The subsequent loss of fluorescence is likely to be due to the loss of cell viability, as shown by significant reduction in the number of monocyte-associated

events noted during flow cytometry. In contrast to studies undertaken Luminespib at 37 °C, monocyte exposure to toxin A488 at 4 °C did not lead to time-dependent increase in cell-associated fluorescence. Studies using trypan blue, which quenches membrane-associated fluorescence [31], showed significantly greater reduction in monocyte-associated fluorescence when the cells were exposed to toxin A488 at 4 °C, compared with those incubated at 37 °C. These studies suggest that, when exposed to monocytes at 4 °C, toxin A488 remains predominantly associated with the cell membrane. By contrast, following incubation for 1 h at 37 °C, the majority

of A488 is internalized by the monocytes. Lymphocytes incubated with click here toxin A488 at 37 °C showed a small increase in fluorescence (compared with control, non-toxin-exposed cells) at 48 h, but not at 24 h. In contrast to monocytes, there was no significant change in the number of events in the lymphocyte gate in toxin A488-exposed peripheral blood mononuclear preparations studied by flow cytometry. Also in contrast to monocytes, the difference in fluorescence between lymphocytes incubated with toxin A488 and control medium (non-toxin-exposed cells) at 4 °C fell short of statistical significance. In studies using whole blood cells, toxin A488-associated fluorescence in monocytes

and lymphocytes was similar to that seen in isolated PBMNCs. Compared with monocytes, toxin A488-associated fluorescence in neutrophils showed interesting differences. Thus, the fluorescence in neutrophils was greater when exposed to toxin A488 on ice than at 37 °C. Moreover, during incubation at 37 °C, toxin A488-associated fluorescence in neutrophils (which increased over time) was markedly quenched by trypan blue. This implies that the labelled toxin remained predominantly on the neutrophil cell surface, which either could be because of its inability to take up the toxin or that the cells rapidly O-methylated flavonoid degrade it once internalized. Future studies should investigate this further. Neutrophil-derived myeloperoxidase has previously been reported to inactivate cytotoxic activity of unfractionated C. difficile culture filtrate [32] and highly enriched toxin B [33]. Resistance to cell death of neutrophils exposed to unfractionated C. difficile culture filtrates (containing toxin-derived activity) has also been previously reported [34]. Our studies used purified toxin A and have shown that although there was a relatively small, but significant reduction in forward-scatter characteristics, majority of the neutrophils appeared to remain viable after 3-h exposure at 37 °C. However, further studies are required to determine the susceptibility of neutrophils to cell death following exposure over different time periods to varying concentrations of toxin A.

Fbp from other bacteria, FnBPA and FnBPB from Staphylococcus aureus and Sfb1 from S Staphylococcus pyogenes, are known to contain a common motif that bind to the N-terminal type I module of Fn (28, 29). Another Fbp, BBK32 from Borrelia burgdorferi, is reported to bind to III1–3 as well as to I1–5 of Fn (30, 31). BBK32, however, has the capacity to make an aggregation of Fn by virtue of binding to III1–3 of Fn. Unlike BBK32, neither FbpA nor FbpB from C. perfringens has such an Fn aggregating capacity (data not shown). It is ICG-001 manufacturer known that Fn aggregates when Fn is incubated with III1-C peptide (32). This means that Fn binds to III1-C peptide. In fact, in the present study, Fn reacted

with immobilized III1-C peptide. The binding of Fn to III1-C was inhibited by the presence of either rFbpA or rFbpB (Fig. 5). This result suggests that C. perfringens Fbps buy PD0325901 may inhibit Fn-matrix formation in vivo. We thank Takahiro Hiraiwa, Tatsuma Tsuchiya and Masaya Okuda for generating the monoclonal

antibodies. We also thank Kana Harutsumi for technical support. “
“A balance of inhibitory and activating signals determines the function of dendritic cells (DCs) in the immune response, which may be regulatory or stimulatory. Defects of inhibitory receptor FcγRIIb are involved in the pathogenesis of autoimmune diseases such as systemic lupus erythematosus (SLE), in which high levels of circulating immune complexes (IC) exist. Our previous study showed that IC/Ig can suppress TLR4-triggered inflammatory Ibrutinib supplier responses in macrophages via FcγRIIb. This led us to question whether IC/Ig can polarize FcγRIIb-overexpressing DCs (DC-FcγRIIb) to be tolerogenic, thus attenuating lupus progression once infused in vivo. First, we found that IC/Ig markedly inhibited LPS- or CpG-induced DC maturation, enhanced tolerogenicity of DCs via FcγRIIb, and induced massive prostaglandin E2 (PGE2) secretion from DCs, both contributing to T-cell hyporesponsiveness. Endogenous Ig and lupus-derived IC also exhibited the same effect.

DC-FcγRIIb, transfected with recombinant adenovirus encoding FcγRIIb, displayed enhanced tolerogenic function and produced more PGE2 in the presence of IC, thus further inhibiting T-cell responses. Importantly, in vivo infusion with DC-FcγRIIb significantly reduced kidney damage and prolonged the survival of lupus-prone MRL/lpr mice either before or after the onset of clinic lupus. Therefore, administration of DC-FcγRIIb may be a new approach to attenuate lupus progression. As a highly heterogeneous population, DCs not only play an important role in initiating and enhancing immune response but also contribute to the maintenance of tolerance via various mechanisms, including direct inhibition of T-cell response, induction of T-cell anergy or Treg and directing Th subset polarization 1–7.

05 were considered as significant (*). This work was supported by grants from the Chilean government FONDECYT 1070954 (R.Q.) and Scholarship for Postgraduate Studies 21050679 (F.M.) and by grants of the Deutsche Forschungsgemeinschaft DFG-PR 727/3-1 (I.P.) and SFB621-A14 (I.P.). The authors thank Andreas Krueger and Nadja Bakočević for critically reading the manuscript and Mathias Herberg for animal care. Conflict of interest: The authors declare no financial

or commercial conflict of interest. Detailed facts of importance to specialist readers are published as ”Supporting Information”. Such documents are peer-reviewed, but not copy-edited or typeset. They are made available as submitted by the authors. “
“OTHER ARTICLES PUBLISHED IN THIS MINI-REVIEW SERIES ON Th17 CELLS Function and regulation of

human T helper 17 cells Selleckchem Caspase inhibitor in health and disease. Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04037.x this website Induction of interleukin-17 production by regulatory T cells. Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04038.x Are T helper 17 cells really pathogenic in autoimmunity? Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04039.x Development of mouse and human T helper 17 cells. Clin Exp Immunol 2009; doi:10.1111/j.1365-2249.2009.04041.x CD4+ T cells display considerable flexibility in their effector functions, allowing them to tackle most effectively the range of pathogenic infections with which we are challenged. The classical T helper (Th) 1 and Th2 subsets have been joined recently by the Th17 lineage. If not controlled, the potent effector functions (chiefly cytokine production) of which these different cells are capable can lead to (sometimes fatal) autoimmune and allergic inflammation. The primary cell population tasked with providing this control appears to be CD4+ regulatory T (Treg) cells expressing the forkhead box P3 (FoxP3) transcription factor. Here we consider the comparative capacity of FoxP3+ Tregs to influence the polarization, expansion and effector function of Th1, Th2 and Th17 cells in vitro and in vivo as well as in relation to human disease. This remains a particularly challenging series

of interactions to understand, especially given our evolving understanding of Treg and T effector interrelationships, as well as recent insights into functional plasticity that cast doubt upon the wisdom of a strict categorization of T effector cells based Thymidylate synthase on cytokine production. The study of CD+ T cells has been greatly facilitated by their division into functional subsets. The basis for this division was the identification of distinct cytokine production profiles among T cell clones, giving rise to T helper (Th) 1 and Th2 subsets [1]. The developmental and functional relationship between these prototypic Th subsets was subject to intense study and provided the framework for classifying T cell responses for almost two decades. These ‘classical’ subsets exemplify the characteristics required to claim subset status.

Patients were randomized to atorvastatin (40 mg once daily for 4 days starting preoperatively) SCH727965 research buy or identical placebo capsule. Primary outcome was to detect a smaller absolute rise in postoperative creatinine with statin therapy. Secondary outcomes included AKI defined by the creatinine criteria of RIFLE consensus classification (RIFLE R, I or F),

change in urinary neutrophil gelatinase-associated lipocalin (NGAL) concentration, requirement for renal replacement therapy, length of stay in intensive care, length of stay in hospital and hospital mortality. Results:  Study groups were well matched. For each patient maximal increase in creatinine during the 5 days after surgery was assessed; median maximal increase was 28 µmol/L in the atorvastatin group and 29.5 µmol/L in the placebo group (P = 0.62). RIFLE R or greater occurred in 26% of patients with atorvastatin and 32% with placebo (P = 0.65). Postoperatively urine NGAL changes were similar (median NGAL : creatinine ratio at intensive care unit admission: atorvastatin

group 1503 ng/mg, placebo group 1101 ng/mg; P = 0.22). Treatment was well tolerated and adverse events were similar between groups. Conclusion:  Short-term perioperative atorvastatin use was not associated with a reduced incidence of postoperative AKI or smaller increases in urinary NGAL. (ClinicalTrials.gov NCT00910221). Ku-0059436 manufacturer “
“Omeprazole is an important cause of drug-induced acute interstitial nephritis (AIN). How omeprazole induces injury is unknown. Detailed clinical assessment of 25 biopsy-proven cases of omeprazole-induced AIN showed that all patients presented with impaired renal function, sterile pyuria with varying amounts of proteinuria but no eosinophiluria and no systemic symptoms to suggest a vasculitis. Histological analyses were

characteristic of an acute tubulitis with an inflammatory cellular infiltrate. Using modified Banff scheme criteria, mild tubulitis (t1) was present in 56% of cases, a moderate tubulitis (t2) in 24% of cases, and a severe tubulitis in 20% of cases. Most (78%) of cases had mononuclear cell infiltrates, no significant eosinophilic infiltrates were Vorinostat supplier found, and glomeruli were not involved. Immunostaining for CD4, CD8, IL-17A, IL-17F, Foxp3 and T-bet (T cell subsets), CD20 and CD163 defined the cellular infiltrates. The predominant inflammatory cells were CD4+ lymphocytic aggregates (77% of cases), combined with co-staining of CD4 IL and 17A/F in 44–48% of all cases, suggesting a Th17-mediated inflammatory process. T-bet+ cell infiltrates were present to a lesser degree, suggesting additional Th1 involvement. How omeprazole induces this inflammatory response is unclear, but may include direct effects by IL-17 expressing CD4+ cells on renal tubular cells.

Choriodecidual leukocytes may produce three times more MMP-9 than reference cell lines such as U937[14] or amounts equivalent to those produced by some metastatic cancer lines. In addition to the above-mentioned choriodecidual leukocyte functional properties, our data support the possibility that these cells could be contributing to the secondary wave of mediators, creating a microenvironment leading to collagenolysis,

which could be related to the rupture of the fetal membranes.[10, 18] In summary, our findings demonstrate that choriodecidual leukocytes isolated from fetal membranes at term are functionally different from cells in other compartments and may collaborate to modulate the microenvironment linked to induction and progression www.selleckchem.com/HDAC.html of human labor. Support for this work was provided partially by Grant No: R01 ES016932 from the U.S. National Institute for Environmental

Health Sciences and the National Institutes of Health. M.C.C. received a scholarship and financial support provided by the National Council of Science and Technology (CONACyT) and U.N.A.M. (PAPIIT IA200612-2). This paper constitutes a partial fulfillment of the Graduate Program in Biological Sciences of the National Autonomous University of México (UNAM). Marisol Castillo-Castrejon acknowledges the scholarship provided by the Consejo Nacional de Ciencia y Tecnologia

(CONACyT No. 203418). N.G-L is funded by Wayne State University Research Initiative in Maternal, this website Perinatal, and Child health (Eunice Kennedy Shriver National Institute of Child Health and Human Development of the National Institutes of Health). The authors thank Marie O’Neill for reviewing the manuscript prior to the submission. “
“UCB-Celltech, 208 Bath Road, Slough, Berkshire SL1 3WE, United Kingdom TNFRSF25 is a member of the TNF receptor superfamily (TNFRSF) that binds to the TNF-like protein TL1A. Although recent studies have demonstrated a role for TNFRSF25 in regulating CD4+ T-cell responses, it remains to be determined if TNFRSF25 functions as a costimulatory receptor for CD8+ T cells. Here, we demonstrate Reverse transcriptase that ectopic expression of TL1A on mouse plasmacytomas promotes elimination of tumor cells in a CD8+ T-cell-dependent manner and renders mice immune to a subsequent challenge with tumor cells. To gain further insight into the role of TNFRSF25 in CD8+ T-cell responses, we analyzed the effect of TNFRSF25 triggering on OT-I TCR transgenic T cells. We demonstrate that TNFRSF25 triggering in vivo with soluble TL1A promotes the proliferation and accumulation of antigen-specific CD8+ T cells as well as their differentiation into CTLs. Furthermore, we show that TNFRSF25 also functions as a costimulatory receptor for memory CD8+ T cells.

[19] and illustrated in the Maximum parsimony tree based on the ITS region (Fig. 2) are mixed in the ACT, TEF and RPB1 trees (data not shown) as well as in the multi-locus tree (Fig. 1) within arrhizus and delemar, respectively. The variety tonkinensis was represented in our study by 4 strains, which were all morphologically assigned to this variety by Zheng et al. [17]: CBS 257.28, CBS 330.53, CBS 399.95 and the ex-type strain of var. tonkinensis,

CBS 400.95. The variety was neither detected in the single locus trees using the ML approach nor in the ITS tree using the maximum parsimony approach (Fig. 1 and Fig. 2). Figure 3 illustrates schematically the maximum intra- and interspecific distances within the Rhizopus arrhizus/R. delemar complex for both possible scenarios: (i) lineages arrhizus and delemar belong to a single PCI-32765 datasheet variable species and represent varieties, or (ii) lineages arrhizus and delemar represent separate species. In the latter scenario (Fig. 3b) the intraspecific variability of arrhizus and delemar, and especially the distance between both entities, is very small compared to distances

to other species. In accordance with single-gene and multi-gene genealogies, the AFLP banding patterns, when clustered with UPGMA in BioNumerics v. 4.61, clearly revealed two different groups for arrhizus and delemar (Fig. 4). Forty-eight strains of arrhizus and 34 strains of delemar were analyzed statistically in order to establish whether the Fostamatinib manufacturer entities differ significantly in ecology, geographic

distribution or clinical relevance. The proportions were as follows (illustrated with colored squares in Fig. 1): 14 clinical strains, 8 food strains and 2 environmental strains in arrhizus and 4 Sinomenine clinical and 8 food strains but no environmental strain in delemar. Remaining strains originated from unknown sources. No significant difference was found between sources and clusters (chi square = 2.86, P = 0.091, critical level = 0.05), and no difference in geographic distributions between arrhizus and delemar was detected. No physiological difference was detected between arrhizus and delemar (Table 3). All tested strains were negative for laccase, cellulose, and tyrosinase and positive for lipase and amylase. The majority of strains were positive for gelatin liquefaction and siderophore production, but no significant correlation was observed between negative strains and taxonomic entities or source of isolation. A few strains showed urease activity, while the activity of this enzyme could not be related to taxonomy or ecology. All tested strains (20 of arrhizus and 20 of delemar) grew well (average 64 mm/days) with 30–36 °C as optimum temperature range. At 40 °C strains were inhibited for about 50%. According to our experimental design, the maximum growth temperature was 45 °C with reduced growth for all strains tested.

However, little is known about and would be interesting to investigate the immunological

characteristics of HIV-1-positive sera in China where non-clade B viruses are prevalent and the circulating viral subtypes are distinct and more complex than both the United States and Europe. Here, we screened 80 Chinese HIV-1-positive sera against a minipanel of pseudoviruses representing various circulating HIV-1 subtypes in China and identified 8 cross-clade neutralizing sera (CNsera). Immunological characterization of the sera showed that gp120-targeting antibodies with multiple epitope specificities contributed to the cross-clade neutralizing activity of these CNsera. V3-directed antibodies were prevalent in these CNsera, but did not mainly contribute to their neutralization breath and potency Daporinad chemical structure while CD4bs-specific, 2F5- and 4E10-like antibodies were rarely detected. 2G12-like neutralizing antibodies were more frequently detected in HIV-1 patients

from China where recombinant subtype viruses are prevalent than in United States and Europe. One broadly neutralizing serum (Serum Palbociclib datasheet 45) was identified to contain antibodies with unknown epitope specificities that were sensitive to terminal glycan modifications on virus Env and insensitive to N160K mutagenesis, and correlated with the cross-clade neutralization activity of Serum 45. Most antiviral vaccines protect people through induction of neutralizing antibodies in the sera or mucosa [1,

2]. HIV-1 is one of the most pandemic viruses in the world. There is still no effective vaccine to prevent the spread of HIV-1 after almost three decades of research [3-5]. The immune correlate of protection against HIV-1 infection is not yet clear although broadly neutralizing antibodies (bNAbs) are believed to be an important component, and a fraction of individuals infected with HIV-1 in nature can develop bNAbs. A handful of bNAbs have been isolated from HIV-1-infected individuals [6-8], such as b12, VRC01, LY294002 2G12 and 447-52D targeting gp120, as well as 2F5 and 4E10 targeting the membrane proximal external region on gp41 [9, 10]. Recently, a number of bNAbs such as PG9 and PG16 were isolated from an African donor using high-throughput screening method, and the epitopes mediating their neutralization activities involve both the variable loops and the conformational structure of the native trimeric envelope glycoprotein [11]. Extensive studies using mostly clade B patients from United States and Western Europe, or clade C patients from sub-Saharan Africa, have documented the immunological properties of the serum antibody response during infection [12-15]. However, there have been limited studies on the serological responses in infected Chinese patients, and little is known about immunological characteristics of the serum antibodies.

In males, 15 item International Index Of Erectile Function (IIEF) and in females 19 item Female Sexual Function Index (FSFI) were used. Results: Out of 100, 78 males (78%;mean age 46.8 ± 10.5 years) and 57 females (57%;mean age 39.68 ± 9.01 years) completed and submitted the questionnaire. In males, SD which included IIEF domains [Erectile function, Orgasmic function, Sexual desire, Intercourse satisfaction and overall satisfaction] was found in 71 (91%) patients this website and in females, SD which included FSFI domains [Desire, Arousal, Lubrication, Orgasm, Satisfaction and Pain] was found in 55 (96.5%) patients which was significantly higher than in control

group. Only 17 (21.8%) males and 5 (8.8%) females had discussed this problem with their care Y27632 providers and none had received any sort of treatment for the same. 28 (35.8%) males and 18 (31.5%) females were on medications known to cause SD particularly beta-blockers, clonidine and diuretics. Menstrual irregularities were present in 100% of pre-menopausal women. 43 (55.1%) males and 45 (78.9%) females thought that sexual activity can be harmful to their condition and 12 (15.4%) males and 22 (38.5%)

females thought that sexual activity can be detrimental to the health of their partners. Conclusion: Sexual dysfunction is a common problem in ESRD and irrespective of etiology, is a cause of distress. In India, being a conservative society, very few patients discuss this issue with their doctors and hence receive little attention and are often undertreated. Additional research on relevance of sexual dysfunction on quality of life of ESRD patients is needed. MORIISHI MISAKI, KAWANISHI HIDEKI, SHINTAKU SADANORI, TSUCHIYA SHINICHIRO Tsuchiya General Hospital Introduction: Heart failure is the most frequent cause of death among Japanese hemodialysis patients. We explored whether frequent dialysis improves cardiac functions and

reduces hospitalization. Methods: We evaluated 15 hemodialysis patients complicated selleck compound with heart failure who could not achieve their optimum dry weight with a standard schedule of 4 hours, 3 times a week. The dialysis schedule was changed from 4 hours, 3 times a week to either 3 to 4 hours, 4 times a week or 2 hours, 6 times a week. The following parameters were evaluated at the baseline (before the change of the dialysis schedule), and 3 and 6 months after the change: body weight, blood pressure, urea, albumin, blood pressure fall during dialysis, and UF volume. In addition, LAD, LVM, EF, TRPS, and E/A were determined by echocardiography before dialysis and compared with the baseline and 6-month values. Furthermore, the frequency and days of hospitalization during 6 months were evaluated. Results: The mean age of the patients was 67.5 ± 8.6 years, and the mean duration of hemodialysis was 115.2 ± 88 months. In 8 patients, the schedule was changed to 3 to 4 hours, 4 times a week.

e. those presenting to a urogynecology clinic), a

simple screening question from the PFDI, “Do you usually have a bulge or something falling out that you can see or feel in your vaginal area?” had a 96% sensitivity and a 79% specificity for prolapse beyond the hymen (POP-Q Fostamatinib solubility dmso stage > II).[42] This is consistent with the fact that women with a POP-Q stage < II often have no POP symptoms.[28] Taken together, these studies suggest that QOL questionnaires may help to identify significant prolapse as well as specific compartment defects associated with POP. These could be valuable tools for screening women in clinical settings in order to identify those who are candidates for treatment. QOL questionnaires have been useful in evaluating the efficacy of both surgical and non-surgical treatment modalities of POP by helping to re-define what is selleck products considered a successful outcome. For example, in evaluating treatment success after surgery for POP, Barber et al. noted that treatment success varied widely from 19.2 to 97.2% depending on the definition of success.[43] If the definition of success was based on anatomic correction resulting in support being

proximal to the hymen, the success rate was lowest (19.2–57.6%). However, there was a 94% success rate when success was defined as the absence of prolapse beyond the hymen based on POP-Q assessment. More importantly, a subjective cure (the absence of bulge symptoms using responses to PFDI questions) occurred in 92.1% of Baricitinib participants, which was significantly associated with women’s assessment of overall wellbeing. These findings underscore the additional value that QOL questionnaires can provide in assessing outcomes. More than 86% of gynecologists and 98% of urogynecologists use pessaries in their daily practice.[44-46] QOL questionnaires have provided important insights into long and short-term outcomes in women who use pessaries to manage POP. In choosing candidates for pessary use, it should be remembered that the stage of POP does not determine the success of pessary fitting and therefore should

not influence the decision to use a pessary in a potential candidate.[47] Responses to QOL questionnaires have revealed that patient satisfaction with medium-term pessary use is high (70–92%)[48, 49] and is also associated with increased frequency and satisfaction with sexual activity,[50, 51] underscoring the fact that sexual activity should not be considered a contraindication to pessary use. Improvement in both bulge and irritative bladder symptoms are the most consistent findings across most studies evaluating the effect of pessary use on QOL,[48, 51-57] though two studies reported new onset of UI.[52, 56] In a prospective observational cohort study, Komesu et al. found that while pessary use improved both bladder and prolapse symptoms, they were more effective in improving symptoms of prolapse.

The recombinant protein was expressed in soluble form with His tag at the N-terminus. The positive clone was bulk-cultured, and the pellet was stored at −20°C. It was thawed, and 4 volumes of lysis buffer (20 mm sodium phosphate (pH 7·4), 1 m NaCl and 1 mg/mL lysozyme) was added. After mixing, the tube was kept in ice Protein Tyrosine Kinase inhibitor for 30 min, and the suspension was sonicated thrice at 10 Hz for 1 min. The sonicated bacterial pellet was centrifuged at 11 000 g for 15 min at 4°C. The supernatant was collected and passed through a Ni–agarose column. The column was washed with excess buffer and then eluted with increasing concentrations of imidazole (5–250 mm). The presence of protein in the eluted fractions was

checked by SDS gel electrophoresis and Western blot using anti-H.c-C3BP antiserum. The enzyme activity of the recombinant GAPDH and its interaction with C3 were studied as described above. SDS-PAGE was carried out in 5–15% linear gradient gels in discontinuous buffer system. Occasionally, protein samples were reduced by adding 2-mercaptoethanol (2% final concentration). Protein bands were visualized by staining with Coomassie Brilliant Blue R-250. For Western blot, proteins PD0325901 mouse were transferred from gel

to nitrocellulose membrane at 200 mA for 90 min. Primary antibody was used at 1 : 250 or 1 : 500 dilutions and secondary conjugated antibody at 1 : 500 dilutions. For antibody production, H.c-C3BP (25–50 ug/mL) was fractionated on a SDS gel, and the lightly stained gel band region around the 14-kDa band was excised with a blade, washed with several changes

of PBS and homogenized in Freund’s complete adjuvant. The emulsion was used for immunizing two healthy male rabbits. Booster doses were given every third week with the same amount of protein in incomplete adjuvant. Blood was collected a week after the last immunization, and the presence of antibodies was checked RVX-208 by Western blot. Animal experimentations were performed as per the guidelines of the animal ethics committee of the institute. All the data were analysed by GraphPad prism 4 software using one-way anova. A P value <0·05 was considered significant. To identify the C3-binding protein in H. contortus, a simple strategy of using C3–Sepharose was followed. On passing the ES products of adult H. contortus through C3–Sepharose column, a band of ~14 kDa was observed in the SDS gel of the eluted fraction after staining with Coomassie Brilliant Blue (Figure 1a). This band was consistently observed in all batches of ES products. This observation was confirmed by immunoprecipitation analysis. The immunoprecipitates formed as a result of C3 and ES products interaction showed a ~14-kDa band, which was absent in the C3 protein lane (Figure 1b). To evaluate the existence of H.c-C3BP in the adult worms, Western blot analysis was performed using antiserum raised against the ~14-kDa band. Adult parasites showed different pattern.