Only COI-negative fibers were histochemically negative for COX activity in all patient groups. Frequency of COI-negative fibers was significantly lower in patients with mtDNA point mutation than in patients with deletions. This suggests that impact of point mutation on protein synthesis is less than that of deletions. “
“Brain ischaemia models are essential to

study the pathomechanisms of stroke. Our aim was to investigate the reliability and reproducibility of our novel focal ischaemia-reperfusion model. To induce a cortical transient ischaemic attack, we lifted the distal middle cerebral artery (MCA) with a special hook. Pembrolizumab chemical structure The early changes after 2 × 15-min occlusion were observed in the somatosensory evoked responses (SERs). The histological responses to 2 × 15-min MCA occlusion and to 30-, 45- or 60-min ischaemia were examined after a 1-day survival period by 2,3,5-triphenyltetrazolium chloride (TTC) and Fluoro Jade C (FJC) staining. Another group, with 30-min ischaemia, was analysed histologically by FJC, S100 and CD11b labelling after a 5-day survival period. The amplitudes of the SERs decreased immediately at the beginning of the ischaemic period, and remained at a reduced level during the ischaemia. Reperfusion resulted in increasing SER amplitudes, but they never regained the control level. The short-lasting ischaemia did not

lead to brain infarction Palbociclib cell line when evaluated with TTC, but intense labelling was found with FJC. The 30-min ischaemia did not result in FJC labelling after 1 day, but marked labelling was observed after 5 days with FJC, S100 and CD11b in the cortical area supplied by the MCA. We present here PAK5 a novel, readily reproducible method to induce

focal brain ischaemia. The ischaemia-reperfusion results in noteworthy changes in the SERs and the appearance of conventional tissue damage markers. This method involves possibilities for precise blood flow regulation, and the setting of the required level of perfusion. “
“In glioblastoma multiforme (GBM), the pathophysiological events preceding and promoting an uncontrolled and remarkable growth is largely unknown. Studies on gliomas and macrophage expression have shown high levels of phagocytic cells, that is, microglial cells. It has also been demonstrated that human astrocytic cells and rat glioma cells are capable of phagocytosis. The purpose of this study was to investigate a potential phagocytic property in human GBM cells in tumor biopsies from surgery. With an immunhistochemical double staining using macrophage markers (CD68 and CD163) and human telomerase reverse transcriptase (hTERT) as a marker for neoplastic cells, we found high levels of double positive cells in human GBM. In hematoxylin-erythrosin stained sections, we also identified fragmented cell components in the cytoplasm of tumor cells. In our judgement, many neoplastic cells in GBM are also positive for macrophage markers.

3c,d). The Th2 cytokine IL-13 and the toll-like receptor ligand poly I:C had no significant effect on H4R expression in any of the studied groups (data not shown). It has been described previously, www.selleckchem.com/products/GDC-0941.html that slanDC are the principal producers of IL-12 and also produce high levels of TNF-α upon activation with the toll-like receptor ligand LPS.2 Stimulation of PBMC with histamine or the H4R-specific agonist 4-methylhistamine significantly down-regulated the production of TNF-α and IL-12 in slanDC, as measured

by intracellular cytokine staining (Fig. 4a,b). The down-regulation of TNF-α could be fully blocked by pre-incubation of the cells with the H4R selective antagonist JNJ7777120, showing that the effect is specific for H4R (Fig. 4a); for IL-12 only partial blockage was achieved (Fig. 4b). In addition to studies with PBMC the effect of histamine on the release of cytokines into the cell culture supernatant was investigated in isolated slanDC. We could observe histamine-induced down-regulation of TNF-α and IL-12 secretion into the supernatant at three consecutive time points: 24, 48 and 72 hr (Fig. 5). The H4R agonist 4-methylhistamine also led to decreased cytokine secretion and the H4R receptor antagonist JNJ7777120 could selectively block the down-regulation (Fig. 6a). As slanDC also express the H1R and H2R (Fig. 1) we tested in addition agonists at these receptors. mTOR inhibitor The TNF-α secretion

was not down-regulated after stimulation with the H1R agonist 2-pyridylethylamine and the H2R agonist amthamine, indicating that the down-regulation of TNF-α Docetaxel price is solely mediated via the H4R. For IL-12 we observed down-regulation after stimulation with the H2R agonist indicating that the down-regulation of IL-12 is mediated by two histamine receptors H2R and H4R (Fig. 6b). We did not observe significant differences in the secretion of the anti-inflammatory cytokine IL-10 (Figs 5 and 6). Several studies show that slanDC are pro-inflammatory cells producing large amounts of inflammatory cytokines and inducing antigen-specific

T-cell responses.2,4 As a result of their presence in chronic lesions of AD and psoriasis they are thought to be involved in the pathogenesis of inflammatory skin diseases. However, relatively little is known about the regulation of their function. We chose to investigate the effect of histamine on slanDC, because histamine is an important inflammatory mediator present in the lesions of AD and psoriasis and histamine has been shown to modulate the function of other types of antigen-presenting cells such as monocytes17 and MoDC.15 Here we show for the first time, that slanDC express histamine receptors and that their pro-inflammatory capacity is down-regulated in response to stimulation with histamine. SlanDC express mRNA for three histamine receptors H1R, H2R and H4R, but not for the H3R.

Health-related quality of life in elderly dialysis patients appears to be decreased compared with elderly persons in the general population[19] although may be better preserved

than in a younger cohort of patients where the perceived reduction in health-related quality of life associated with dialysis is greater.[20] Many factors will impact on a patient’s quality of life and may influence their decision to dialyse or not. An important concept is that of hospital free survival. Dialysis in elderly patients is associated with increased hospitalization with rates of hospitalization in elderly RRT patients of 20–35 days per year[9, 21] compared with 10–16 days per year[9, 17] in those on non-dialysis pathways. One UK study published by Carson et al.[9] concluded that elderly haemodialysis patients spent almost 50% of the time they survived in hospital or attending to dialysis compared with those on non-dialysis Neratinib pathways who spent just 4.3% of their days. This crucial information is frequently not imparted

to patients or considered by nephrologists when discussing the option of RRT. Evidence learn more also exists that elderly dialysis patients have one of the highest prevalence rates for frailty of any single population and that initiation of dialysis may be associated with considerable functional decline. Jassal et al.[22] showed that in those aged ≥80 who commenced dialysis (80% of whom were living independently at home), 30% had functional

loss 6 months after dialysis initiation (required community/carer support or transfer to a nursing home). Another study by Kurella Tamura et al.[14] showed that the majority of elderly nursing home residents have died (60%) or lost function (27%) 12 months after dialysis initiation. The elderly can have specific medical issues and needs that are best assessed by an Aged Care Physician. This is recommended particularly when assessment of cognitive function is a part of the considerations in determining whether dialysis is appropriate or not. Finally carers of elderly dialysis patients also have impaired quality of life with all components of The Short Form (36) Health Survey (SF36) affected and 32% of carers with signs of depression in one study.[23] We have no information on the impact of carers of elderly patients on non-dialysis pathways and further studies are required. Selleck Gefitinib Jennifer Robins and Ivor Katz Documenting five key variables important in determining mortality associated with dialysis: Nephrologist response to the Surprise Question. Age. Comorbidities. Functional status. Nutritional status. Use of the Surprise Question in all patients: on dialysis or those patients on, or being considered for, a non-dialysis pathway. Use of the clinical score by Couchoud et al. (2009) for patients being considered for a non-dialysis pathway. Use of the modified Charlson score (MCS) and the clinical score by Cohen et al.

By 7 months, most infants finally have sufficient postural FK866 cell line control to reach while sitting independently. Given infants’ success at adopting context appropriate reaching responses by the end of the first year, it has been a longstanding puzzle as to why infants typically experience an increased rate of less adaptive two-handed reaching patterns at the start of their second year (e.g., Babik, 2010; Corbetta & Thelen, 1996; Fagard & Pezé, 1997; Goldfield & Michel, 1986; Ramsay, 1985). Corbetta and Bojczyk (2002) were

the first to suggest that infants’ tendency to return to two-handed reaching around the end of the first year was associated with changes in postural control upon the emergence of walking. By tracking nine infants weekly over the course of their transition to upright locomotion, including documenting arm position during walking and reaching patterns, Corbetta and Bojczyk (2002) demonstrated that infants who displayed competent and adaptive reaching responses prior to walking, such as reaching primarily with EPZ-6438 solubility dmso one hand for small objects, typically began to reach more often with two hands

for small objects after walking onset. As infants’ balance control improved, the two-handed reaching pattern declined, suggesting that something unique about the motor constraints associated with the onset of walking played an important role in the developmental reorganization of reaching (Corbetta & Bojczyk, 2002). Walking is the culmination of a whole sequence of upright postures, making it difficult to fully interpret the mechanism underlying the relationship between its onset and infants’ return to bimanual reaching. In particular, we do not yet know whether there was something unique about walking or whether it was the general postural shift mafosfamide to an upright position that reorganized the motor system. It could be that the onset of

the high guard posture used for balance control prompted the reorganization of infants’ reaching patterns. However, it is also possible that it was the more general switch to being upright that prompted the reorganization. In that case, we may see a relationship between the development of bimanual reaching and other upright postures like pulling-to-stand or cruising (moving sideways holding onto furniture with one or both hands for support). In fact, some recent preliminary work suggests that the onset of independent standing may be related to infants’ reaching patterns and that subsequent walking strategies shape the trajectory of changes in reaching preferences (Thurman et al., 2012).

“
“Invariant natural killer T (iNKT) cells are a specialised subset of T cells that are restricted to the MHC class I like molecule, CD1d. The ligands for iNKT cells are lipids, with the canonical superagonist being α-galactosylceramide, a non-mammalian glycosphingolipid. Trafficking of CD1d through the lysosome is required for the development of murine iNKT cells. Niemann-Pick type C (NPC) disease is a lysosomal storage disorder caused by dysfunction in either of two lysosomal proteins, NPC1 or NPC2, resulting in the storage of multiple lipids, including glycosphingolipids. In the NPC1 mouse model, iNKT cells are virtually undetectable, which

Fulvestrant in vivo is likely due to the inability of CD1d to be loaded with the selecting ligand due to defective lysosomal function and/or CD1d trafficking. However, in this study we have found that in NPC1 patients iNKT cells are present at normal frequencies, with no phenotypic or functional differences. In addi-tion, antigen-presenting cells derived from NPC1 patients

are functionally competent to present several different CD1d/iNKT-cell ligands. This further supports the hypothesis that there are different trafficking requirements for the development of murine and human iNKT cells, and a functional lysosomal/late-endosomal compartment is not required for human iNKT-cell development. Invariant natural killer T (iNKT) cells are defined by their invariant T-cell receptor and restriction to the MHC class I like molecule, CD1d. iNKT Histone demethylase cells express Alvelestat order multiple markers associated with NK cells and have the ability to rapidly release both TH1 (e.g. IFN-γ) and TH2 (e.g. IL-4) cytokines after engagement, acting as a bridge between innate and adaptive immunity [1]. iNKT cells play important roles in host protection against pathogens, cancer and auto-immunity. iNKT cells are lipid-reactive, with the canonical superagonist being α-galactosylceramide (α-GalCer) a non-mammalian glycosphingolipid.

Mammalian glycosphingolipids (GD3 and iGb3), mammalian phospholipids and pathogen-derived glycolipids (α-galactosyl diacylglycerol, α-glyucuronsyl ceramides) have also been shown to activate iNKT cells [2]. iNKT cells develop in the thymus, where they undergo a process of positive selection with double positive thymocytes presenting selecting ligand(s) on CD1d [3]. Rodents only have one member of the CD1 family, CD1d, whereas humans have five members, CD1a to CD1e [4], that have differential intracellular trafficking patterns [5]. Murine CD1d exhibits a broad intracellular trafficking pattern, transiting through early and late endosomes, and also the lysosome, which is necessary for successful thymic selection [6, 7]. In addition, functional lysosomes are required for the presentation of activating ligands to murine iNKT cells [8].

Here, we report a case of reconstruction of the right midfoot with the trauma-related osteomyelitis using a free chimeric scapula and LD muscle flap in a 59-year-old

woman with diabetes mellitus. After radical debridement and sequestrectomy, a 7 × 3 cm2 wound with a 5 × 3 cm2 bony defect was reconstructed with the chimeric scapula and LD muscle flap. The postoperative course was Lumacaftor supplier uneventful. The bony union was achieved 6 months after surgery. In 14 months follow-up, no clinical complications including a new ulcer or stress fracture were noted. At the end of follow-up, the gait analysis showed an unbalanced stress distribution on the right foot and a valgus gait. We suggest that this chimeric scapula and LD muscle flap may be an alternative option for midfoot reconstruction. © 2012 Wiley Periodicals, Inc. Microsurgery, 2012. “
“Whether post-traumatic regeneration can eventually result in rat peripheral nerve fibers regaining their pretrauma size is still an open question. While it has been shown that, after a sufficient duration in post-traumatic time, the number of regenerated rat peripheral nerve fibers can return to

pretrauma numbers and the animal can regain normal prelesion function, no information regarding long-term changes in the size parameters of buy Decitabine the regenerated nerve fibers is available. To fill this gap, we have investigated the post-traumatic changes in myelinated axon and nerve fiber diameter, myelin thickness, and g-ratio (the ratio of the inner axonal diameter to the fiber diameter) at three different time points following nerve injury: week-6, week-8, and week-24. A standardized nerve crush injury of the rat median nerve obtained using a nonserrated clamp was used for this study. The results showed that, consistent with previous studies, fiber number returned to normal values at week-24, but both axon and fiber diameter and myelin thickness PAK6 were still

significantly lower at week-24 than prelesion, and the g-ratio, which remained unchanged during the regeneration process, was significantly reduced at week-24 in comparison to the prelesion value. On the basis of these results, the hypothesis that regenerated rat peripheral nerve fibers are able to return spontaneously to their normal pretrauma state, provided there is a sufficiently long recovery time postaxonotmesis, is not supported. © 2012 Wiley Periodicals, Inc. Microsurgery, 2012. “
“The biology behind vascularized bone allotransplantation remains largely unknown. We aim to study cell traffic between donor and recipient following bone auto-, and allografting. Vascularized femoral transplantation was performed with arteriovenous bundle implantation and short-term immunosuppression.

4). In the male mice the number of DP thymocytes was slightly increased (Fig. 5). These results demonstrate the partial impairment of positive and negative selection in LAR-deficient mice. During selection, the strength of the TCR signal plays a pivotal role in determining cell fate 3–5. In LAR-deficient thymocytes, the

level of TCR stimulation, as measured by the intracellular Ca2+ concentration, MAPK inhibitor was reduced compared with control thymocytes (Fig. 6). We think the reduction of Ca2+ responding cells is mainly attributed to DP thymocytes because neither CD4SP nor CD8SP thymocytes express LAR 17, 18 and LAR deficiency might not affect the Ca2+ mobilization in CD4SP as well as CD8SP thymocytes. This reduction in the strength of the TCR signal may result in a decrease in the efficiency of negative and positive selection (Fig. 7). Although LAR deficiency might affect T-cell development in the thymus, the animals do

not appear to be immune-compromised and there has been no report of which in the literature. LAR deficiency might not be reflected in the immunological phenotype; first, because the effect of LAR deficiency in the thymus was subtle and its effect was compensated in the periphery; second, because LAR is a member of receptor type membrane tyrosine phosphatase family including CD45 that is expressed on thymocytes as well as peripheral T cells and CD45 could compensate the effect of LAR deficiency. How does LAR deficiency affect TCR signal transduction? During TCR signal transduction, a receptor-like PTP, CD45, activates two PTK, Lck and Fyn, by dephosphorylating a tyrosine moiety 29,

30. Activated Lck and Fyn then phosphorylate the immunotyrosine-activating check details motif on CD3ξ, which leads to the activation of thymocytes as well as T cells. Tsujikawa et al. 12 reported that LAR also regulated the activity of Lck and Fyn in CD45-deficient cells. Taken together, our results suggest that LAR is also involved in Inositol monophosphatase 1 TCR signal transduction in thymocytes. The effect of LAR deficiency on TCR signal transduction seems subtle since we did not observe significant differences in the proliferation of LAR-deficient thymocytes following TCR stimulation (Supporting Information Fig. 6). Regarding the regulation of Ca2+ mobilization by LAR, Archuleta et al. have demonstrated that activated Lck and Fyn increase tyrosine phosphorylation of phospholipase C-γ1, and activated phospholipase C-γ1 increase formation of IP3, which may be responsible for the rapid increase in intracellular Ca2+ mobilization 31. Taken together, we hypothesize that LAR may regulate Ca2+ mobilization by activating Lck and Fyn, which then leads to tyrosine phosphorylation of phospholipase C-γ1 and increases formation of IP3, which finally regulate intracellular Ca2+ mobilization. Our data suggest that LAR is only expressed during the DN-to-DP transition of T cells in the thymus and that LAR plays a role in pre-TCR- or αβTCR-mediated selection during the differentiation of thymocytes.

Purified NK cells were used in subsequent experiments. NK cell cytotoxicity was determined using the calcein release assay, a fluorometric assay comparable to the chromium release assay [8, 9]. Target K562 cells were labelled with 2 μg/ml calcein-AM for 1 h at 37°C with occasional shaking. Effector cells and target cells were co-cultured at the indicated effector-to-target (E : T) ratios and incubated at 37°C for 4 h. After incubation, 100 μl of the supernatant was transferred to a new plate. The fluorescence of the samples was measured with a Spectramax Gemini EM Proteasome inhibitor Fluorescence Microplate Reader (Molecular Devices, Sunnyvale, CA, USA)

(excitation filter 485 nm, emission filter 538 nm). The percentage lysis was calculated according to the formula [(experimental release − spontaneous release)/(maximum release − spontaneous release)] × 100. To investigate the effect of STAT-3 inhibitor JSI-124 on the viability of human NK cells, 1 × 106 primary purified or expanded NK cells were seeded per well in 24-well plates. JSI-124 was added at the indicated final concentrations (0, 0·05, 0·1, 0·2 and 0·5 μM). At the 24, 48 and 72 h time-points, cells were stained with 7-AAD, then analysed by flow cytometry. Primary NK cells were EPZ 6438 purified and incubated with 20 ng/ml of IL-21 with or without 0·1 μM of JSI-124 for 24 h, and were then lysed with 50 mM Tris-Cl (pH 6·8), 100 mM dithiothreitol, 2% sodium dodecyl sulphate (SDS) and 10% glycerol. Samples were analysed

by SDS-polyacrylamide gel electrophoresis (PAGE), followed by immunoblotting using the Chemo Glow chemiluminescent substrate (Alpha Innotech, San Leandro, CA, USA) according to the manufacturer’s instructions. Results are expressed as the mean ± standard deviation.

Statistical comparison was performed by Student’s t-test. P-values of less than or equal to 0·05 were considered significant. We engineered K562 cells to express mbIL-21 and CD137L, and used these cells to expand NK cells efficiently from the peripheral blood mononuclear cells (Fig. 1). For cell engineering, CD137L and mbIL-21 sleeping beauty expression vectors were harvested as described in Materials and methods, and then transfected into K562 cells, together with the sleeping beauty transferase SB11. CD137L was first transfected, and CD137L-positive K562 cells (CD137L-K562) were sorted by the flow cytometer; mbIL-21 was transfected Y-27632 2HCl subsequently into CD137L-K562 cells, and mbIL-21-positive CD137L-K562 (mbIL-21-CD137L-K562) cells were sorted. Isolated cells were stained with CD137L and IL-21 flow cytometer antibodies. Results showed that both CD137L and IL-21 were expressed clearly on the surface of mbIL-21-CD137L-K562 cells (Supporting Fig. S1). After constructing the mbIL-21-CD137L-K562, NK cell expansion was performed as described in Materials and methods. To evaluate NK cell purity, expanded cells were stained with CD3, CD56 and CD16 antibodies. Figure 2 was a representative of six different expansions.

Chemokines, basic proteins that strongly bind to heparin, can induce leukocyte chemotaxis and activation and are intimately involved in various biological processes, including inflammatory responses, hematopoietic regulation and neoangiogenesis 18–20. The chemokines CCL4, CCL5 and CCL20 have been reported as being capable of attracting memory/activated T cells, www.selleckchem.com/products/r428.html whereas immature DC and B cells express

CCR6 – its specific CC chemokine receptor 20, 21. Previous DNA microarray analysis has revealed that IFI16 overexpression in EC triggers the expression of proinflammatory adhesion molecules, and functional analysis of the ICAM-1 promoter by site-specific mutagenesis has demonstrated that NF-κB is the main mediator of IFI16-driven gene induction 9. However, definitive prove that IFI16 regulates the proinflammatory activity of EC at the functional level has been missing. In this study, protein array analysis of the IFI16 secretome reveals that

IFI16 triggers the expression of both intercellular adhesion molecules and chemokines responsible for leukocyte recruitment in vivo. Consistent with these observations, significant increases in the protein levels of CCL4, CCL5 and CCL20 were identified by ELISA in the supernatants of HUVEC overexpressing IFI16. Moreover, studying CCL20 as a representative chemokine, we demonstrate that NF-κB is the relevant mediator of CCL20 gene transcriptional activation following IFI16 overexpression. The relevance of this interaction is highlighted by the finding that the supernatants of IFI16-overexpressing HUVEC trigger the migration of both Rapamycin supplier CCR6-positive L-DC and B cells and that this migration is significantly downregulated by the addition of Ab that neutralize CCL4, CCL5 and CCL20. Inflammation is a complex defence mechanism, which aims to contain and resolve harmful processes

(such as infections, toxic Myosin stress and tissue damage) and protect the integrity of the human body. At sites of inflammation, infection or vascular injury, both local proinflammatory and pathogen-derived stimuli render the vessel endothelium surface attractive for incoming leukocytes 22. This innate immune response of the endothelium consists of a well-defined and regulated multi-step cascade involving consecutive steps of release of leukocyte-recruiting chemokines by EC and adhesive interactions between the leukocytes and the endothelium; thus the proinflammatory activation of EC is important for the tight regulation of the mechanisms underlying the chemoattraction of leukocytes to lesions – mechanisms that are known to involve components of the NF-κB complex; indeed, the NF-κB complex is considered to be the major transcription factor regulating the expression of EC adhesion molecules and chemokine release 23–25. Consistent with this, in this study we show that IFI16 triggers the expression of proinflammatory genes by activating the NF-κB complex.

Pemphigus-vulgaris-specific IVIG (PV-sIVIG) was affinity-purified from IVIG on a column of single-chain variable

fragment (scFv) anti-desmogleins 1 and 3. The anti-idiotypic activity of PV-sIVIG was confirmed by JAK inhibitor enzyme-linked immunosorbent assay, inhibition assay. After induction of pemphigus by injection of anti-desmogleins 1 and 3 scFv to newborn mice, the animals were treated with PV-sIVIG, IVIG (low or high dose) or IgG from a healthy donor (n = 10 each). The skin was examined 24–48 h later, and samples of affected areas were analysed by histology and immunofluorescence. In vitro study showed that PV-sIVIG significantly inhibited anti-desmogleins 1 and 3 scFv binding to recombinant desmoglein-3 in a dose-dependent manner. Specificity was confirmed by inhibition assay. In vivo analysis revealed cutaneous lesions of pemphigus

vulgaris in mice injected with normal IgG (nine of 10 mice) or low-dose IVIG (nine of 10 mice), but not in mice treated with PV-sIVIG (none of 10) or high-dose IVIG (none of 10). On immunopathological study, PV-sIVIG and regular IVIG prevented the formation of acantholysis and deposition of IgG in intercellular spaces. In conclusion, the PV-sIVIG preparation is more effective than native IVIG in inhibiting anti-desmoglein-induced pemphigus vulgaris in mice and might serve as a future therapy in patients Selleckchem GW 572016 with the clinical disease. Pemphigus is a group of organ-specific autoimmune mucocutaneous disorders with an established immunological

basis. Its clinical hallmark is the presence of intraepithelial blisters and erosions on the skin and the mucous membranes. Immunohistological studies of pemphigus lesions have shown that immunoglobulin G (IgG) autoantibodies directed against the adhesion molecules desmoglein 1 and desmoglein 3 in the affected epithelium cause cell-to-cell detachment of epidermal and mucosal epithelial cells (acantholysis) [1–3]. The goal of therapy is to eliminate these pathogenic autoantibodies [4]. However, at present there are no available selective inhibitors of desmoglein autoantibodies, and therapy is therefore based upon antibody removal and non-specific immunosuppression. Left untreated, pemphigus vulgaris (PV) has a natural history of relentless progression, with 50% mortality at 2 years Selleckchem Depsipeptide and almost 100% at 5 years [5]. Since the 1950s, the survival of patients with PV improved remarkably with the introduction of corticosteroids and cytotoxic drugs, which have powerful anti-inflammatory and immunomodulatory effects. However, their use is limited severely by immunosuppression, myelosuppression and numerous side effects. Intravenous immunoglobulin (IVIG), a blood product prepared from donor serum, is used as replacement therapy in immunodeficient conditions [6,7]. Recent studies have revealed an extremely wide spectrum of IVIG antibody activity.