10 Treg therapy would probably be most effective in the early stages of disease, but because these patients have many other therapeutic options, it may be difficult to find cohorts in which testing of this therapy can be justified. Furthermore, IBD is a heterogeneous disease and each individual is likely to have

distinct disease aetiology, microbiota composition, Ribociclib molecular weight and relevant antigens. It may therefore be challenging to determine standard dosing and delivery schedules, as well as to monitor outcomes. Animal models of Treg therapy for IBD have relied on transfer of cells into T-cell-deficient animals. Will a similar conditioning step be necessary in IBD to make space for the Tregs to engraft and allow their expansion through homeostatic expansion mechanisms?

As IBD is not usually a life-threatening disease, would such SAHA HDAC price a pre-conditioning regimen be ethical? Here we will be able to learn from the results of a trial in type 1 diabetes, which is currently enrolling patients, where Tregs will be infused into immunocompetent individuals (http://www.clinicaltrials.gov/ct2/show/NCT01210664). Once Treg therapy is administered, what parameters will determine the extent to which treatment has been effective? In contrast to the scenario of transplantation,92,93 there are currently no known effective biomarkers of relevant immune status in IBD, and apart from monitoring disease symptoms and crude analysis of T cells from biopsies, there is no way to test if the therapy has re-set immune homeostasis. The efficacy of current therapeutic agents such as anti-tumour necrosis factor-α antibodies will be likely to set the bar high for Treg therapy, possibly requiring life-long cure with minimal

side-effects. Although there are still many unknowns and theoretical risks (Fig. 1), Tacrolimus (FK506) it is the hope that delivery of Tregs will indeed be able to reset intestinal immunity that justifies the study of these approaches. Current treatment strategies for IBD rely on the use of non-specific immunosuppressive agents such as steroids and anti-cytokine antibodies; these treatments are not effective in all patients, are non-specific, and never provide a cure. Antigen-specific Treg cellular therapy would, in contrast, offer a cure through specific and potent targeting of the response to disease-driving antigens at the site of inflammation. Because evidence to date suggests that Tregs are indeed functional in IBD patients, expansion of autologous cells is likely to be a feasible approach. In the context of haematopoietic stem cell transplantation, a major concern has been the purity of such expanded autologous Tregs, because contaminating effector T cells could theoretically cause graft-versus-host disease.94 Several groups have worked to identify markers that can be used in conjunction with CD25 to improve the purity of the expanded cells.

People with Diabetes Mellitus tend to suffer from acute and chronic complication. One of complication is a major cause of death in Diabetes Mellitus is a disease of the kidney. Objective: This study aimed to determine the relationship Diabetes Mellitus Type 2 with Chronic Kidney Disease at Dr. Abdul Moeloek General Hospital Bandar Lampung 2012–2013. Methods: This type of research is descriptive analytic. Research data collection was conducted using cross sectional study design by medical record. The number of the sample in this study amounted to 650 people with the sampling technique

is total sampling method. In this research, statistical test using the chi-square. Result: From the results, the patients Diabetes Mellitus Type 2 in internal medicine room at Dr Abdul Moeloek General Hospital Bandar Lampung 2012–2013 totaled 460 people with patients Diabetes Mellitus Type 2 and Chronic Kidney selleck compound Disease totaled selleckchem 155 people. Where as only Chronic Kidney Disease totaled190 people. Conclusion: There is a relationship between Diabetes Mellitus Type 2 and Chronic Kidney Disease at DR Abdul Moeloek General Hospital Bandar

Lampung 2012–2013. Key words: Diabetes Mellitus Type 2, Chronic Kidney Disease. 230 THE USE OF THRICE WEEKLY DOSES OF CINACALCET IN NON-COMPLIANT END-STAGE RENAL FAILURE PATIENTS ON HAEMODIALYSIS M HARFIELD1,2, R JAYALATH1,2, G KAN1,2 1Department of Nephrology, The Townsville Hospital, Townsville, Queensland;2The School of Medicine and Dentistry, James Cook University Queensland Australia, Australia Aim: To determine whether cinacalcet given post haemodialysis under direct observation, three times a week is an effective treatment strategy in poorly compliant, end stage renal failure patients. Background: Cinacalcet is used for the treatment of refractory secondary hyperparathyroidism in end-stage renal disease. Intolerance and poor compliance with daily

dosing leads to treatment failure. Methods: In this retrospective cohort study, we reviewed the PTH levels obtained during standard monitoring for haemodialysis patients currently on cinacalcet therapy. 20 out of 70 patients currently maintained on haemodialysis were directly observed Roflumilast taking their cinacalcet dose immediately post dialysis, in comparison with 50 patients who had been prescribed the once daily dosing. Patients selected for this treatment had failed conventional therapy either through side effects or issues with poor compliance. The peak PTH level was taken before commencement of the thrice weekly regimen and was compared to the lowest PTH obtained, after one year of treatment. The results were analysed using a one sample T-Test. Results: Of the 20 patients who were on the thrice weekly regimen, an average of 75.6% reduction in PTH was demonstrated in this group (p value <0.05). The once daily dosing regimen demonstrated an average reduction of 81% in comparison.

Results: Both the scores of IPSS and the levels of quality of life in EPIC were significantly worse at 1 month postoperatively compared to the pretreatment baseline, and thereafter progressively improved in both groups. Eviprostat-treated

patients showed significantly better recovery compared to Eviprostat-untreated control at 6 months postoperatively, with respect to urinary summary score, urinary function and urinary irritation/obstruction subscales in EPIC. Moreover, the feeling Smad inhibitor of incomplete emptying in IPSS and the urinary irritation/obstruction subscale in EPIC were significantly improved at 3 months postoperatively compared to the peak impairment at 1 month in the Eviprostat-treated group. Conclusions: It is possible that Eviprostat has the potential to ameliorate postoperative LUTS caused by brachytherapy. “
“Objectives: This was a single-center, institutional review board-approved study, conducted in the USA that used a 3 × 3 orthogonal Latin squares crossover design to assess variability in overactive bladder symptoms and adverse events when subjects were exposed to three rate settings

of sacral neuromodulation. Methods: Thirteen female subjects selleckchem who had urgency frequency and urinary urge incontinence were enrolled into the study. Twelve subjects completed the study. Upon enrollment, each subject was randomized to one of three rate-setting sequences: 5.2, 14, and 25 Hz.

Each rate setting was tested for 1 week in every subject. Results: When subjects were programmed to 5.2, 14, and 25 Hz, Nintedanib (BIBF 1120) they had an average of 3.83 ± 2.27, 2.37 ± 1.83, and 2.82 ± 2.1 incontinence episodes per day and an average of 2.61 ± 1.64, 1.84 ± 1.43, and 1.94 ± 1.61 pad changes per day, respectively. Rate had a statistically significant effect on the number of incontinent episodes (P < 0.001) and number of pad changes (P = 0.039) with more incontinent episodes in the 5.2-Hz setting compared to the 14- and 25-Hz settings (P < 0.04) for both measurements. Nine subjects reported 21 adverse events. None of the adverse events was considered either a serious or an unanticipated adverse device effect (UADE). Conclusion: Rate significantly affected the number of incontinence episodes and pad changes per day. The number of adverse events was similar across the three rate settings with programming-related adverse events lowest in the 14 Hz group. "
“Objectives: To measure urinary nerve growth factor (NGF) levels in patients with several urinary tract diseases under different conditions and compare with NGF levels in patients with overactive bladder (OAB) and interstitial cystitis/painful bladder syndrome (IC/PBS). Methods: Urinary NGF levels were measured using enzyme-linked immunosorbent assay (ELISA) and normalized by urinary creatinine concentration.

CD38 mean fluorescence intensity (MFI) increased not only in CD14+ monocytes that became infected but also in monocytes in the same cultures that remained uninfected (Supporting Information Fig. check details 4). These results indicate that exposure to HIV-1 is sufficient to cause upregulation of CD38 in peripheral blood monocytes in vitro and, taken together

with the observed effects of depleting HIV-specific IL-10+ CD8+ T cells, suggest that the latter could protect monocytes from activation by HIV-1 in vivo. Finally, we investigated whether the effects of HIV-specific IL-10+ CD8+ T cells on monocyte CD38 expression were IL-10-dependent. Treatment of CD8-depleted PBMCs with an IL-10 receptor (IL-10R) blocking antibody prior to co-culture overnight with CD8+ T cells led to a marginal

increase in monocyte CD38 expression, when compared with the effect of depleting HIV-specific IL-10+ CD8+ T cells. This could reflect incomplete receptor blockade on monocytes; alternatively, it could indicate Palbociclib concentration that this population may not mediate its effects solely through IL-10 production (Supporting Information Fig. 5). In this study, we have shown that a distinct subpopulation of HIV-specific CD8+ T cells contributes substantially to IL-10 production by PBMCs in chronic uncontrolled HIV-1 infection. The magnitude of this population was positively correlated with the magnitude of the IFN-γ response to the same HIV-1 antigens and the majority of the CD8+ T-cell subset co-produced IL-10 and IFN-γ upon short-term HIV-1 gag stimulation. However, a shift towards lone IL-10 production was associated with better virological control. Together, these observations suggest that a subset of HIV-1 gag-specific IFN-γ-secreting CD8+ T cells may have acquired the capacity to produce IL-10 in response to chronic viral replication, possibly as Cediranib (AZD2171) a protective response to inflammation in the context

of ongoing antigenic stimulation. Their virtual absence in patients treated with an effective ART regimen is consistent with this notion, although this remains to be confirmed in a longitudinal study. Furthermore, their lack of a conventional Treg-cell phenotype contrasted with CMV-specific IL-10+ CD8+ T cells that were detected in some co-infected individuals and suggests that these populations have distinct ontogenies. Co-expression of IL-10 and IFN-γ by tissue-homing virus-specific T cells has been extensively reported in murine viral infection models and in human CD4+ T cells [11, 19, 25-28]. By contrast, human virus-specific CD8+ T-cell populations with dual IL-10-/IFN-γ-secreting capacity appear to be rare: to our knowledge, the only precedent for this is in Epstein-Barr virus (EBV) infected solid organ transplant recipients, in whom CD8+ Treg type 1 cells expressing FoxP3 could be induced in vitro by type-1-polarising DCs [11].

SV2C is almost completely absent from neocortex, hippocampus, thalamus and cerebellum [5, 6]. Our data show that SV2C is barely detectable in the normal adult hippocampus and seems restricted to axonal projections of the GCL to CA4 (mossy fibre

pathway). A major finding of this study is that SV2C expression is increased in TLE patients with MTS1A and mossy fibre sprouting, and that SV2C is selectively overexpressed in Zn2+-rich glutamatergic synapses in the IML. In the normal hippocampus, granule neurones from the GCL receive afferents to the outer and middle ML respectively from the lateral and medial entorhinal Gemcitabine cortex and their axons target CA3 and CA4 pyramidal neurones forming the mossy fibre pathway. The IML receive afferents mainly from hilar ipsilateral associational and commissural systems, mostly the mossy neurones, which are excitatory interneurones located in the hilus [37, 42]. However, in the context of HS, abnormal mossy fibre sprouting occurs in the IML, maybe in response to the loss of normal afferents to granule neurones of GCL [42]. Indeed, a significant loss of hilar mossy neurones has been found in TLE patients with HS and mossy fibre sprouting, and it has been suggested that in humans, as in animal models, this results in deafferentation of the IML followed

by reactive synaptogenesis of mossy fibres Selleck JNK inhibitor forming abnormal monosynaptic recurrent excitatory synapses on granule for cells, a re-entry circuit contributing to epilepsy [27, 42, 43]. Because mossy fibres and abnormal mossy fibre sprouts are Zn2+-rich, they were initially detected by the Timm’s method [44] due to their high heavy metal content. Antibodies against ZnT3 also detect them as ZnT3 controls the amount of Zn2+ in the synaptic vesicles of mossy fibres. Indeed, the massive release of glutamate during seizures is accompanied by an equally massive release of Zn2+ from the presynaptic buttons in HS [38, 45]. Our findings suggest therefore that SV2C is selectively expressed in abnormal sprouts of mossy fibres in the IML.

SV2C has been recently reported to be preferentially associated with GABAergic SVs [7]. However in this study, we found no colocalization of SV2C IR with GABAergic synapses, such as those contributed to the IML by inhibitory neurones like the pyramidal basket cells. On the opposite, SV2C colocalized with VGLUT1 in the IML, indicating that it is expressed in glutamatergic synapses and bringing additional arguments for a selective expression in abnormal sprouting fibres. No particular clinical or therapeutic characteristic differentiated the cases of TLE patients with HS and SV2C overexpression from the rest of the cohort. This might be related to the rather small size of this patient series and the retrospective collection of data. In conclusion, this study provides the first report on the expression pattern of SV2 isoforms in patients with pharmacoresistant TLE and HS.

Again, the differences Stem Cell Compound Library price did not reach statistical significance, possibly because of the variability among patients, despite a general trend towards elevated values in the HIV-negative women compared with the HIV-positive women. When we stratified the

HIV-positive CVL according to menstrual status, we observed a significant increase of Trappin-2/Elafin secretion in the secretory phase of the cycle, suggesting that this molecule might be hormonally regulated (Fig. 5c). The presence of Trappin-2/Elafin in CVL suggests that Trappin-2/Elafin might be a relevant molecule for in vivo protection against HIV-1. The research presented demonstrates that epithelial cells from the upper and lower FRT synthesize and secrete Trappin-2/Elafin. We also found that rTrappin-2/Elafin has potent anti-HIV activity against both X4/T-tropic IIIB and R5/M-tropic BaL HIV-1. To our knowledge this is the first published report of anti-HIV activity of rTrappin-2/Elafin against HIV-1. Furthermore, unlike epithelial cells from the Fallopian

tubes, cervix and vagina, uterine epithelial cells respond to Poly(I:C) by secreting increased amounts of Trappin-2/Elafin. Lastly, we observed that Trappin-2/Elafin is present in CVL from both HIV-positive and HIV-negative women, and generally higher levels, although not statistically significant, were observed in HIV-negative women, suggesting PLX4032 price that this molecule is normally found in FRT secretions and that it might have anti-HIV protective functions in vivo. Another possible explanation might be that HIV-1 infection can inhibit production of Trappin-2/Elafin. Previous work from our laboratory has demonstrated that epithelial cells from

the upper human and rodent female reproductive tract in culture synthesize and secrete antimicrobials that bathe the mucosal surfaces of the FRT.11–13,54–56 As part of the first line of immune protection, secretions from polarized epithelial cells from the Fallopian tubes, uterus and cervix contain a spectrum of antimicrobials, including SLPI, macrophage inflammatory Baf-A1 datasheet protein (MIP)-3α, defensins and lactoferrin14,18 (M. Ghosh, unpublished data). Our findings indicate that, as a part of this protection, Trappin-2/Elafin is produced by epithelial cells throughout the upper FRT. Others have shown, by immunohistochemistry, that Trappin-2/Elafin is present in neutrophils and glandular epithelial cells in the uterus during the menstrual cycle30 and in the CVL.57 Our findings extend these observations in several ways. First, this study demonstrates the production of Trappin-2/Elafin by epithelial cells throughout the FRT. Second, our studies suggest that some, if not all, Trappin-2/Elafin in the CVL is the result of the downstream movement of secretions from the upper FRT to the lower FRT. Third, whereas others have reported Trappin-2/Elafin in the CVL of HIV-positive women, our findings demonstrate that Trappin-2/Elafin is present in the CVL of healthy women.

The compromised signaling response correlated with the inability of the S291A variant to associate with the chaperone prohibitin. No direct interaction between phosphorylated serine 291 and 14-3-3 proteins was observed in

this study 47 despite the evolutionary conservation JAK inhibitor of the canonical mode 1 motif for 14-3-3 binding in murine and human Syk orthologes. The marked discrepancies to our data cannot be attributed to the use of different experimental systems. It remains however possible that murine and human Syk behave differently. This may also explain why we repeatedly identified prohibitin in our quantitative SILAC-based interactome analysis as unspecific “background” protein (Supporting Information Table 2). Future experiments are needed to directly compare the functions of murine and human Syk. However, the negative-regulatory signal circuit described in this paper for the human Syk ortholog in two different cell lines demonstrates the complexity of the Syk signaling

network. selleck Moreover, our quantitative proteomic approach to comprehensively identify the Syk phosphoacceptor sites and at least some of the their phosphorylation kinetics as well as the interactome of human Syk in resting and activated B cells provides an indispensable clue to finally decipher Syk-regulated signaling pathways under normal and pathological conditions. B-cell culture conditions, lysis and stimulation procedures have been described 30, 48. Immunoprecipitations of citrine-tagged or endogenous Syk, chicken SLP65 and PLC-γ2 from lysates of 3×107 DT40 cells were performed with antibodies to GFP (Roche), Syk (4D10, Santa Cruz), chicken-SLP65 (kindly provided by T. Kurosaki) or PLC-γ2 (Santa Cruz) Alanine-glyoxylate transaminase coupled to protein A/G sepharose

(Santa Cruz). Antibodies for immunoblot analyses were used according to manufacturer’s instructions and recognized Syk (Santa Cruz), 14-3-3γ cell signaling technology (CST), GFP (Roche), 14-3-3-binding motif (CST), GST (Molecular Probes), phosphotyrosine (4G10, Biomol) and PLC-γ (Santa Cruz). For Far Western experiments, immunoprecipitated citrine-Syk was subjected to SDS-PAGE, blotted onto nitrocellulose and incubated with 10 μg GST or GST fusion proteins encompassing 14-3-3γ (plasmids kindly provided by S. Beer-Hammer, Düsseldorf) that were expressed in E. Coli BL21 bacteria upon induction with IPTG for 3 h and purified via glutathione sepharose (GE Healthcare). The cDNA encoding human Syk with an N-terminal OneStrep tag (Iba TAGnologies) was ligated into pAbes-puro vector and transfected via electroporation into Syk-deficient DT40 cells (300 V, 975 μF). For further experiments, three independent clones were selected and pooled. The cDNA of N-terminally citrine-tagged human Syk was ligated into pCRII-Topo.

In that study, in comparison with immunocompromised patients, relatively few copies of EBV DNA (500, 8000, and 77 000 copies/ml) were detected in CSF obtained from three immunocompetent patients with EBV-associated encephalitis. Krumbholz et al. have also reported that similar amounts of copies

of EBV DNA (2100 and 5300 copies/ml) were detected in CSF obtained from two patients with EBV-associated encephalitis (15). Thus, the number of copies of EBV DNA detected in the CSF of our case is consistent with previous studies. Although serological analysis would have been necessary for a conclusive diagnosis in this patient, we believe that EBV might have been involved in the pathogenesis of her limbic encephalitis. EBV can cause various types of central nervous system manifestations, such as encephalitis, Ponatinib datasheet meningitis, cerebellitis,

transverse myelitis, and neuropathy (16, 17). It has been demonstrated that EBV infections of the central nervous system can occur without manifestations LDE225 concentration of infectious mononucleosis (16). However, only two limbic encephalitis cases with EBV infection have been previously reported (by Norwegian neurologists), and one of these cases did not exhibit the typical clinical features that are associated with infectious mononucleosis (18). Therefore, in order to diagnose EBV related non-herpetic acute limbic encephalitis, CSF should be examined for EBV DNA by using real-time PCR even when the patient does not exhibit typical clinical symptoms of infectious mononucleosis. The authors thank Mrs. Akiko Yoshikawa and Mrs. Akemi Miki for their technical support. This work was supported in part by a grant from the Ministry of Health, Labor and Welfare of Japan (H20-Kokoro-021). “
“The emergence of antibiotic-resistant bacteria such as Staphylococcus aureus calls for inventive research and development strategies. Inhibition of this bacterial pathogenesis may be a promising therapeutic approach. The screening of antimicrobial compounds from endophytes is a promising way to meet the increasing

threat of drug-resistant strains of human and plant pathogens. In the present study, a novel endophytic fungus, Colletotrichum Exoribonuclease gloeosporioides, was isolated from the medicinal plant Vitex negundo L. Extracts of C. gloeosporioides were obtained using hexane, ethyl acetate and methanol solvents. The fungal extracts exhibited an effective antimicrobial activity against bacterial and fungal strains. The extracts were also analysed for antibacterial activity against methicillin-, penicillin- and vancomycin-resistant S. aureus strains (1–10). The methanol extract showed an effective antibacterial activity against S. aureus strain 9, with a minimal inhibitory concentration of 31.25 μg mL−1. The synergistic action of endophytic fungal extract with antibiotics such as methicillin, penicillin and vancomycin was observed against S. aureus strain 6.

Care must be taken to avoid contamination of fetal DNA with maternal DNA; detection of such contamination can be performed by short tandem repeat (STR) analysis. The same strategy as for prenatal diagnosis of X-CGD can be used for prenatal diagnosis of other CGD subtypes [40], although this may be more complicated if the parents each carry different mutations. In cases where the family-specific mutations are not known, different methods must be applied. Partial

or complete gene deletions can be recognized by MLPA or array CGH analysis of genomic DNA, but more subtle abnormalities require the use of allele-specific markers. The MLPA or CGH probes and the allele-specific markers should be chosen in the surroundings of the gene that is supposed to be mutated. Step-by-step protocols for laboratory diagnostics (short and extensive) are BVD-523 research buy given in Tables 3 and 4 and in Fig. 1. D. R. obtained financial support from the Chronic Granulomatous Disorder Society, London, UK, and from the European Commission E-Rare find more program (EURO-CGD grant). The authors declare no conflicting interests. D. R. and M. d. B. wrote the paper together. “
“Citation Pertyńska-Marczewska M, Głowacka E, Grodzicka A, Sobczak M, Cypryk K, Wilczyński JR., Wilczyński J. Profile of peripheral blood neutrophil cytokines in diabetes type 1 pregnant women and its correlation with selected parameters in the newborns. Am J Reprod Immunol 2010; 63: 150–160

Problem  Interleukin (IL)-12, IL-10, tumor necrosis factor-α (TNF-α), IL-6 and IL-8 alter as pregnancy progresses, implying continuous immune regulation associated with the maintenance of pregnancy. We aimed to evaluate the peripheral blood neutrophil-derived production of these cytokines in the course of pregnancy complicated by type 1 diabetes. Method of study  These parameters were measured in samples from healthy non-pregnant (C), diabetic non-pregnant (D), healthy

pregnant (P) and pregnant diabetic (PD) women. Results  Neutrophil-derived secretion of TNF-α and IL-12 increased along with progression of pregnancy PFKL in PD and P groups. The concentration of IL-10 from lipopolysaccharide (LPS)-stimulated neutrophils increased during the course of uncomplicated pregnancy but decreased in diabetic pregnancy. Concentration of IL-8 decreased with the advancing gestational age in P and PD groups. LPS-stimulated neutrophil-derived IL-6 concentration increased only in PD patients. Conclusion  Our results show that diabetes creates pro-inflammatory environment thus potentially influencing the outcome of pregnancy. We conclude that neutrophil-derived cytokine production could contribute to the complications seen in pregnant women with type 1 diabetes. “
“Prior murine studies have demonstrated the pivotal role that Blimp-1 has in the exhausted phenotype of T lymphocytes in chronic viral infection. In this issue of the European Journal of Immunology, Seddiki et al. [Eur. J. Immunol. 2013.

This work was supported by grants from the Ontario HIV Treatment Network of the Ontario, Ministry of Health and from the Canadian

Institutes of Health Research to D.W.C. and A.K. We would like to thank Mr Andy Ni and Ms Kathryn Williams, the Ibrutinib biostatisticians at Clinical Research Unit, Research Institute, Children’s Hospital of Eastern Ontario, for their help in statistical analysis. We would also like to thank the healthy volunteers and the patients with TB infection for generously providing blood samples, and Ms N Lamoureux in the Division of Infectious Diseases for case identification and phlebotomy. The authors declare that there are no conflicts of interest. Fig. S1. Gating strategy for the identification of interleukin (IL)-17+, IL-22+ and interferon (IFN)-γ+ CD4+ T cells, in the unstimulated peripheral blood mononuclear cells (PBMCs) of healthy controls. Fig. S2. Interleukin (IL)-17-, IL-22- and interferon (IFN)-γ-expressing CD4+ T cells are induced in individuals with active tuberculosis (TB) infection following stimulation with mycobacterial antigens. Peripheral blood mononuclear cells (PBMCs) (1 × 106/ml) were cultured in the presence or the absence of mycobacterial culture filtrate for 7 days. Intracellular IFN-γ (a), IL-17 (b) and IL-22

(c) expression in CD4+ T cells was detected by flow cytometry. The line graphs of percent frequency ROCK inhibitor of IFN-γ+ (n = 7), IL-17+ (n = 10) and IL-22+ (n = 8) expressing CD4+ T cells Cyclic nucleotide phosphodiesterase before and after stimulation were generated. US, unstimulated group; ST, stimulated group. “
“Citation Hansen PJ. Medawar redux – an overview on the use of farm animal models to elucidate principles of reproductive immunology. Am J Reprod Immunol 2010 Farm animals have been important models for the development of reproductive immunology. Two

of the major concepts underpinning reproductive immunology, the idea of the fetal allograft and progesterone’s role in regulation of uterine immunity, were developed using the bovine as a model. This volume of the American Journal of Reproductive Immunology is composed of review articles that highlight the continued relevance of farm animals as models for research in mammalian biology. It is important that a diverse array of genotypes are used to elucidate biological principles relevant to mammalian biology and human health because the nature of mammalian evolution has resulted in a situation where the genome of the most commonly used animal model, the laboratory mouse, is less similar to the human than other species like the cow. Moreover, the evolution of placental function has been accompanied by formation of new genes during recent evolution so that orthologs do not exist in any but closely related species.