammation has the appearance of an abscess more than a granuloma (Fig. 2). Often, the only feature in the acute inflammatory lesions that is reminiscent of granulomatous inflammation is the presence of scattered multi-nucleated giant cells. As lesions age, they often develop Panobinostat manufacturer a central zone of necrosis that seems to evolve from extensive karyorrhectic (leucocytoclastic) debris to a central zone with a slightly basophilic hue, and finally to a central zone of amorphous acidophilic material (Fig. 3). Concurrent with this degeneration of the central zone of neutrophils, the periphery of the lesion accrues palisades of elongated macrophages and scattered multi-nucleated giant cells that justify being called granulomatous inflammation. Mark et al. [6] concluded that in GPA (WG):

‘Micronecrosis, usually with neutrophils (microabscesses), constitutes the early phase in the development of the pathognomonic organized palisading granuloma.’ They suggested that the multi-nucleated giant cells might be a secondary reactive response to the acute necrotizing lesions. This is supported PAK5 by the finding of engulfed apoptotic and necrotic neutrophil debris that can be seen occasionally within the multi-nucleated giant cells at sites of necrotizing inflammation in GPA (WG) (Fig. 2b). This prominence of neutrophilic

infiltrates (microabscesses) in the acute phase of the disease and the atypicality of the granulomatous inflammation that follows have been reported in detail in the literature [6,7] but probably, in part because of the term ‘granulomatosis’ in the name, concepts and theories about the pathogenesis of the extravascular inflammation in GPA (WG) have drawn analogies to typical granulomatous inflammation as seen in sarcoidosis or tuberculosis, which has little or no resemblance to the granulomatosis of GPA (WG). In a careful pathological study of pulmonary specimens from 35 patients with GPA (WG), Mark et al. [6] concluded that: ‘Compact granulomas of tuberculoid or sarcoidal type did not occur in the cases of Wegener’s granulomatosis.

This is evident in all vowels; our example compares the first formant (F1) location at .75 of the duration of the vowel/ae/ in hamlet and candle. Although there is no effect of word (hamlet,

candle) on F1 for the native speakers (both p > .19), the Spanish-accented speaker produces different F1s depending on the word, F(1, 38) = 8.9, p < .005, either because these sounds are coarticulated more in Spanish or because the slower Cisplatin concentration movements involved in the production of nonnative sounds affects coarticulation. In addition, findings from a listening experiment provided perceptual evidence that stimuli produced by Can and MidW are more similar as compared with MidW-Span.3 A repeated-measures ANOVA with average looking time as dependent measure, age group (younger, older), condition (kingdom/hamlet, candle/raptor), and order (American test, Canadian test) as factors, and familiarity (familiar,

unfamiliar) as repeated measures revealed a main effect of familiarity, F(1, 44) = 10.88, p = .002, main effect of order, F(1, 44) = 8.41, p = .005, significant interaction between age group and familiarity, F(1, 44) = 4.55, p = .04, and no other significant interactions, F(1, 44) < .18. Follow-up paired, find more two-tailed comparisons of looking time averaged across blocks revealed that familiar and unfamiliar trials differed significantly in the older age group, t(1, 23) = 3.77,

p = .001, but not in the younger group, t(1, 23) = 0.88, p = .39, as shown in Figure 3. The main effect of order emerges because both groups showed higher looking times when tested with the American speaker. As evidenced by the lack of interaction with order and familiarity, the pattern of looking remained the same in both the novel and familiar test trials, and only 12-month-olds showed a significant difference in looking time between passages containing familiar and novel Celecoxib words. These findings suggest that 12-month-olds successfully recognized words in the face of variation in dialectal accent, as evidenced by the significant preference for test passages containing familiar words. In contrast, 9-month-olds showed no preference, suggesting that dialectal differences were large enough to impede word recognition. This work extends the finding that infants are sensitive to dialect differences by showing the functional relevance of this sensitivity for word recognition in 9-month-olds. The 9-month-olds’ poor performance could be attributed to their lack of familiarity with dialectal accents, perhaps complicating the representation of words in unfamiliar speech streams.

4). The two populations were individually labeled with CellTrace and then co-cultured at the original ratio (one Treg to nine effector cells), combining either labeled Treg with unlabeled T-effector cells, or conversely labeled T-effector cells with unlabeled Treg cells. These experiments demonstrate that a very low frequency of Foxp3+ T cells arise from the labeled effector T-cell population, cultured alone or with labeled Treg cells, in the absence or presence of 1α25VitD3 (<2% at day 14; data not shown). These data suggest that 1α25VitD3 is not acting to enhance adaptive/activation-dependent

Foxp3 expression. Furthermore, across a dose titration of 1α25VitD3, Treg cell proliferation was only reduced at 10−6 M 1α25VitD3, whereas at all other concentrations proliferation Seliciclib mw was unaffected or even enhanced (Fig. 6C and D). In contrast, proliferation of labeled effector T cells in co-culture was reduced at all concentrations of 1α25VitD3 PI3K inhibitor tested (10−9–10−6 M 1α25VitD3; Fig. 6C and D).

These data imply that culture of T cells with 1α25VitD3 preferentially expands Treg over T-effector cells. Our earlier studies demonstrated that 1α25VitD3 enhances IL-10 expression by CD4+ T cells not only in culture, but also following ingestion of standard formulary doses of 1α25VitD3 by both steroid refractory asthma patients and healthy subjects [12, 14]. Subsequent work has demonstrated that no parallel increase in Foxp3 gene expression occurred in the same peripheral blood CD3+CD4+ T cells, analyzed directly ex vivo pre- and post-1α25VitD3 ingestion (data not shown). To investigate whether vitamin D might influence Foxp3 expression in the tissues, we analyzed the frequency of CD4+Foxp3+ cells in bronchoalveolar lavage (BAL) samples available from a pediatric severe asthma cohort under study, where serum 25-hydroxyvitamin D3 status was also being assessed (Supporting Information Table 1) [21]. Strikingly the majority of these patients showed a vitamin D status reflecting insufficiency (<75nmol/L) or deficiency (<50 nmol/L) [22]. A statistically significant correlation between serum vitamin

D status, and the frequency of CD4+Foxp3+ T cells in the BAL was observed (r = 0.71, p = 0.02), suggesting an in vivo correlate of our in vitro observations on the capacity of 1α25VitD3 to influence Foxp3+ Treg cell prevalence mafosfamide (Fig. 7 and Supporting Information Fig. 5). Interest in enhancing Treg cells in patients is clearly driven by the therapeutic potential of these cells. An attractive approach would be the use of pharmacological agents such as 1α25VitD3, or vitamin D supplementation, to induce the expansion and/or maintenance of Treg cells. This approach is especially suited to ongoing chronic diseases such as asthma that occur at high prevalence, where a simple treatment such as vitamin D supplementation would be relatively safe, acceptable to patients, and cost effective.

Spleens from DENV-2-infected mice were surgically removed at different time-points and single cell suspensions were prepared. Approximately 0·5 × 106 to 1 × 106 spleen cells were incubated with either 10 μg/ml of the indicated peptide, RPMI-1640 medium (Gibco) or PMA (0·1 μg/ml) + ionomycin (1 μg/ml). Golgi plug (BD Biosciences, San Jose, CA) was added to each of the AZD0530 in vivo above samples and incubated at 37° for 6 hr. Cells

were washed with FACS buffer, blocked with Fc block (2.4G2) for 10 min and then surface stained with peridinin chlorophyll protein-Cy5.5-hCD45 (clone 2D1), phycoerythrin-Cy7-mCD45 (clone 30-F11), FITC-hCD3 (clone UCHT1), phycoerythrin-hCD8 (clone H1T8a) and Pacific Blue-hCD4 (clone RPAT4) antibodies for 20 min at room temperature. Cells were washed with FACS buffer, then permeabilized using Cytofix/Cytoperm buffer (BD Biosciences) and stained with allophycocyanin-hIFN-γ (clone B27) and Alexa700-TNF-α for 20 min at room temperature. BMS-777607 price In all experiments the viability marker LIVE/DEAD® Aqua (Molecular Probes, Eugene, OR) was added to exclude dead cells. All cell preparations were fixed with Cytofix (BD Biosciences). Cytokine levels were also assessed by ELISA; 0·5 × 106 to 1 × 106 spleen cells from DENV-2-infected mice

were incubated with either 10 μg/ml of the indicated peptide, RPMI-1640 medium (Gibco) or PMA (0·1 μg/ml) + ionomycin (1 μg/ml) and incubated at 37° for 96 hr. Culture supernatants were collected and IFN-γ level was determined by IFN-γ ELISA (R&D Systems, Minneapolis, MN). Levels of DENV-2 envelope (E) protein-specific antibody in the serum of DENV-infected

engrafted, uninfected engrafted and non-engrafted mice were determined using a standard ELISA. Ninety-six-well microplates were coated overnight with 100 ng/well of DENV-2 E protein (Hawaii Biotech, Aiea, HI) or 1 : 40 dilution of DENV-2-infected Vero cell lysate. The plates were blocked with 1% bovine serum albumin for 90 min and a 1 : 20 dilution of sera diluted with PBS was added to the wells for 1 hr. Plates were washed with PBS containing 0·1% Tween-20. Horseradish peroxidase-labelled goat anti-human IgM or IgG (Bethyl Laboratories Inc., Montgomery, Depsipeptide price TX) was added as the secondary antibody. TMB Solution (Sigma-Aldrich Inc., St Louis, MO) was used as the substrate. The enzyme reaction was stopped by addition of 1 m HCl and the plates were read at 450 nm. Positive controls included sera from a known DENV-positive human. Sera from uninfected engrafted and non-engrafted mice were used as negative controls. All assays were carried out in duplicate or triplicate. Splenocytes from DENV-2 S16803-infected or naive mice were stimulated in vitro with CpG (2·5 μg/ml) + interleukin-2 (1 μg/ml) and Epstein–Barr virus (50 μl/ml). Supernatants of stimulated splenocytes collected 14 days after in vitro stimulation were tested for DENV-specific IgM antibodies and for DENV neutralization activity.

Fungal infections, particularly invasive aspergillosis (IA), still present a diagnostic and therapeutic dilemma for the physicians who take care of the patients with severe underlying diseases and immunosuppression. Because the severity of the underlying disease,

critical illness and acute conditions preclude the diagnosis most of the time, empirical antifungal treatment has been the mainstay of management of such patients until recently. Empirical approach has its own disadvantages including unnecessary exposure to toxic effects and drug interactions as well as increased cost. However, the search for an ideal diagnostic marker, which can guide pre-emptive selleck therapy, has been inconclusive so far.1 The accuracy of the microbiological methods in diagnosing IA depends on the type of the specimen obtained. Tissue biopsies are the best as culture specimens, because histopathological Ganetespib cell line confirmation can be done simultaneously. However, the critical illness of the patients usually does not allow an invasive procedure.2 Imaging modalities such as high resolution computed tomography (CT) are non-invasive options for diagnosing Aspergillus infections.3–5 Serial tomograms starting on the early days of the febrile neutropenic period are required to detect the halo sign that

suggests IA in the appropriate host and setting.6,7 Galactomannan (GM), which is a polysaccharide cell-wall component of Aspergillus, is a promising molecule to search for the clues of Aspergillus infection and tissue invasion.8 Methods like enzyme immunoassay, radioimmunoassay and latex agglutination have been used to identify GM in different specimens.9,10 Commercial kits (Platelia®Aspergillus; Bio-Rad Laboratories, Marnes-la-Coquette,

France) that use the monoclonal anti-GM antibody EB-A2 as both capture and peroxidase-linked antibodies in sandwich enzyme-linked immunosorbent assay (ELISA) are available.10,11 While the specificity of the test is quite high, reported sensitivities in different studies display wide variations.9,12–20 The dispute about the ideal cut-off point was a subject of matter nearly as well as the reproducibility of the test. Recently, an index cut-off of 0.5 was accepted in Europe after the study by Maertens and colleagues.12,14,21–26 In this study, we aimed to evaluate the diagnostic accuracy of serial GM measurements in our high-risk patients along with the possible caveats in diagnosing and treating IA in our centre, and focused on the possible ways to use the method more effectively in our routine clinical practice in the future. This prospective cohort study was carried out in Hacettepe University Hospital for Adults. The study was approved by the ethics committee of the Faculty of Medicine (Approval date 12 July 2001, HEK 01/30-4).

The aGVHD is produced by an allogenic immune response in a predominant milieu of Th1-type cytokines [37]. These findings ITF2357 in vivo suggest that CD30 expression is not only dependent on cytokines produced by Th2-type cells. Accordingly, significant serum CD30s levels have been associated with another immune disease mediated by Th1-type response as in rheumatoid arthritis

[38]. Equally, we have found in the CD30 correlation study carried out in patients with SLE, a positive correlation between IL-4 (Th2), IFNγ (Th1) and immunosuppressive cytokines (IL-10 and TGFβ). Results support the presence of an imbalance in both the Th2-/Th1- and Treg-type cytokines. CD30 has pleiotropic biological functions, and it is capable of promoting cell proliferation and survival as well as inducing antiproliferative responses

and cell death [39, 40]. The CD30/CD30L signalling pathway is barely known and could be a potential therapeutic target in autoimmune diseases such as SLE [12, 13, 25]. Indeed, at present, there are developed preclinical and clinical studies with monoclonal antibodies targeting the CD30/CD30L signalling pathway. This work was supported by the grant PI-2009/25 from Raf inhibitor review the Castilla-La-Mancha Foundation for Health Research (Fundación para la Investigación Sanitaria en Castilla La Mancha (FISCAM)). “
“The immune system of pregnant women is tightly controlled to defend against microbial infections and at the same time, to accept an embryo or the fetus, which are expressing semi-allogenic paternal antigens. Furthermore, inflammation-like processes are crucial for tissue growth, remodeling, and differentiation of the decidua during pregnancy. Dysregulation of elaborate immune control may lead reproductive failure, such as implantation failure, recurrent

pregnancy loss (RPL), preterm birth, intrauterine fetal growth restriction, and preeclampsia. Until recent years, a balance between Th1 and Th2 cells was believed to be the key immune regulatory mechanism of T-cell immunology Thiamet G especially during pregnancy. Since the identification of regulatory T cells was made, the mechanism of immune regulation has become a major issue in immunologic research. Also, the recent identification of Th17 cells has drawn our attention to a new immune effector. The balance between Th17 and regulatory T cells may explain more about the pathophysiology of reproductive failure. This review will discuss relevant human literature on regulatory T and Th17 cells in normal reproductive physiology and in women with RPL and infertility. During pregnancy, the immune system of the mother is tightly controlled to defend against microbial infections and to accept an embryo and a fetus, which are expressing semi-allogenic paternal antigens. Furthermore, immune-mediated processes such as tissue growth, remodeling, and differentiation are crucial to maintain pregnancy.

5% of NaCl. As the original NB contains 0.5% NaCl, NBs with 0% and 2.5% NaCl were termed NB (0.5) and NB (3.0), respectively. After cultivation at 37°C for 24  hrs with shaking (140  r.p.m.), the culture supernatant was separated from the cells by centrifugation. Proteins in the culture supernatant of A. sobria were

precipitated by treatment with TCA solution, which was added to 1.0  mL culture supernatant to reach 10% concentration. The mixture was left for 30  min at room temperature and the precipitates yielded collected by centrifugation. After rinsing with ethanol, the precipitates were solubilized with 100 μL loading solution for SDS-PAGE and a portion (15 μL) of the sample loaded onto a lane of SDS-polyacrylamide gel. The concentration of acrylamide in the gel used was 15%. A portion of overnight preculture of A. sobria 288 (asp−, amp−) (20  mL) was inoculated into selleck products Crizotinib solubility dmso 2 liters of NB (0.5). After cultivation at 37°C for 24  hrs with shaking (140  r.p.m.), the culture supernatant was separated from the cells by centrifugation (12,000  g for 10  min) at 4°C. The culture supernatant was salted out with 30% saturated ammonium sulfate

and the insoluble materials removed by centrifugation. Ammonium sulfate was added to the supernatant to reach 50% saturated ammonium sulfate. The insoluble materials yielded were collected by centrifugation and dissolved in 10  mL of 10 mM phosphate buffer (pH 7.4). The samples were dialyzed against the buffer. The prepared samples were designated the crude samples. One milliliter of the crude sample was loaded onto a hydroxyapatite column (CHT10-I) (Bio Rad, Hercules, CA, USA) equilibrated with 10  mM phosphate

buffer (pH 7.4). Non-adsorbed materials were washed out with 10  mM phosphate buffer, and materials adsorbed to the column eluted with a linear gradient of 10 to 300  mM phosphate buffer (pH 7.4). The fractions containing the target protein were detected by SDS-PAGE. The fractions containing the target Amino acid protein were collected and concentrated by an Amicon ultra-15 centrifugal filter tube (Millipore, Billerica, MA, USA). A portion of the concentrated sample (250 μL) was loaded onto a Superdex 75 column (column size, 10 mm ×  300  mm; GE Healthcare UK, Buckinghamshire, UK) equilibrated with 50  mM phosphate buffer (pH 7.4) containing 150  mM NaCl. After loading the sample, the column was eluted with the buffer used for equilibration. The fractions containing the target protein obtained by column chromatography using Superdex 75 were collected and concentrated by an Amicon ultra-15 centrifugal filter tube. The concentrated sample was separated by SDS-PAGE. Proteins on the gel were transferred to a PVDF membrane on trans-blot apparatus for 30  min at 160  mA at room temperature, and the membrane stained with Coomassie brilliant blue.

Our tally of social referencing did not include instances of the child turning to the parent/experimenter during a display change, or if the parent or the experimenter initiated

spoken communication to the child, both of which elicited the child’s attention. We hypothesized that if infants detected the perceptual anomaly in the picture of the impossible cube, it might elicit an increased frequency of vocalizations and/or social referencing to the parent accompanying the child during the study. Infants’ responses were analyzed using a repeated-measures 2 (Sex) × 2 (Order: Possible versus Impossible First) × 3 (Display) analysis of variance (ANOVA). Preliminary analyses revealed no reliable differences in the extent of reaching, social referencing, vocalizations, or mouthing behaviors based on sex or stimulus order,

Metformin mouse F(1, 10) = n.s., Proteasome inhibitor all p-values > .25, and no interactions, so these between-subjects factors were omitted from further analyses. Data points from the perceptual control displays (tree bark, gray patches, and brown lines) were collapsed into one within-subjects variable for comparison with the possible and impossible cube displays. In order to assure reliability of the experimenter’s judgments, an independent observer who was blind to the hypotheses also coded manual gestures offline for 100% of the final sample. Pearson correlations between the experimenter’s and the coder’s judgments indicated strong interrater reliability for all measures (manual gestures r = .90, p < .01; sequential gestures r = .92, p < .001; social referencing r = .89, p < .01; vocal utterances r = .80, Amino acid p < .01). All

tests of statistical significance used an alpha level of .05, and all t-tests were two-tailed. Results of a within-subjects ANOVA yielded a main effect of display, F(2, 26) = 8.76, p < .001, due to differences in mean quantity of categorical types of manual gestures across displays. Pairwise comparisons (with least squares differences [LSD]) revealed that the infants engaged in a greater number of different types of manual exploration toward the impossible cube relative to the possible cube display, t(13) = 2.74, p < .001, and the perceptual controls, t(13) = 4.25, p < .02, as shown in Figure 2a. The mean impossible preference score was .63, which differed significantly from chance, t(13) = 2.48, p < .03. Infants attempted an average of one additional different type of manual gesture toward the impossible cube display above that of the possible cube display and the perceptual controls. The pattern of increased manual exploration toward the impossible cube display was observed in nine of the 14 infants, with four infants responding equally to the two displays, and one with more reaching to the possible cube, Z = 2.13, p = .03.

Unless otherwise noted, such pairwise comparisons were made between infected pregnant and uninfected pregnant; and between infected pregnant and infected non-pregnant mice within strains; and between infected pregnant mice and infected non-pregnant mice across strains. Pregnancy outcome data were analysed by Fisher’s exact test or chi-squared test as appropriate. Differences with P < 0·05 were considered significant. In agreement with previous studies of virgin mice (15,24), pregnant A/J mice were susceptible to a lethal infection with P. chabaudi AS, whereas B6 mice were resistant (20). Among A/J mice, 100% of infected pregnant mice died by experiment day

12 (n = 7; Figure 1a) whereas B6 mice were resistant, with only 1 of 6 mice succumbing by experiment day 12 (Figure 1a). Because the interest of the study was to evaluate mid-gestational pregnancy outcome in both strains, serial sacrifices were subsequently performed up Protein Tyrosine Kinase inhibitor to experiment day 11. In A/J mice, a maximum peripheral parasite density of 39 ± 2% (mean ± SEM; n = 21) was observed PXD101 price in the infected pregnant group at experiment day 11, while the peak parasitemia for infected pregnant

B6 mice occurred on experiment day 10 at 25 ± 3% (n = 16; Figure 1b), a level significantly lower than in A/J mice. Consistent with previous reports (25,26), parasitemia was also significantly higher in infected non-pregnant A/J mice on experiment

day 9 through 11 relative to infected non-pregnant B6 mice (data not shown). Moreover, peripheral second blood parasite density was significantly higher in pregnant A/J mice relative to non-pregnant mice at experiment day 6 (0·5 ± 0·2% (n = 64) vs. 0·1 ± 0·0% (n = 104), respectively; P = 0·03) and at peak parasitemia (39·1 ± 1·9% (n = 21) vs. 33·4 ± 1·8% (n = 27), respectively; P = 0·04; Figure S1), suggesting that, as in B6 mice (20), pregnancy increases the susceptibility of A/J mice to malaria. While anaemia was not observed in uninfected pregnant A/J and B6 mice, haematocrit was substantially reduced over time in infected pregnant (Figure 1c) and infected non-pregnant (Figure S1 and data not shown; (20) mice of both strains. On experiment day 11, haematocrit in infected pregnant A/J mice was significantly lower than in infected pregnant B6 mice (Figure 1c). As expected in normal pregnancy, uninfected pregnant A/J and B6 mice gained weight over the course of the experiment (Figure 1d). In contrast, infected pregnant mice of both strains did not experience significant weight gain, and starting at experiment day 9, body weights fell steadily with reductions to below starting body weight at experiment day 11 (Figure 1d) (20). From experiment days 9 through 11, mean body weight was significantly lower in infected pregnant relative to uninfected pregnant mice for both strains (P < 0·05).