The ELISA technique required relatively large amounts of tissue e

The ELISA technique required relatively large amounts of tissue extracts, and one mouse could therefore be used only for the measurements of the two actual cytokines

as the oral mucosa, ear skin or lymph nodes cannot be dispersed in too large volume of extraction buffer to display measurable amounts of the cytokines. Counting of lymph node cells.  In a separate set of experiments (n = 2), submandibular and auricular (2 + 2) and axillary (4) lymph nodes were excised and kept in PBS. The lymph nodes were then squeezed through a nylon mesh (NYHC 150–80; Tidbecks, Ljungsarp, Sweden) to acquire single cell suspensions. The volume was adjusted to 10 ml before counting in a Bürker haemocytometer. Total cell counts for the combined submandibular/auricular and axillary lymph selleck inhibitor nodes Decitabine nmr were estimated. Calculations.  The oral mucosa and ear skin IL-2 and IFN-γ content was estimated per mg wet weight tissue. The total content of respective cytokine in quadruple regional (submandibular and auricular) and distant (axillary) lymph nodes was calculated. The tissue levels of IL-2 and IFN-γ differed in individual mice and not least between the different experimental series. However, the peaks of cytokine appearance/disappearance were consistently sharp but could vary from 4 to 24 h after hapten exposure in individual mice. The figures shown (Figs. 1–3)

are representatives of single experimental series, as assembling ADAMTS5 the results from the three different experimental series into one curve causes considerable obscuring of the real biological response. Mice with normal oral mucosa or ear skin showed very low levels of IL-2. One exposure of the hapten to the oral mucosa or the ear skin (sensitization) resulted in increased levels of IL-2 locally,

(maximum 24-fold increase for the oral mucosa, and maximum 27-fold increase for ear skin, both n = 3) peaking 4–6 h after exposure and thereafter quickly subsiding. At 24 h, the IL-2 levels were back to baseline. After a second hapten exposure (elicitation), a similar peak of IL-2 occurred (maximum 39-fold increase for oral mucosa and 35-fold for the ear skin, both n = 3). The levels of IL-2 after elicitation were normalized by 12–24 h regardless whether oral mucosa or ear skin was examined. One exposure to the hapten resulted in only minor variations in the levels of IFN-γ in both ear skin and buccal mucosa. Increased levels of IFN-γ were found mainly after the second hapten exposure where a rapid increase in this cytokine was demonstrated. The peaks of IFN-γ were found between 8 and 24 h after re-exposure to the hapten (maximum 14-fold increase for oral mucosa and 8-fold for ear skin, n = 3) in tissue sensitized a week earlier. The levels of IFN-γ after elicitation were normalized by 24–48 h regardless whether oral mucosa or ear skin was examined.

BKV positivity was tested by RT PCR machine (copies/ml), & lower

BKV positivity was tested by RT PCR machine (copies/ml), & lower limit of detection was. Results: Mean age

of patients was 44 ± 10.89 years and majority were males (n = 16, 80%). Continuous creatinine elevation (graft dysfunction) was the reason for doing the BKV test in all patients. 45% (n = 9) patients were BKV positive after 2–3 years post-transplant. Patients those who became BKV positive after 3 years of Transplant showed faster recovery from infection and their viral load reached below detection level within 8–9 months. 33% (n = 3) patients suffered from unstable creatinine level & they were monitored very closely. 55% (n = 11) of the patients detected with BKV infection in less than 1 year after transplant. This group of patient showed little delay in recovery and took more than 10 months to reach lower limit of MK-2206 molecular weight viral detection level. 18% (n = 2) patient of this group had BKV associated nephropathy and dialysis restarted for a short span of time.

Treatment RG7204 clinical trial for BKV involved no prophylactic therapy, only dose reduction of Tac & MMF was done. Average 4–5 log/copy viral load reduction reported by 6 months from initial load in almost all patients and almost all patient’s viral load became below significant level( Rejection was seen in 7 (35%) of the patients and death in 1 patient. Conclusion: This retrospective study shows that BKV infection is seen more

commonly in elderly males and is present quite early in 50% of the patients (within 8 months). Routine screening with early modification of the intensity and nature of the immunosuppression regimen could reduce the toll of BKVN in the kidney transplant population. TAN SI-YEN1, RAO MOHAN2 1Prince Court Medical Centre; 2Royal Adelaide Hospital Introduction: ABO incompatible kidney donors are increasingly used to expand donor pool with excellent long term patient buy Forskolin and graft survival. We report here the results of a pioneering ABOi kidney transplant programme in Malaysia. Methods: 10 patients entered into our ABOi kidney transplant programme between July 2011 till December 2013. Data including ABO titres pre and post transplant, graft function, rejection rates, patient and graft survival were collected. Results: Median ABO titres pre transplant was 1:128 and fell to < 1:16 at time of transplant following desenstization with IV Rituximab, immunoadsorbtion, double filtration plasmapharesis and IVIg. Median follow up was 17 months with 100% patient and graft survival. Median serum creatinine at follow up was 106 umol/L with rejection rate of 10% at 1 year and none had antibody mediated rejection. Conclusion: The wide variety of desenstization protocols which may be readily implemented facilitates the development of ABOi kidney transplantation.

The individual

parameters were scored from 1 to 3, and a

The individual

parameters were scored from 1 to 3, and a cumulative score between 0 and 19 was recorded for each biopsy. The observer was blinded (J.H.E). Values are expressed as the mean ± 2 SD. To compare the treatment group with controls, we used the Mann–Whitney U-test. To evaluate the differences between before treatment, during and after treatment, the normality of each type of measurement was evaluated using a KS test based on the residuals from a simple linear model using patient and time as factors. In no case was normality close to being rejected (P > 0.4 in all cases). Hence, one-way repeated-measures anova was used. However, to evaluate the differences between the two treatment groups, two-way repeated-measures anova was used. Three patients who received combined treatment were not evaluated at week 8 because they had started another psoriasis Kinase Inhibitor Library chemical structure treatment due to exacerbations: two of those patients at week 4 (Fig. 1A; BL3 and BL6) and one patient at week 7 (Fig. 1A; BL1). For these patients, PASI KPT-330 mouse evaluation was made at the time point their study participation was terminated, and they were not included

in the analysis at week 8. All measurements were taken using sigmastat 3.1 (Systat Software, San Jose, CA, USA). A P-value ≤ 0.05 was considered statistically significant. In order to evaluate whether clinical improvement of psoriasis following bathing in geothermal seawater combined with NB-UVB and NB-UVB alone is preceded by changes in systemic inflammatory markers, the clinical efficacy of each treatment regimen was evaluated first. As shown in Fig. 1C, both treatment regimens demonstrated significant clinical improvements. Furthermore, the data suggested that patients receiving combined treatment Farnesyltransferase demonstrated better clinical response, measured by the PASI score, than patients treated only with NB-UVB. This was seen both

after one week (% improvement: combined treatment 37.3 ± 10.3 versus NB-UVB treatment 18.3 ± 8.9, P < 0.05) and after three weeks (67.3 ± 11.9 versus 22.0 ± 12.0, P < 0.0001). However, this was not the main aim of the study, and larger cohort and another control group would be needed to fully address this interesting observation. Interestingly, bathing in the Blue Lagoon immediately following skin punch biopsy resulted in no infections and only minor skin irritation resolving in few days. In addition, the above clinical findings were confirmed by the histological Trozak’s score where patients in both treatment groups showed a significant histological improvement at week 3 (Trozak’s score: BL treatment = 10.3 ± 5.5 versus NB-UVB treatment = 8.0 ± 4.6; Fig. 2).

Hoffmann et al investigated the association of diet with fungal

Hoffmann et al. investigated the association of diet with fungal populations, using fecal samples from 98 healthy individuals [158]. They characterized 62 fungal genera and 184 species by deep sequencing, and usually found that the presence of either the phyla Ascomycota or Basiodiomycota was mutually exclusive. The authors could not conclude which of those fungi are true gut residents selleck inhibitor and which are passengers resulting from diet. We cannot exclude the possibility that the presence of Saccharomyces is due to the ingestion of yeast-containing foods such as bread and beer [82].

A recent study conducted on the Wayampi Amerindian community showed a high diversity among yeast species in the gut, with a prevalence of S. cerevisiae over Candida species [80], suggesting a role for

this fungus in gut immune homeostasis. Thus, integrating information on the repertoire of the gut mycobiota in the context of the broader microbiota and developing functional tests to measure its role in shaping immune function is necessary to better understand the role of the microbial communities in sustaining human health. Although we have described RXDX-106 in vivo the composition of the fungal microbiota in various locations in the human body, we remain aware that these locations are not isolated and that DCs trained in the Peyer’s patches of the intestine (Fig. 1) can shape T-cell responses in other locations. A clear example of this crosstalk was recently shown in an elegant study by Kim et al. [159], who showed that antibiotic treatment of mice increases susceptibility to allergic airway disease by promoting varying degrees of fungal outgrowth in the intestine, ultimately resulting in the acquisition of an M2 phenotype by alveolar macrophages [159]. The authors isolated C. parapsilosis

from the feces of antibiotic-treated mice and showed that transferring this fungus to mice that did not carry this species increased their susceptibility to allergic airway inflammation induced by papain or house dust mite extract [159]. Oral treatment of mice with Candida species isolated from humans also led to fungal outgrowth in the gut and exacerbated allergic airway inflammation, increasing serum levels Thalidomide of prostaglandin E2, which promoted the development of M2 macrophages [159]. The mycobiota alteration mediated imbalance in alveolar macrophage function contributed to the increase in airway inflammation, as untreated animals receiving alveolar macrophages from antibiotic-treated mice developed more severe airway inflammation than animals that received alveolar macrophages from control mice. Based on this result, it appears that intestinal dysbiosis, particularly the altered ratio of fungi to bacteria, could be a causative factor in the development of allergic disease. Patients with severe asthma with fungal sensitization are often sensitized to C. albicans and benefit from antifungal drug therapy [160]. Colonization of mice with C.

1A) consistent with a naïve state Upon culture with OVA323–339,

1A) consistent with a naïve state. Upon culture with OVA323–339, CD4+ T cells rapidly upregulated the expression of the early activation marker CD69 and, as indicated by their FSC profile, began to enlarge and undergo blastogenesis (Fig. 1A). CD69 expression remained high on CD4+ T cells in OVA peptide-containing

cultures until day 5 and during this time a CD44hi phenotype was acquired. This indicated ongoing activation of CD4+ T cells in the presence of antigen which was confirmed by continued CFSE dilution until peptide removal (data not shown). CD62L expression Osimertinib research buy was transiently reduced upon culture but after 3 days, even in the presence of OVA peptide, returned to the levels equivalent to that on naïve OT-II cells (Fig. 1A). Upon washing and reculture in the absence of OVA peptide, but in the presence of IL-7, CD69 expression rapidly declined to baseline levels and OT-II T cells developed a CD44hi CD62Lhi phenotype as displayed by central memory T cells 12. Restimulation of OT-II cells recovered from culture demonstrated that a large proportion of the “central memory-like” T cells were capable of rapidly producing the effector cytokines IFN-γ

and IL-2 (Fig. 1B) unlike naïve T cells (data not shown), Selleck Midostaurin indicating substantial acquisition of rapid effector function. Notably, post-activated OT-II T cells produced little IL-4, IL-17 or IL-10, indicating that these conditions promoted Th1-like differentiation. No Foxp3 expression was detected in CD4+ T cells recovered from these cultures (data not shown). Therefore, we conclude that these culture conditions generate a population of OT-II T cells phenotypically similar to central memory T cells and skewed toward a Th1 phenotype. Using a model in which OVA expression is targeted to DC by the CD11c promoter, we have shown that steady-state presentation of OVA by OVA-expressing DC induces peripheral tolerance in naïve CD4+ and CD8+ T cells 13, 14 and memory and effector CD8+ T cells 4, 15. As the CD11c promoter appears to drive low-level transgene expression in CD11cint cells Resveratrol 16, which includes plasmacytoid DC, some activated macrophages,

subsets of intraepithelial lymphocytes and NK1.1+ cells, we previously showed that the presentation of immunogenic MHC/OVA peptide complexes was restricted to CD11chi conventional DC 13. Additionally, Taqman qPCR studies have shown OVA message is restricted to DC and not expressed in B and T cells of 11c.OVA mice 15. Therefore, we used this model to test the susceptibility of activated CD4+ T cells to DC-induced peripheral tolerance. To determine whether CD4+ memory T cells were activated by OVA peptides presented by steady-state OVA-expressing DC, cultured OT-II cells were CFSE labeled and transferred to 11c.OVA and nontransgenic controls. Three days after transfer, little CFSE dilution was observed in the spleens or LN of nontransgenic recipients, although a small number of cells appeared to have undergone one or two divisions (Fig. 2A). In 11c.

We also discuss the role of cholesterol metabolites in the direct

We also discuss the role of cholesterol metabolites in the direct regulation of tumor cell growth (intrinsic role), aiming to envisage an integrated view of these two aspects. Oxysterols BI 6727 mouse are generated during cholesterol metabolism through enzymatic reactions by means of cholesterol 24-hydroxylase (24S-HC), sterol 27-hydroxylase (27-HC), cholesterol 25-hydroxylase (25-HC), CYP7A1 (7α-HC), CYP3A4 (4β-HC),

and CYP11A1 (22R-HC), and through autoxidation [2-5], initiated by nonradical reactive oxygen species such as singlet O2, HOCl, and ozone (O3) or by inorganic free radical species derived from nitric oxide, superoxide, and hydrogen peroxide [5]. Some oxysterols, such as 7β-HC and 7KC, are exclusively generated by nonenzymatic cholesterol oxidation, whereas 7α-HC, 4β-HC, and 25-HC can be produced by both pathways

Target Selective Inhibitor Library screening [2]. Finally, 24S-HC and 27-HC can be generated only by enzymatic cholesterol oxidation [2, 3, 5]. These cholesterol precursors, as well as desmosterol [6], can all activate LXRs [7]. LXRα (also known as NR1H3) and LXRβ (also known as NR1H2) are LXR isoforms belonging to the nuclear receptor superfamily, which comprises 48 ligand-dependent transcription factors that control metabolism, homeostasis, development, and cell growth [8]. LXRs regulate cholesterol homeostasis by modulating the expression of various genes (including the ATP-binding cassette (ABC) transporters C1 and G1, the sterol response element-binding protein-1c, and the apolipoprotein E). In particular, LXR-dependent gene expression has been associated with cholesterol efflux and the synthesis of fatty acids and triglycerides [9]. LXRβ is expressed ubiquitously, whereas LXRα is expressed in the liver, adipose tissue, adrenal glands, intestine, lungs, and cells of myelomonocytic lineage

[9]. Of note, Lxrα transcripts are upregulated in CD11c+ and CD11c− cells purified from mice treated with complete Freund’s adjuvant [10], whereas Lxrβ transcripts do not undergo transcript changes (Russo et al. unpublished observations). These results were reproduced in vitro by using these proinflammatory cytokines, such as TNF-α and IL-1β, and TLR ligands, such as LPS [10]. The transcriptional activity of LXRα and -β isoforms requires their heterodimerization with the retinoid X receptor (RXR). LXRs regulate gene expression through direct activation, ligand-independent and -dependent repression, and also by trans-repression [11]. Whereas the transcriptional activity inducing activation of target genes requires the binding of LXR–RXR heterodimers upon ligand engagement on the DNA promoter of the target genes, in the trans-repression model, LXR–RXR heterodimers have been shown to block nuclear factor κβ, signal transducer and transcription activator, and activator protein 1 induced transcription of the proinflammatory genes (COX-2, MMP9, IL-6, MCP-1, iNOS, and IL-1β) in macrophages [12, 13].

DCs from GLA-SE but not SE-treated mice became active stimulators

DCs from GLA-SE but not SE-treated mice became active stimulators of the allogeneic mixed leukocyte reaction, inducing robust proliferation of both CD4+ and CD8+ T cells (Fig. 5C). To further evaluate the capacity of DCs to become immunogenic following antigen capture in vivo, mice were injected with anti-DEC-HIV gag and either GLA-SE or SE. After 4 h, splenic DCs were purified by cell sorting and injected into naïve mice i.v. In addition, to check that antigen presentation was performed by the transferred and not recipient DCs, MHCII−/− DCs were used as negative controls. Only WT DCs, after targeting with anti-DEC-gag and stimulated with GLA-SE in vivo, were capable

of inducing gag-specific T-cell immunity (Fig. 5D). These data indicate that GLA induces the full maturation of spleen and lymph node Small molecule library manufacturer DCs in vivo. The discovery of receptors

responsible for stimulating innate immunity, such as the TLR and RIG-like receptor pattern recognition receptors, makes it possible to test chemically defined agonists as new adjuvants to trigger the DC link between innate and adaptive immunity. To understand adjuvant action, these agonists need to be characterized in vivo at the level of antigen presenting DCs. Our experiments at this direct level indicate that a synthetic TLR4 agonist, GLA-SE, serves as an effective adjuvant and enhances Y-27632 cell line the capacity of DCs in vivo to immunize against protein antigens. The adjuvant role of GLA-SE was dependent on TLR4. Similar results have been reported by Baldwin et al. where GLA induced production of IL-6 by oxyclozanide monocyte-derived DCs in culture, and this was blocked with anti-TLR4 but not TLR2 antibodies 27. Our results extend prior research by showing a complete dependency of TLR4 stimulation for the induction of adaptive responses in vivo by GLA-SE. DCs are the major link between the innate and the adaptive immune system, and its appropriate activation and maturation by agonists for innate signaling receptors should allow for the induction of

an adaptive response 41, 42. However, much of the evidence involves studies of DCs stimulated in cell culture with adjuvants 43. In the current study, we demonstrated that GLA-SE injection together with a protein antigen allows the antigen-capturing DCs to quickly become immunogenic in vivo. Enhanced T-cell responses were detected when antigen was targeted to DCs. We did not detect qualitative difference in adaptive responses between untargeted or targeted protein. However, lower doses of antigen were required using anti-DEC-HIV gag p24 to achieve detectable responses. This finding highlights the importance of DCs for initiating adaptive T-cell immunity. After showing that DCs were essential for the generation of T-cell responses in lymph nodes to an s.c.

To date, this has only been achieved with attenuated N  caninum i

To date, this has only been achieved with attenuated N. caninum isolates used as live vaccines (10,11). However, application of a live vaccine poses a series of logistic and economical problems, which render inactivated and/or subunit vaccines much more attractive, provided a reasonable degree of protection against infection and disease can be achieved. Several research groups have reported promising results using recombinant antigens for vaccination studies, but others have reported failures or even anti-protective effects (3,9). This shows that the antigen repertoire of N. caninum contains both protective and immunomodulatory or

even immunosuppressive molecules, and these need to be defined and investigated. In addition, the route of antigen delivery and Raf inhibitor the type of adjuvant employed also need further investigation, SCH772984 considering that they can also alter the efficacy of a given vaccine candidate (41,43,44). Infection studies in cattle do not represent a cost-effective system to work with, and only

a limited number of research groups have taken up the enormous task to work with cattle directly (9,12). Accordingly, murine models have been extensively used for proof-of-concept studies on how an immune response against a vaccine could limit parasite dissemination and pathology. The currently used experimental murine models include (i) cerebral infection models with challenge infections of nonpregnant mice leading to cerebral disease and death, (ii) foetal infection models where mice are challenged during pregnancy and (iii) transplacental transmission of N. caninum tachyzoites leading to stillbirth, abortion or birth of infected offspring (9,49). In

the present study, we employed the acute disease model of cerebral infection in nonpregnant animals. For the vaccine, we employed an innovative approach by analysing the relative efficacy of recNcPDI vaccine antigen associated with nanogel vaccine delivery formulations. RecNcPDI has been previously shown to be ineffective when applied i.p. emulsified in SAPs, but highly effective and mediating protection against cerebral infection and disease when applied i.n. in the presence of cholera toxin (19). The purpose of the current work was to use chitosan-based nanogels, combined with different adjuvants (saponin and CT), as carriers for the E. coli Progesterone expressed recNcPDI antigen. Thereby, the aims were to investigate whether this nanogel association would influence the immunogenic and efficacy characteristics of the vaccine antigen upon i.p. and i.n. vaccination. SDS–PAGE and immunoblotting showed that recNcPDI was efficiently associated with both types of nanogels employed – alginate-coated chitosan nanogels and mannosylated, alginate-coated nanogels. The vaccine antigen was well associated with the nanogels, in terms of no nanogel-free material being detected. It also retained its antigenic reactivity with a polyclonal anti-recNcPDI antiserum.

Finally, experiments using DC deficient in ER-β revealed that the

Finally, experiments using DC deficient in ER-β revealed that the expression of ER-β on DC was selleck products essential for protective effects of ER-β ligand treatment in EAE. Our results demonstrate for the first time an effect of ER-β ligand treatment in vivo on DC in the target organ of a prototypic cell-mediated autoimmune disease. Pregnancy confers protection in a variety of cell-mediated autoimmune diseases in humans and in their respective animal models, including psoriasis, myasthenia gravis, Grave’s disease, rheumatoid

arthritis, and multiple sclerosis (MS) 1–4. Late pregnancy in humans has been associated with a decrease in Th1 immune responses. In MS, the reduction in Th1 immunity during late pregnancy is paralleled by a reduction in relapses 5. Estrogen treatment in the MS mouse model, experimental autoimmune encephalomyelitis, has been shown to reduce clinical disease by inhibiting a variety of disease-promoting mechanisms, including reductions in proinflammatory cytokines, chemokines, and migration factors, as well as increases ABC294640 research buy in CD4+CD25+Foxp3+ T regulatory cells 6–10. Estrogens signal

primarily through two nuclear receptor subtypes, estrogen receptor (ER)-α and -β, whereas more rapid membrane effects have also been described 11, 12. Although both ER are expressed in all immune cell types, most of the protective effects of estrogen treatment in EAE have been shown to be mediated through ER-α without evidence for involvement of ER-β signaling 13–15. Recently, our lab has shown that ER-β ligand treatment during EAE reduced clinical

Oxymatrine disease relatively late and preserved axon densities despite a lack of an effect on decreasing CNS inflammation and altering peripheral cytokine production. This suggested a neuroprotective effect that was independent of influences on the peripheral immune system 16. However, an effect of ER-β ligand treatment on the composition and the function of immune cells in the target organ during EAE remained unknown. There is a great deal of evidence that APC localized to the CNS at sites of immune cell infiltration play a pivotal role in the outcome of neuroinflammation. The induction of EAE requires priming of antigen-specific CD4+ T cells (TC) in secondary lymphoid tissues, and re-activation of these CD4+ TC at the target organ by professional APC. DC can drive Th-cell differentiation and are potent APC that can influence innate and adaptive immune responses. DC in the healthy CNS normally reside in the meninges and around CNS blood vessels. Recent studies have shown that during adaptive immunity, mature myeloid DC preferentially accumulate at the perivascular inflammatory foci of the spinal cords during peak EAE disease severity, inducing the production of effector TC in the CNS 17–19. In a model where DC were the only cells expressing MHCII molecules, DC alone were sufficient to initiate EAE 20.

In this process, phenomena described following observational

In this process, phenomena described following observational ZVADFMK studies in humans drives hypotheses to be tested in animal experiments.

Animal experimentation in turn refines hypotheses that can then be tested in humans. This in turn leads to further questions and more productive animal experimentation. In this iterative approach, studies in humans and animals complement each other and can synergize to move our understanding of disease forward. That being said, my bias is that a good animal is not meant to primarily replicate all of what happens in humans, nor is it meant to be directly transferable. A well-working model generates logical and testable hypotheses that are consistent first foremost with existing data in the animal, and possibly in humans as well. The drive for those who primarily use animal models should be to ‘know thy model’, able to communicate

it effectively to others, and to generate productive integrative and iterative study. In studies in humans, several properties are taken into consideration to determine the appropriateness of the group of patients accessed for a study. These properties may be related to certain demographics or to ICG-001 prevalence of disease. When considering animal models to study adverse pregnancy outcomes, several issues come to mind. With decreasing funding through federal and other sources, Casein kinase 1 cost may play a large role in the choice of mode. Larger animal

models are likely more costly and research based on these models is receiving less support.[1] However, certain strains of genetically manipulated mice are also very expensive (http://jaxmice.jax.org). The animal welfare regulatory requirements for non-human primate work are increasingly stringent as is the administrative oversight. Another constraint is the ability to deal with the public relations issues necessary to utilize primate models. Only certain institutions have the capacity, specialized facilities, and highly trained veterinary staff. Depending on the species, there are some zoonotic disease issues that require a very rigorous occupational health program. Another practical issue related to choice of animal models is the presence of experts working with that model. Just as it is often better to watch a relative cooking a family tradition, rather than relying on a recipe, there are likely to be small bits of ‘inside’ or not widely published information about the model that are more easily obtained by direct contact with the investigator utilizing the model. Current thinking would refute the notion that the placenta is just a passive membrane between mother and fetus. Early studies of nutrient uptake suggest that most of the resources delivered to the uterus are utilized by this organ. The placenta is selfish.