The manuscript was published with permission of the Director of V

The manuscript was published with permission of the Director of VIDO as manuscript number 529. The authors do not have any conflicting interests.

“Citation Ticconi C, Rotondi F, Veglia M, Pietropolli A, Bernardini S, Ria F, Caruso A, Di Simone N. Antinuclear autoantibodies in women with recurrent pregnancy loss. Am J Reprod Immunol 2010; 64: 384–392 Problem  To investigate the possibility that antinuclear antibodies (ANA) are involved in recurrent pregnancy loss (RPL). Methods  Case–control study carried out on 294 women (194 cases and 100 controls) in two University hospitals. The presence, the serum titers and the indirect

immunofluorescence (IIF) patterns of ANA were determined in women with RPL and in control women. Results  Antinuclear antibodies at titers ≥ 1:80 were detected in 97 (50%) women with RPL and in 16 (16%) control women. Elevated ANA titers (≥1:180) were detected only in RPL women, whereas all control women had ANA titers no greater than 1:80. No differences could be detected in the IIF patterns between RPL and control women. No differences in ANA positivity JNK inhibitor could be detected according to the type (primary or secondary) or number (>2 versus ≥3) of losses. Conclusions  ANA could be of some value in identifying women with RPL with potential, although still not fully defined, immune abnormalities. “
“Eosinophils are multi-functional leucocytes that play a role in inflammatory processes including allergy and infection. Although bone marrow (BM) inflammatory cells are the main source

of eosinophil-basophil (Eo/B) differentiation-inducing cytokines, a recent role has been Y-27632 supplier demonstrated for cytokine induction through Toll-like receptor (TLR)-mediated signalling in BM progenitors. Having previously demonstrated that cord blood (CB) progenitors induce Eo/B colony-forming units (CFU) after lipopolysaccharide (LPS) stimulation, we sought to investigate the intracellular mechanisms by which LPS induces Eo/B differentiation. Freshly isolated CD34-enriched human CB cells were stimulated with LPS (and/or pharmacological inhibitors) and assessed for alterations in haematopoietic cytokine receptor expression and signalling pathways by flow cytometry, Eo/B CFU in methylcellulose cultures, and cytokine secretion using Luminex assays. The LPS stimulation resulted in a significant increase in granulocyte–macrophage colony-stimulating factor (GM-CSF)-responsive, as opposed to interleukin-5-responsive, Eo/B CFU, which also correlated with significant increases in CD34+ cell GM-CSFRα expression.

Posted in Antibody | Leave a comment

The five

The five GPCR Compound Library chemical structure SLE patients ascertained to have TSGA10 autoantibodies were further analysed for autoantibodies against common APS1 autoantigens by ITT and immunoprecipitation. The female patient with high-titre autoantibodies against TSGA10 was found to have very low-titre GAD autoantibodies. One of the SLE patients with low-titre TSGA10 autoantibodies

was determined to have low-titre autoantibodies against both GAD and NALP5, whereas another patient had very low-titre autoantibodies against AADC. No autoantibodies were detectable against the autoantigens SCC, TPH, TH, 17-OH, CYP1A2, 21-OH or IA2. The single healthy blood donor with a positive TSGA10 autoantibody index did not have autoantibodies against any of the APS1 autoantigens. To determine the age at which TSGA10 autoantibodies manifest and if there are any fluctuations in TSGA10 autoantibody titres over the duration of the disease, ITT was conducted on

Y-27632 solubility dmso all serum samples collected from the five autoantibody-positive APS1 patients collected from the time of diagnosis (Fig. 2). Serum samples were available from a range of 4.5 years post-diagnosis to 23.5 years post-diagnosis with a median of 14.5 years for each patient. Three of the five patients had autoantibodies against TSGA10 from the first available serum sample at ages 7, 9 and 14 years. Seroconversion to a positive TSGA10 autoantibody index was observed in the remaining two patients at age 8 years and the second at 29 years of age. Autoantibody titres remained constant for each patient with every sample available with the longest follow-up period of 23.5 years. The tissue expression of TSGA10 was examined in various organs by quantitative PCR. TSGA10 mRNA was predominantly Aspartate expressed in testicular tissue (Fig. 3), with expression also being detected in almost all tissues studied, albeit at very low levels in most organs.

Virtually undetectable TSGA10 mRNA expression was observed only in the heart, skeletal muscle, leucocytes and adrenal cortex. Pituitary manifestations are a rare feature of APS1 presenting as either single or multiple hormonal deficiencies. Autoantibodies against pituitary tissue have been repeatedly shown by immunofluorescence in the sera of APS1 patients, yet a major pituitary specific autoantigen remains to be identified. A cDNA clone encoding TSGA10 was isolated and identified as a minor autoantigen in APS1 from the immunoscreening of a human pituitary cDNA expression library. While conducting the present study, the TSGA10 autoantigen was also independently isolated from a human testis cDNA expression library and characterized using sera from within the same Finnish APS1 patient series [20].

Posted in Antibody | Leave a comment

In summary, our data identify Th2-cell differentiation patterns l

In summary, our data identify Th2-cell differentiation patterns linked to partial DC maturation stages with quantitative differences between pathogen-derived, TLR-dependent VSG antigens, and non-TLR-dependent TNF stimulation in vitro. No induction of FoxP3+ Treg cells could be observed by

any of our DCs in the absence of exogenous TGF-β in vitro. To assess how these DC maturation signatures prime T-cell responses in vivo, we injected differentially matured and OVA-loaded DCs together with OVA-specific TCR-transgenic OT-II T cells i.v. and determined proliferation and cytokine production Alectinib manufacturer of injected T cells. DCs matured with TNF, mfVSG, or MiTat1.5 sVSG all induced proliferation of CFSE-labeled T cells (Fig. 4A). The most profound priming in T cells was detected upon injection of LPS-matured DCs as determined by flow cytometry (Fig. 4A) or calculated as the division index (Fig. 4B). Furthermore, one single injection of DCs conditioned with TNF, mfVSG, or MiTat1.5 sVSG increased intracellular IL-13 and IL-5 release by ex vivo restimulated OVA-TCR-specific T cells (Fig. 4C and D), in contrast to mice which received LPS-matured

DCs which showed only background levels of IL-13- or IL-5-producing OVA-TCR-specific T cells (Fig. 4C this website and D). Similar to our in vitro findings (Supporting Information Fig. 4B), a low frequency of IFN-γ-releasing T cells was detectable after a single injection, irrespective of the DC maturation regimen. Clearly polarized Th1-cell responses resulted only after injection of LPS-matured

DCs (data not shown and Fig. 4C and D). Furthermore, injection of DC conditioned with TNF, mfVSG, or MiTat1.5 sVSG did not raise the frequency or total cellular amounts of FoxP3+ Treg cells among OVA-TCR-specific T cells in vivo similar to LPS-matured DCs (Supporting Information Fig. 5B and C) further strengthening the observation that partially mature DCs efficiently induce proliferation and priming of (CFSE labeled) OVA-TCR-specific T cells in vivo (Fig. 4A). Together, DCs conditioned by TNF- Bay 11-7085 or T. brucei-derived VSG antigens induce profound and comparable Th2-cell priming in vivo. Asthma induced by alum-guided immunization of mice with OVA is a widely used model for a Th2-cell mediated disease characterized by proinflammatory lung infiltrates of eosinophilic granulocytes and a subsequent Th2-cell dependent production of OVA-specific IgG1 and IgE 42. Mice subjected to repeated sensitization and antigen challenges showed a profound influx of total cells, in particular eosinophils in the bronchoalveolar lavage (BAL) as a major parameter for asthma (Fig. 5A). Three repetitive injections of OVA-loaded TNF, mfVSG, or MiTat1.5 sVSG-matured DCs did not change the total cellular influx in the lungs compared with noninjected animals.

Posted in Antibody | Leave a comment

[48] This demonstrates that the tolerated, re-transplanted skin g

[48] This demonstrates that the tolerated, re-transplanted skin graft carried over within it perfectly functional effector T cells, but that FOXP3+ Treg cells were actively blocking their ability to reject and so maintained

the tolerant state within the graft. By studying the changes in gene expression of dendritic cells when they interact with Treg cells,[49, 50] it was found that in addition to the known down-regulation of co-stimulatory ligands and antigen presentation, there was up-regulation of a number of enzymes that either catabolize or use essential amino acids[51] (Fig. 3). In the context of a microenvironment with a restricted availability of nutrients, the local depletion of essential amino acids by these enzymes would buy GW-572016 be an effective mechanism to control the immune response via the mTOR nutrient sensing pathway. It has also been shown that the intracellular availability of leucine and consequently mTOR activation is controlled by T-cell-receptor-induced expression of the neutral amino acid transporter slc7a5 in Th1 and Th2 cells, where it is essential for their activation find more and differentiation, while Treg cells seem not to require this particular transporter.[52] The first example of such amino acid catabolism being able to

control the immune response was the expression of indoleamine 2,3 dioxygenase (IDO) in the placenta during pregnancy, which acts locally to deplete the essential amino acid tryptophan in order to block the maternal immune response to paternal

alloantigens.[53] This tryptophan-depleted microenvironment is sensed by general control non-repressed 2 (GCN2), ADP ribosylation factor which is one of the initiators of the integrated stress response, and leads to a block in the proliferation of CD8 effector T cells,[54] and is required for the survival of T cells, including CD4+ Treg cells, during periods of amino acid starvation.[51] GCN2, however, was not essential for T cells to sense the absence of essential amino acids in vitro,[51] neither is it required for the induction of tolerance to skin grafts in mice by co-receptor blockade (S. Cobbold, E. Adams and H. Waldmann, unpublished results). The induction of FOXP3 by stimulating naive CD4+ T cells in the presence of low doses of TGF-β in vitro was also unaffected by stimulating the GCN2 pathway with histidinol; whereas, inhibition of the mTOR pathway gave a synergistic increase in FOXP3 induction.[51] It has also now been shown that 1-methyltryptophan mediated blocking of IDO and tryptophan sensing can act via mTOR and PKCθ signalling.[55] Indoleamine 2,3 dioxygenase may have been recognized as the first example of immune regulation due to amino acid catabolism because, of all the essential amino acids, tryptophan is thought to be present at the lowest concentration.

Posted in Antibody | Leave a comment

We estimated the density of TMC0356 to be over 105 CFU per 1 g of

We estimated the density of TMC0356 to be over 105 CFU per 1 g of feces. Moreover, when TMC0356F-100 was subcultured repeatedly in skim milk, and then digested with ApaI, TMC0356F-100 and TMC0356 were different from each other in two bands on PFGE. However, no difference between TMC0356F-100 and TMC0356 could be detected by carbohydrate fermentation and enzymatic activity tests (data not shown). These results indicate that there are some changes in the genome of TMC0356 after repeated reculture, although

these changes do not alter tested physiological functions of this bacterium. Therefore, the method developed in the present study might be, at least partly, dependent on the frequency of subculturing. TMC0356 can be MK-2206 mouse distinguished from other strains by PFGE using three restriction enzymes—SmaI, SacII, and ApaI. PFGE is also useful for the detection of L. gasseri TMC0356 in human feces.

Our results indicate that orally administered TMC0356 can survive in, and colonize, the human intestine. We thank Professor Hisakazu Iino (Life Science for Living System, Graduate School, Showa Women’s University) for isolation and identification of lactobacilli in the fecal samples of our subjects. We also thank Professor Takao Mukai (School of Veterinary Medicine, Kitasato University) for technical advice relating to PFGE. This work was supported by a Grant-in-Aid for Research and Development from the Japanese Ministry of Agriculture and Forestry. “
“Intraperitoneal larval infection (alveolar PLX-4720 mouse echinococcosis, AE) with Echinococcus multilocularis in mice impairs host immunity. Metacestode metabolites may modulate immunity putatively 4��8C via dendritic cells. During murine AE, a relative increase of peritoneal DCs (pe-DCs) in infected mice (AE-pe-DCs; 4% of total peritoneal cells) as compared to control mice (naïve pe-DCs; 2%) became apparent in our study. The differentiation of AE-pe-DCs into TGF-β-expressing cells and the

higher level of IL-4 than IFN-γ/IL-2 mRNA expression in AE-CD4+pe-T cells indicated a Th2 orientation. Analysis of major accessory molecule expression on pe-DCs from AE-infected mice revealed that CD80 and CD86 were down-regulated on AE-pe-DCs, while ICAM-1(CD54) remained practically unchanged. Moreover, AE-pe-DCs had a weaker surface expression of MHC class II (Ia) molecules as compared to naïve pe-DCs. The gene expression level of molecules involved in MHC class II (Ia) synthesis and formation of MHC class II (Ia)–peptide complexes were down-regulated. In addition, metacestodes excreted/secreted (E/S) or vesicle-fluid (V/F) antigens were found to alter MHC class II molecule expression on the surface of BMDCs.

Posted in Antibody | Leave a comment

This group of patients with a low risk of complications


This group of patients with a low risk of complications

[1] is also the most common category of febrile neutropenic patients. Our patients were recruited from a clinical antibiotic trial [16] in which patients were randomized MK-2206 concentration into two different dosing regimes of tobramycin. The results obtained comparing these two dosing regimens of tobramycin add information to the field of interaction between aminoglycosides and the host immunopathological response. Moreover, our patients participated in this study only once, thus avoiding bias related to the same patient providing several sets of results. Unfortunately, we did not collect samples beyond 2 days after the beginning of febrile neutropenia,

and our group AZD6738 purchase of patients was relatively small. In general, our results were in accordance with results from similar studies in cancer patients with febrile neutropenia. Schuttrumpf et al. [24] previously found that most patients with a non-infectious cause of febrile neutropenia had PCT concentrations <0.5 μg/l. Bacteraemia with coagulase-negative staphylococci may not increase the PCT levels [25], whereas occasional patients with higher PCT values may not have any infection [26]. The median level of the proinflammatory IL-6 increased about 30% from 61 to 80 ng/l. Still these IL-6 levels were compatible with non-bacteraemic febrile episodes compared with previous studies [27–31]. Median IL-8, INFγ and TNFα were low both in the first and in the second samples. All IL-8 values were <1000 ng/l, a cut-off value usually suggesting an increased risk of bacteraemia [32]. Engervall et al. [27] underlined, however, that both pro- and anti-inflammatory cytokines tend to be elevated at the beginning of febrile

neutropenia. Other studies show that cytokine concentrations are not predictive of bacteraemia in febrile neutropenic patients [33]. IL-6 and IL-8 seem to be the two cytokines most strongly associated with bacteraemia, and low levels of these cytokines Liothyronine Sodium have a high negative predictive value [28]. Likewise, high levels of the anti-inflammatory IL-10 are associated with persistent bacteraemia, the mechanism thought to be a condition of immunoparalysis with reduced ability to clear the infecting agent [30]. Different cytokine measurement standardizations in different studies make absolute levels difficult to compare [34]. Most studies of inflammatory response markers include episodes of febrile neutropenia where the same patient may participate several times [9, 10, 12, 14, 15, 27–31, 34–37], adding to the problems of comparing different studies. The clinical condition of our patients during the first couple of days of febrile neutropenia was only mildly deteriorated. The MASCC scores ≥21 in 92% of our patients suggested a low risk of complications [1]. The study of Uys et al.

Posted in Antibody | Leave a comment

, 2000) Chemotherapy with praziquantel is the cornerstone of sch

, 2000). Chemotherapy with praziquantel is the cornerstone of schistosomiasis control. Assessment of the impact of mass treatment with praziquantel is usually by determining the prevalence of the infection and presence of PPF (Mohamed-Ali et al., 1991). In Sudan, Mohamed-Ali et al. (1991) and Doehring-Schwerdtfeger et al. (1990) reported a reduction of egg excretion and reversibility of PPF 7 and 23 months, respectively, after praziquantel Venetoclax manufacturer treatment, while the same finding was reported by Homeida

et al. (1996) after both annual and biennial treatment. Reports by the Homeida group, in their studies in Sudan, have shown that the factors that control fibrosis regression are age, gender and the grade of fibrosis. Young patients with lower PPF grades tend to respond more to antischistosomal chemotherapy (Homeida et al., 1991, 1996; Kheir et al., 2000).

Based on the above findings, and because the SM2 locus was reported to control the progression of the disease (Henri et al., 2002), it was suggested that the regression of PPF (reversibility) could also be under genetic control. Thus, the aim of this study is to evaluate the factors controlling the regression of liver fibrosis in S. mansoni-infected subjects after praziquantel therapy. This study was carried out between 1999 and 2002 in Um-Zukra village, Gezira state, Managil province, Central Sudan. The village is about 350 km south of Khartoum (the capital)

and 110 km west of Wad Medani town, in the Managil extension MLN0128 nmr agricultural scheme. The Gezira and Managil irrigated scheme involves about two million acres, cultivated by cotton and other crops, and populated by about 1.5 Farnesyltransferase million individuals. The study area was selected according to the prevalence of S. mansoni infection. Random stool samples were obtained from different villages in the Gezira state, and examined for S. mansoni eggs. The highest prevalence (50%) was found in Um-Zukra village. The population of Um-Zukra is about 4000individuals (according to a census performed in 1999), belonging to three tribes, mainly the Kawahla (80%), in addition to Rawashda and Galeen (20%). The village is surrounded by cultivated area and the canal is only 450 m from the center of the village. There are two water pumps (wells) that are used for drinking water. The other water source for domestic use (washing and bathing) is the canal. Each house was given a number from 1 to 629. The numbers were written on metallic plates and fixed on all houses, and pedigrees for the study subjects were drawn. Plastic containers for stool samples were distributed to the villagers according to the house and individual numbers. The Schistosoma mansoni egg count g−1 stool was conducted in November 1999 using Kato’s method (Katz et al., 1972) on three stool samples collected on different days before treatment.

Posted in Antibody | Leave a comment

The SNPs rs731236, rs7975232 and rs1544410 are located at the 3′

The SNPs rs731236, rs7975232 and rs1544410 are located at the 3′ untranslated region of VDR gene, so none of them would be seen in the protein product. Although this region has been recognized as being involved in the regulation of gene expression, particularly through the modulation of mRNA stability [27], the functional role of the SNPs has not been Ceritinib established. The likely explanation for our observed association regarding SNP rs731236 is to assume a linkage to one or more truly functional polymorphisms elsewhere in VDR

gene [3, 27]. Another SNP, rs2228570, is localized within the 5′ end of the gene and consists of a T-to-C change. This change occurs inside a start codon (ATG) such that when the C variant is present, an alternative start site is used, resulting in a protein with a different size [3, 27]. This is the only known protein polymorphism in VDR gene. In the present study, however, SNP rs2228570 was not associated with the risk of periodontal disease. A positive association between the CC genotype of rs2228570 ZVADFMK and aggressive periodontitis was reported in Chinese [13] and Korean [15] populations, while no association was observed between SNP rs2228570 and chronic periodontitis in a Chinese population

[6, 10]. The mechanisms responsible for the occurrence of aggressive periodontitis and chronic periodontitis might be different [19]. To our knowledge, the present study is the first to find a significant additive interaction between VDR SNP rs7975232 and smoking that affects

the risk of periodontal disease, indicating a biologic interaction, although the multiplicative interaction was not significant. Biologic interaction is defined as two causes CYTH4 acting in the same sufficient-component model to cause disease. Our observed positive interaction means that the risk of periodontal disease in subjects who both have ever smoked and have the AA genotype of SNP rs7975232 is more than what would be expected if the effect of smoking and having the AA genotype of SNP rs7975232 were summed. Therefore, subjects with the AA genotype of SNP rs7975232 who do not smoke will reduce the risk of periodontal disease that would have been caused not only by smoking but also by the interaction of the two factors. To date, only one study has examined the interaction between VDR polymorphism and periodontal disease. In that study, an interaction was found between SNP rs731236 and smoking in Caucasians with regard to the presence and progression of periodontal disease [7]. This result is at variance with our findings showing that neither multiplicative nor additive interactions between SNP rs731236 and smoking with respect to the risk of periodontal disease were significant. The current study had methodological advantages in that study subjects were homogeneous in gender and age group and in that several confounders were controlled for. Several weaknesses should also be considered, however.

Posted in Antibody | Leave a comment

Such maternal immunological imprinting and in-utero exposure of t

Such maternal immunological imprinting and in-utero exposure of the fetus resulting in adverse pregnancy outcomes are best exemplified in pregnancies with autoimmune conditions such as APS, SLE, myasthenia gravis and primary Sjögren’s syndrome. Risks for fetus and neonate Patients with APS often have anti-phospholipid autoantibodies that are reactive against phospholipid proteins, such as β2-glycoprotein, cardiolipin, tissue plasminogen activator, thrombin, protein C and platelet antigens. The pathogenicity of anti-phospholipid autoantibodies is often associated with IgG classes and they target proteins that are involved in thrombosis, platelet and complement pathway

activation, monocyte and endothelial cell functions Vemurafenib cost [75]. These autoantibodies can be either agonistic or antagonistic in nature. They contribute to the pathologies of APS by promoting thrombotic events, impairing endothelial U0126 research buy cell function and provoking overt inflammatory responses in the maternal circulation and placental tissues. This may lead to vasoconstriction, impaired endothelial function and placental dysfunction that restrict blood supply to the placenta and result in placental ischaemia

and/or hypertensive disorders. Such a cascade of events can lead to a range of poor pregnancy outcomes such as RSA, IUGR, pre-eclampsia or stillbirth. Mild to moderate thrombocytopenia is common in APS, and this can worsen in pregnancy [9]. The causes of APS-associated thrombocytopenia are poorly understood: unlike immune thrombocytopenia (ITP), specific antibodies against the major platelet adhesion receptors (GPIIb-IIIa or GPIb-V-IX) are uncommon. Pregnant

women with SLE carry not only a risk of maternal and fetal morbidity, but also risks of long-term disability to the newborn. The immunopathologies of SLE pregnancy display several features of those seen in APS. Thus, it is not surprising that SLE pregnancy shares many of the adverse risks and poor outcomes of APS, such as maternal morbidity, IUGR, pre-eclampsia, stillbirth or preterm birth [9]. In addition, the autoimmune conditions of SLE and APS are often exacerbated during pregnancy and contribute further to the disease burden and Florfenicol dysfunction of the maternal circulation and renal system. The deposition of anti-nuclear proteins, anti-dsDNA, anti-basement membrane autoantibodies and autoreactive antibodies in kidney glomeruli can cause nephritis that results in further damage to the already compromised kidney function. This, in turn, exacerbates the hallmark signs of pre-eclampsia, such as hypertension and proteinuria. In addition, neonates of mothers with SLE or primary Sjögren’s syndrome are at risk of developing neonatal lupus syndrome and congenital heart block [9, 10]. These neonatal conditions often occur in mothers who are seropositive for anti-Ro/SSA and/or anti-La/SSB autoantibodies.

Posted in Antibody | Leave a comment

Our data cannot distinguish these possibilities and further studi

Our data cannot distinguish these possibilities and further studies will be required

to resolve SRT1720 these issues. Yet, the transfer of pre-activated Treg cells resulted in a demonstrable effect on the trafficking capabilities of Teff cells. Understanding the dynamics of this interaction is important as transferred, pre-activated polyclonal Treg cells are the most likely to be used in clinical situations. The mechanisms by which Treg cells inhibit Teff cell trafficking remain to be fully elucidated. The decrease in S1P1 expression at the mRNA level in Teff cells that had been primed in the presence of Treg cells is an attractive mechanism for the retention of the Teff cells in the LN, but other effects of Treg cells on chemokine expression 6 or on adhesion molecule expression 9 must also be considered. Although our studies were performed in a model system using TCR transgenic Teff cells, recent studies have shown

that polyclonal Treg cells may also regulate trafficking of CD8+ Teff cells in vivo during acute infection with respiratory syncytial virus 21. It is clear from these studies that polyclonal Treg cells do not influence the immune response by selleck chemicals simply “shutting down” immunity. In fact, it has recently been shown that polyclonal Treg cells enhance antibody responses when mice are immunized intranasally in the presence of the cholera toxin potentially by promoting Teff cell retention in the LN and promoting T-dependent B-cell responses 22. It would therefore be expected that the therapeutic administration of polyclonal Treg cells would not necessarily lead to global immunosuppression or the inhibition of responses to all antigens or pathogens. Rather, they influence the Teff-cell responses by specifically targeting trafficking pathways, thus allowing immunity to develop in lymphoid organs, but limiting the number of potentially auto-aggressive cells that are allowed to enter tissues. C57BL/6 and B10.A mice were obtained

from DCT, NIH. C57BL/6 CD45.1+ and CD45.1+ 5CC7 TCR-Tg mice Oxalosuccinic acid on RAG−/− background were obtained from Taconic Farms. 2D2 TCR-Tg and B6 Thy1.1 (B6.PL) mice were obtained from The Jackson Laboratory. 2D2-Thy1.1 mice were generated in house by crossing 2D2 TCR-Tg mice with Thy1.1 (B6.PL) mice and screening the progeny by flow cytometry with anti-Vβ11 and Thy1.1 antibodies. EAE was induced in C57BL/6 mice by subcutaneous immunization in the hind flank with 200 μL of an emulsion containing 400 μg of MOG35–55 peptide and 400 μg of Mycobacterium tuberculosis strain H37Ra in CFA (Difco). On days 0 and 2, the mice received an i.p. injection of 200 ng pertussis toxin (CalBiochem) dissolved in 100 L PBS.

Posted in Antibody | Leave a comment