0 mg/day. However, urine protein further increased beyond 1 g/g Cr, and serum creatinine increased and C-reactive protein also increased, accompanied by skin rash BMN 673 solubility dmso and dyspnoea. Allograft biopsy was conducted (2.5 years post transplant). The biopsy showed diffuse glomerular endocapillary proliferation and swelling of glomerular endothelial cells (Fig. 1). The presence of glomerular basement

membrane injury was present. Immunofluorescence showed no significant immune deposit including C4d. Intraluminal proliferating cells were mostly CD34+, indicating that the majority of them were endothelial cells. On the contrary, CD4+ or CD8+, i.e. T cells or CD68+ macrophages were few by immunohistochemistry. These findings suggested that the injury was mediated by direct insult to the endothelium, such as drug-induced injury, and was not mediated by alloantigen-directed immunological insult. No endarteritis or tubulointerstitial lesion was observed. No donor-specific antibody was detected with flow-bead analysis. EVR was discontinued and TACER was returned to the previous dose. Erismodegib Proteinuria only decreased to 0.5 g/g Cr and methylprednisolone mini-pulse therapy was given (125 mg ×3), resulting in improvement of proteinuria to 0.1 g/g Cr. Other symptoms have also disappeared. Allograft biopsy taken 6 months later still showed mild and focal endocapillary

proliferation but those lesions had significantly improved compared with the previous biopsy (Fig. 2). Glomerular injury accompanied by de novo proteinuria in this case is assumed to be caused by everolimus. The presence of glomerulitis supports antibody-mediated rejection (AMR) as a possible cause. However, glomerular endothelial injury was not associated with either lymphocyte margination or C4d deposition and the proliferating cells were mostly endothelial cells, indicating the injury was mediated by drug rather than alloimmune response. Furthermore, the lack of donor-specific antibody and the reversal of clinical and pathological findings only by low-dose steroid therapy are unsupportive of

AMR. The presence of basement membrane injury could be mediated by Monoiodotyrosine CNI toxicity. In this case, the deterioration of the clinical data occurred after adding EVR. The presence of underlying CNI-mediated glomerular injury could not be excluded but the injury, severe enough to induce significant clinical presentation was likely to be triggered by EVR. Typically, proteinuria induced by mTORi is believed to be mainly mediated by podocyte injury.[5] Reports of glomerulonephritis induced by EVR, as in our case, are scarce.[6] Reluctance to biopsy would have resulted in attributing the cause of proteinuria to typical adverse effect of EVR in general. We could fortunately reverse the graft injury after recognizing the presence of glomerulonephritis and this case suggests the importance of clarifying the pathology by allograft biopsy.

5 mice. The Rag deficiency precludes the generation of other T-cell clones from the endogenous TCR locus, so the animals harbor a monoclone of the self-antigen-specific BDC2.5 Teff cells. Alternatively, purified CD4+ naïve Teff cells from BDC2.5/NOD mice were used. We transferred 5–10 × 104 BDC2.5 Teff cells into the animals at the time of tumor cell implantation (Fig. 1A) or 3–7 IWR-1 molecular weight days after tumor cells injection (Fig. 1B). The implanted tumor cells established a palpable subcutaneous tumor and effectively reduced the blood glucose level of the tumor-bearing animals, which enables an objective assessment of tumor burdens regardless

of the location of tumors. Adoptively transferred autoimmune Teff cells eradicated

palpable Ribociclib clinical trial inuslinoma. Complete killing of insulinoma cells in the animals was reflected by the rise in blood glucose levels (Fig. 1A and B). To examine the efficacy of autoimmune Teff cells without having to adoptively transfer T cells, we implanted NIT-1 tumor cells into Foxp3-deficient BDC2.5 mice (the BDC2.5/NOD.Foxp3sf congenic line) [29], in which autoimmune Teff cells are free of Treg cell suppression. In Foxp3-deficient BDC2.5 mice, the implanted NIT cells initially established an insulinoma but the tumor was effectively rejected, whereas fatal insulinoma developed in all control BDC2.5 mice that harbor natural Treg cells (Fig. 1C and D). A prominent role for Treg cells has been established in suppressing antitumor immunity. We examined the function of Treg cells in suppressing tumor-killing capacity of self-antigen-specific Teff cells. NIT-1 tumor-bearing NOD.SCID mice were treated with the self-antigen-specific CD4+ Teff cells alone, Teff:Treg mixture at a 10:1 ratio, or no T-cell control. Blood glucose readings indicated that autoantigen-specific Treg cells efficiently suppressed insulinoma killing by the autoimmune Teff cells (Fig. 2A). In the group of animals that received autoimmune Teff cell alone, only a residual tumor was recovered. Pathological analyses Montelukast Sodium of residual insulinoma

and healthy pancreatic β cells revealed virtually complete destruction of both malignant and nonmalignant tissues (Fig. 2B, middle). In the presence of Treg cells, the tumor was preserved. However, this relatively low ratio of Treg cells did not substantially suppress autoimmune Teff cells in healthy pancreatic islets (Fig. 2B–D). Flow cytometry analyses revealed a substantially increased ratio of CD4+Foxp3+ Treg cells to Teff cells at the tumor site (Fig. 2E and F). In addition, given the generally established, prominent role of CD11b+Gr1+ myeloid-derived suppressor cells (MDSCs) in tumor microenvironment [30], we analyzed CD11b+Gr1+ cells in insulinoma versus healthy pancreata. Four-week-old BDC2.5/NOD mice (n = 5) were inoculated with NIT-1 cells.

Since innate immune responses in particular differ between mice and humans, these responses should be investigated more intensively after viral infection of mice with reconstituted human immune system components. Two bacterial pathogens in particular have been explored in mice with reconstituted human immune system components, namely Mycobacterium tuberculosis (Mtb) and Salmonella enterica

Typhi (S. Typhi), the etiological agents of tuberculosis and typhoid fever, respectively (Table 1). Intranasal Mtb infection led to lung granuloma formation in mice with reconstituted human immune system components [79, 80]. These granulomas were quite similar to granulomas of tuberculosis patients in that they were comprised of human giant cells and macrophages in a necrotic core, surrounded Gemcitabine by human T cells and encapsulated by a fibrotic response. Mouse leukocytes of the NSG hosts were sparse in these granulomas and restricted to the periphery. Moreover, no granulomas were observed in nonreconstituted

mice. Apart from Mtb, i.p. or i.v. injection of S. Typhi established this infection in reconstituted, but not BRG or NSG mice without reconstitution [81-83]. Infection was documented by colony-forming units (cfu) in the spleen, liver, BM, gall bladder, and blood. Mutant S. Typhi strains were also explored in this setting, and a strain that was avirulent in human volunteers replicated to lower cfu levels, while a typhoid toxin mutant showed increased infection. Therefore, both Mtb and S. Typhi infections can be explored in ice with reconstituted human immune system components. Interestingly, while the reported S. Typhi JNK inhibitor immune response was only analyzed for bacteria-specific antibody responses of an undefined isotype in a subset of mice (25%) [81], the CD4+ T-cell responses to Mtb infection seemed to serve an unexpected purpose [79]. CD4+ T-cell depletion compromised for granuloma formation and

this diminished bacterial load [79]. In contrast, TNF neutralization preserved granuloma formation and diminished Mtb load. These data suggest that granulomas promote Mtb replication and TNF mediates protective functions, which are independent of granuloma formation. These studies mark the beginning of investigations of antibacterial immune responses in mice with human immune system components. The limited information that has been generated thus far already leads to a better understanding of bacterial pathogenesis in humans and allows exploring mutants as vaccine candidates to elicit immune responses in this preclinical model of human immune responses. Born out of the need for new in vivo models for infection with human pathogens and the immune responses raised against them, which might be better translatable to human patients than the classical animal models, mice with reconstituted human immune system components are increasingly being explored.

3 cmH2O as a result of increased

intra-abdominal pressure, which is necessary for emptying the neobladder. In the present study, the mean maximum voiding pouch pressure (above baseline) was 84.4 ± 46.4 and 81.4 ± 37.8 cmH2O, respectively. However Porru[13] reported higher neobladder pressure at Qmax (140 cmH2O). One limitation in comparing the pressure values among various studies is the definition of “voiding pressures” which could be either equivalent to Pves or Pdet. Urethral length and function has been evaluated more extensively www.selleckchem.com/products/obeticholic-acid.html in patients undergoing radical prostatectomy (RP) for prostate cancer. Recent data from Memorial Sloan Kettering Cancer Center suggests that urethral length (on magnetic resonance imaging) after surgery as well as percentage loss of the length due to surgery corroborate with status of continence in men undergoing RP.[33] Similarly, others have reported an inverse correlation between functional urethral length and MUCP, and incontinence.[16] Sphincter/urethral function have been reported with UPP measurement in patients with orthotopic neobladder.[13, 19, 21, 24] Koraitim et al.[19] studied cystometric and urethrometric urodynamic parameters in 88 patients having undergone ONB. They studied a total 28

parameters, out of which MUCP correlated with both diurnal and nocturnal incontinence, and resting pouch pressure with nocturnal incontinence. However, absolute values of none of the parameters were mentioned. In a series of 12 men Porru and Usai[13] noted two RO4929097 nmr patients had reduced urethral pressure (MUCP < 45 cm H2O). The incidence of nocturnal incontinence was 56%; they reported only descriptive association between incontinence, and MUCP and pouch pressure. El Bahnasawy et al.[21] found 3-mercaptopyruvate sulfurtransferase a significant difference in MUCP between continent and incontinent groups. We have found a correlation between lower FUL and incontinence;

however, none with MUCP. The strength of the present study is tabulation of all relevant UDS parameters for ready reference, despite the limitation of small samples. The effect of pelvic floor strengthening and relaxation exercises have been advised in such patients by most experts in the field. However, an objective urodynamic correlation of the effect of these exercises has not been reported. With the limitation of small sample size and short follow-up we tried to elucidate the effects of these exercises on voiding function. There was a trend of increase in Qmax with more pronounced decrease in EMG activity and less pronounced abdominal pressure with the exercises (Fig. 3). Ureteroileal anastomotic stenosis with upper tract deterioration was significantly higher in patients with antirefluxing compared with those with refluxing anastomosis (13.5% vs 3%).[34, 35] Abol-Enein and Ghoneim described serous-lined extramural ureteral reimplantation[9, 10] and reported reflux in 3% of patients and deterioration of renal function in 4%.

16 Finally, the few NS populations that have been tested for GM are almost monomorphic for haplotype GM 1,17 5*. This represents an extreme differentiation compared with NC, which is explainable by rapid genetic drift through

isolation. Actually, NS populations are spread discontinuously over a vast geographic area extending from East (Ethiopia) to West (Mali) Africa throughout the Sahara Desert, and may have been submitted to repeated episodes of demographic contraction and gene flow with local neighbours, depending on climatic variation, which extensively modified the environments. Variation of GM has also been highly informative for anthropological studies in East Asia. A north–south genetic cline is clearly observed, with high frequencies of GM 1,17 21 and GM 1,2,17 21 and low frequencies of GM 1,3 5* in the north, the reverse situation being click here observed

in the south. Here again, the linguistic information is relevant: we observe continuous genetic differentiations between (from one end of the cline to the other) Altaic, Japanese and Korean; North Tibeto-Burman; Northern Chinese (all Mandarin but Southeastern); Wu and Southeastern Mandarin; Southern Chinese and Southern Tibeto-Burman; and Austro-Asiatic, Tai-Kadai and Austronesian populations.17,18 However, contrary to the situation found in Africa, in East Asia the linguistic families are found in specific geographic areas and it is hard to establish whether the observed genetic patterns have mostly been shaped by linguistic or by geographic differentiations in the past. As discussed in more Staurosporine manufacturer detail below for the HLA polymorphism, GM genetic variation is compatible with the ‘pincer’ model of migrations from West Asia, suggesting that some populations followed a southern (maybe coastal) route through India to Southeast Asia, and others a route north to the Himalaya Mountains to Northeast Asia (although at a different period), both groups

of populations later intermixing through north–south migrations in East Asia. As for HLA, a higher level of internal diversity (higher heterozygosity) is observed in Northeast Asia compared with Southeast Asia, indicating higher levels acetylcholine of gene flow, whereas Southeast Asian populations may have undergone rapid differentiation through genetic drift.19 Another crucial example pertains to the peopling history of Taiwan. In a previous study, we investigated the GM polymorphism of several Aboriginal populations from this island (Siraya, Pazeh, Taroko, Atayal, Tsou, Bunun and Puyuma, as well as Yami located in Lan-Yu island off the southeastern coast of Taiwan).20 We found a decrease in heterozygosity from (north)western to southern and southeastern regions (with a higher frequency of GM 1,3 (–23) 5* in the west, whereas GM 1,3 23 5* is (almost) fixed in the south and/or southeast).

2A). However, the number of antigen-specific cells recovered at day 5 was not different between CpG-treated and control mice. Co-injection

of poly(I:C), LPS, or imiquimod did not modify the number of tetramer+ cells recovered from the spleens or LN at these early time points compared with mice immunized with peptide alone (data not shown), demonstrating a selective potency of CpG to enhance the early expansion of CD8+ T cells in response to soluble peptide in vivo. Consistent with the increased clonal population size at day 3 post-immunization, tetramer+ cells recovered from mice treated with CpG displayed a more robust proliferation profile compared with control mice that received peptide alone, as indicated by CFSE dilution (Fig. 2B). The effects of CpG were not as striking ICG-001 in the spleen, though similar trends were observed. By day 5, however, there was no accumulation of CFSElo cells regardless of CpG treatment, with proliferation profiles similar to those observed previously at day 5 in all groups (data not shown). Further, the numbers of tetramer+ cells recovered from the spleens of immunized mice 10 days post-immunization were

not changed by treatment with any TLR, including CpG (Fig. 2C). Thus, in spite of inducing more robust early proliferative activity, CpG treatment could not modify the widespread cell death observed after peptide immunization. Addition of MHC class II-restricted peptides to the BMS-777607 solubility dmso inoculum to elicit help from CD4+ T cells did not enhance the survival of the peptide-stimulated CD8+ T cells, even in the presence of CpG (Supporting Information Fig. 2). In mice that were immunized with peptide alone, we could not detect antigen-specific T cells by ELISPOT, suggesting that they were unable

to produce IFN-γ (Fig. 2D). However, antigen-specific SB-3CT cells from the dLN of mice treated with CpG and peptide were readily detected by IFN-γ ELISPOT. These differences were not merely due to differences in frequency, as there was a ten-fold increase in tetramer+ cells measured by FACS, but there were greater than 300-fold differences in the number of IFN-γ-producing cells. Curiously, antigen-specific IFN-γ secreting T cells were not detected in the spleen when immunizing mice with either peptide alone or CpG with peptide. CpG clearly modulates the CD8+ T-cell response to soluble peptide by promoting cell division and clonal expansion, as well as supporting IFN-γ production. However, CpG could not induce T-cell survival, as there was no significant increase in the final magnitude of the CD8+ T cell after the contraction phase. Since CpG has been shown to have many effects on the immune system 21 that may change over time, we modified the timing of the CpG administration relative to the peptide to investigate whether there were temporal effects of the CpG that could enhance T-cell survival.

The most ecologically valid approach to determining the trainability

of the CIVD response is to track individuals before, throughout, and after a prolonged period of natural exposure to cold stress. However, from a methodological and research design perspective, this approach is difficult to control, and it is not easy to isolate individual factors and mechanisms that can contribute to local thermal adaptation of the extremities. For example, it can be difficult selleck to accurately quantify the duration and intensity of both whole-body and local cold exposure, such that results from field studies present equivocal evidence for adaptation. Table 1 summarizes a number of the existing field and laboratory studies on CIVD trainability. A number of studies suggest minimal adaptation even from occupations experiencing extensive local and/or general exposure to cold. One such study tracked a group of SCUBA divers stationed with the British Antarctic Survey for a year, with monthly laboratory immersions of the index finger into ice water [11]. Compared with a control group of nondiving Survey members, no significant differences

were reported in CIVD response between the groups over the study period, nor were there differences in subjective pain response. While one potential explanation may have been that an overall drop in core temperature during diving blunted the potential RG7204 in vivo CIVD response, an earlier study on the same population reported that rectal temperature during

diving did not decrease below 36.0°C, even though finger temperature decreased to 10°C over the approximate 30-minute dives [10]. Therefore, it must be concluded that significant peripheral cooling repeatedly occurred in the diving group over the course of the year, but that such repeated local cold exposure did not significantly affect core temperature nor enhance CIVD response. Furthering the lack of response, Livingstone [50] and Livingstone et al. [51] reported lower mean finger temperatures in groups of Canadian soldiers upon immersion of the middle finger into ice water following a Ribociclib solubility dmso two-week Arctic expedition. However, one potential caveat in interpreting these studies, especially with the Canadian soldiers, is that the subjects were already living in winter environments, and may have experienced natural cold acclimatization and therefore limited further potential for adaptation. Other literature suggests that field acclimatization is indeed possible. Tropical inhabitants—soldiers from the plains of India—exhibited an improved peripheral blood flow and CIVD response after seven weeks of exposure to the Arctic environment [63], but this remained below the level found in Arctic natives, and suggests that full adaptation requires much longer exposure periods.

33–39 Of the 418 haplotypes of the parents of the 104 families (haplotype information was derived from three parents in one family), there were 122 different haplotypes, taking into account both genes and alleles. Of these, 48 were A and 74 were B. Sixty-six haplotypes only occurred on one occasion. In total, 230 (55%) of haplotypes were A and 188 (45%) were B. The percentage of individuals who were homozygous for the A haplotype was Ixazomib purchase 32·3%, the percentage homozygous for the B haplotype was 12·1% and 55·6% of individuals had both A and B haplotypes. B haplotypes have previously

been shown to be more prevalent in non-Caucasian populations such as Australia Aborigines and Asian MK0683 cost Indians,40–43 whereas in Caucasian populations approximately 55% of the population will have A haplotypes and 30% have two A haplotypes.44 It is believed that populations with higher frequencies

of B haplotypes will be those under strong pressure from infectious diseases. The addition of 27 new families to the haplotype study resulted in the definition of 19 new individual haplotypes, some of which occurred more than once. This would indicate that even in a small ethnically homogeneous population, the number of families (77 in the original report) needs to be greatly increased to cover all potential haplotype variation. It is important to note that genes normally associated with the A haplotype can also be found on the B haplotype. These genes, KIR3DL1, KIR2DS4, KIR2DL1, KIR2DL3, were present on 102, 99, 113 and 52 of the 188 B haplotypes, respectively. Ninety-six B haplotypes had both P-type ATPase KIR3DL1 and KIR2DS4. The only activating gene, bar KIR2DL4,

on the A haplotype is KIR2DS4. There are two versions of KIR2DS4, one with the full sequence and one with a short deletion. The deleted version has a 22-base-pair deletion in exon 5, which causes a frame shift leading to a stop codon in exon 745 and it is believed that this version is not expressed at the cell surface. The deleted version (KIR2DS4 alleles *003,004,006,007) is quite common, at 80% in the Northern Ireland population, nearly 60% of the population having only the deleted KIR2DS4. However, there is a trend for decreased frequency of the deleted version in those populations that are homozygous for the A haplotypes.46 Interestingly we found that 30 (62·5%) of the different A haplotypes and 155 (67·4%) of total A haplotypes contained both a deleted version of KIR2DS4 and a deleted version of KIR2DL4, (2DL4-9A). Consequently, in those individuals who have the genotype AA, 43·1% did not have an activating KIR, leading to 13·9% in the overall population not having an activating receptor.

Samples were analyzed using a BD FACS Calibur flow cytometer and data were analyzed using FlowJo software. Isotype-matched Selleck FDA approved Drug Library PE- and FITC-conjugated mAbs of irrelevant specificity were used

as negative controls. Lymphocytes from either EAMG or CFA control rats (2 × 106/mL) were cultured in the presence of AChR R97-116 (10 μg/mL) with or without CGS21680 (30 nM). After a 72 h incubation, supernatants were collected and IFN-γ, IL-4, IL-17, and TGF-β levels were determined using respective ELISA kits (Shanghai Senxiong Biotech Industry Co. Ltd., China) according to the manufacturer’s instructions. The analyses were performed in triplicate and the results are expressed as the mean cytokine concentration (pg/mL) ± SD. For preventive treatment experiments, rats were given CGS21680 (0.5mg/kg intraperitoneally (i.p.)) in PBS starting 1 day before EAMG induction and every 3

days throughout the course of the experiment. Therapeutic treatment of EAMG consisted of 1.0 mg/kg CGS21680 administered Sirolimus solubility dmso i.p. every 3 days starting 29 days post immunization. Hind limb muscles were harvested, snap frozen in liquid nitrogen, and a cryostat used to generate 10-μm thick sections. We incubated the sections with biotin-conjugated goat antirat IgG (Sigma-Aldrich) for 1 h. Sections were then stained with tetramethylrhodamine-labeled α-BTX (Molecular Probes), FITC-labeled goat antirat C3 (Nordic Immunological Laboratories), and Alexa Fluor 350-labeled streptavidin. Sections were then analyzed using a fluorescence microscope (LSM 700, Zeiss). Data were expressed as mean ± SD. Differences between groups were analyzed using Graphpad software (Graphpad software, CA) and the two-tailed Student’s t-test for paired and unpaired data. p < 0.05 were considered MYO10 statistically significant. This work was supported by Heilongjiang Provincial Innovation Found for Postgraduates (YJSCX2011-324HLJ, Na Li is the recipient), National Nature Science Foundation of China (81000511, Lili Mu is the recipient), China Postdoctoral

Science Foundation (20100480062, Lili Mu is the recipient), National Nature Science Foundation of China (81000536, Qingfei Kong is the recipient), China Postdoctoral Science Foundation (20100471094, Qingfei Kong is the recipient), National Nature Science Foundation of China (30901330, Bo Sun is the recipient), National Nature Science Foundation of China (81100883, Yumei Liu is the recipient), and the Harbin Medical University Cell Biological Engineering Center (1151gzx05). The authors declare no financial or commercial conflict of interest. Disclaimer: Supplementary materials have been peer-reviewed but not copyedited. Figure S1. The A2ARagonist CGS21680 reduced the number of AChR antibody-secreting cells. Figure S2.

The biotinylated rFbp were dissolved in BVBS containing 0.02% (v/v) Tween 20. The binding of biotinylated Fn to III1-C in the presence of 1 μg or 10 μg rFbp was measured. Absorbance at 280 nm was used to calculate the protein concentration of Fn and

Fn fragments using ɛpercent= 10. The concentration of rFbp was measured by the Bradford method (Bio-Rad, Hercules, CA, USA) using BSA as a standard. All experiments were performed in triplicate. Statistical significance (P < 0.05, P < 0.01) was determined by comparison with controls using Student's two-tailed t-test. To determine which Fn fragments are recognized by the rFbp, a plate binding assay was performed in which binding of biotinylated-rFbpA or -rFbpB to immobilized Fn fragments (70 kDa, 30 kDa, 45 kDa, 110 kDa or selleck chemicals III1-C) was assayed. The Fn fragments were mapped according to their position within the Fn polypeptide (Fig. 1a). Of the Fn fragments tested, both rFbpA and rFbpB bound only to the III1-C fragment of Fn (Fig. 1b). Both rFbpA and rFbpB were found to bind to the III1-C fragment. However, the III1-C fragment of serum Fn is known to be cryptic. Therefore, rFbp-binding proteins from Fn were purified by affinity chromatography on rFbpA- and rFbpB-Sepharose columns. Following

elution of bound proteins with 4 M urea, the yield of affinity purified binding protein from rFbpA-Sepharose and rFbpB-Sepharose chromatography was 0.96% and 1.08% of the applied Fn protein, respectively. In order to characterize the purified rFbp-BP, epitope mapping with various anti-Fn mAbs using immobilized Apitolisib research buy Fn fragments in a plate binding assay was first carried out.

for The mAb HB91 reacted strongly with both the N-terminal 70-kDa and 30-kDa fragments of Fn, but reacted weakly with the 45-kDa fragment. The other three mAbs tested, HB39, ZET1, and ZET2, reacted with the 110-kDa Fn fragment. The HB39 mAb was the only mAb that also reacted weakly with both the N-terminal 70-kDa and 30-kDa fragments (Fig. 2a). No mAb tested here reacted with III1-C (Fig. 2b). To determine if the rFbp-BP might contain Fn-epitopes, whether the rFbp-BP were recognized by the anti-Fn mAbs, using SDS-PAGE and Western blotting analysis was checked. Silver staining of SDS-gels showed that both rFbpA-BP and rFbpB-BP consisted of a major, slightly broad protein band with a size of 450 kDa, and minor bands with the sizes of 180, 160 and 84 kDa (Fig. 3a and b). When binding of the anti-Fn mAbs was tested by Western blotting, the 450-kDa protein band of the rFbp-BP reacted with both HB91 and HB39, but not with ZET1 or ZET2. To determine whether rFbp-BP expressed III1-C, a rFbp-binding assay to rFbp-BP in the presence of III1-C peptides was performed. Binding of both rFbpA and rFbpB to rFbpA-BP and rFbpB-BP, respectively, was significantly inhibited by the presence of III1-C peptide in a dose-dependent manner (Fig. 4).