Bone marrow was harvested from mouse femurs by flushing through with complete RPMI medium and the cells were treated with 1 ml of 0·83% NH4Cl for 3 min to lyse the red blood cells. The cell suspension was plated out at 5 × 105 cells/ml (1 ml/well) in the wells of 24-well plates, in RPMI-1640 medium containing 20% (v/v) GM-CSF. Cultures were stimulated with Poly I, Poly I:C, LPS, CpG ODN, Jap, X31 or PR8, as indicated above, and incubated at 37° for 6 days. Experiments over a time course from 6 to 9 days were initially

undertaken, and a culture period of 6 days was selected because the cultures demonstrated an effect that was not increased over longer time-periods of culture. Surface antigen staining was performed using either directly conjugated mAb or biotinylated mAb followed by staining with phycoerythrin (PE) or Cy-chrome-conjugated streptavidin

(both from BD Biosciences Pharmingen, Oxford, UK). Torin 1 manufacturer The following antibody conjugates were used: mouse CD11c–PE or CD11c–biotin, Gr1–fluorescein isothiocyanate www.selleckchem.com/products/abt-199.html (FITC) or Gr1–PE (Caltag, Buckingham, UK), B220–allophycocyanin (APC), CD19–biotin (BD Biosciences Pharmingen) and PDCA–biotin (Miltenyi Bergisch Gladbach, Germany), and a mAb to major histocompatibility complex class II (MHCII) (KB6, a gift from Dr M. Parkhouse, Department of Infection and Immunity, Instituto Gulbenkian de Ciencia) was purified and coupled to FITC using standard methods. Fluorescence was analysed using a FACSCalibur flow cytometer (Becton Dickinson, Oxford, UK). Cells were stained with haematoxylin and eosin, and morphological analysis was performed under a light microscope at 400× magnification. Cells were counted in five fields of view and the numbers of different cell types were assessed. Neutrophil-like cells were defined as cells with cytoplasm that stained neutral pink and a multilobed nucleus. Cells containing a large oval nucleus surrounded by a voluminous

cytoplasm were classed as monocytes, and cells containing a large, dark nucleus, with little or no cytoplasm, were classed as lymphoid. Photographs were taken at 200× Celecoxib magnification using a Canon Powershot G3 mounted onto a Nikon TMS-F inverted microscope. To examine the effects of TLR ligands (representing bacterial and viral PAMPs) and inactivated influenza viruses on the generation of BMDCs, BALB/c bone marrow was cultured in the presence of GM-CSF, with or without the inactivated influenza A viruses Jap (H2N2), X31 (H3N1), or PR8 (H1N1), the TLR3 ligands Poly I and Poly I:C, the TLR4 ligand LPS or the TLR9 ligand CpG ODN. The production of BMDCs was determined by assessing the surface expression of CD11c and MHCII by flow cytometry. The results (Fig. 1a) showed that the addition of influenza virus to BMDC-generating cultures resulted in a marked reduction in the proportion of cells expressing the expected CD11c+ /MHCII+ phenotype. The addition of ligands for TLR3, TLR4 and TLR9 (Fig.

For example, at 6 or 7 years after transplantation,

Keene et al. [46] demonstrated grafted cell survival, as shown by the various striatal markers found within the grafted MAPK inhibitor tissue. However, basic markers of cell cytoarchitecture such as haematoxylin & eosin and Nissl reveal that grafted cells depict a morphology very different from host cells [43]. Cells within p-zones are ballooned, vacuolated, lack structural cytoplasmic integrity and even stain positively for apoptotic markers such as caspase-3. When identical immunohistological stainings are compared between the reports by Keene and Cicchetti, and those published for the 6- [22] and 18-month post-transplantation cases [42], it is apparent that grafted striatal projection neurones exhibit a much weaker staining and that they lack dendritic extensions almost completely

[43,45], pointing to a rather unhealthy morphology. In contrast, various subclasses of striatal interneurones including NADPH-d-, ChAT-, parvalbumin- and calretinin-positive cells, show a better long-term survival, suggesting a degeneration or neuronal sparing pattern similar to that observed with HD pathology [42,43,46]. Although there may be signs of degeneration PI3K inhibitor within the grafted tissue, ingrowth of host-derived TH fibres can be observed, suggesting connections and interactions between the host and donor cells [43,46]. These results are in accordance with earlier animal model studies as well as transplanted PD patients [55,56]. Such TH innervation was not found in the 10-year post-transplantation case depicting cysts and mass lesions [45], suggesting that TH innervation of grafted tissue is not a random process. However, DARPP-32-

and calbindin-positive Dimethyl sulfoxide cells within the grafts do not appear to cross the graft–host interface, suggesting a limited connectivity of the graft with the host brain [46]. One study reported the presence of cortical glutamatergic input onto the grafted striatal cells, using both immunohistochemistry and transmission electron microscopy [43]. Moreover, a notable microglial and astrocytic gliosis was observed in the vicinity of grafted tissue 9–10 years after transplantation [43,44], while such a response was found to be less intense in the graft than in the host at earlier intervals (6 and 7 years) [46]. Finally, elements associated to vasculature and vasculature network, such as endothelial cells and capillaries [stained with Von Willebrand factor (vWF)], pericytes [using platelet derived growth factor receptor-beta (PDGFR-β) as a marker] and larger-calibre blood vessels [detected with the α-smooth muscle actin (α-SMA) marker], demonstrated poor revascularization of the grafted tissue [44].

The mechanism underlying the pathogenic role of CD103+ DCs in AN mice may relate to their ability to activate CD8 T cells. LIN YI-TING1,4, WU PING-HSUN3,5, KUO MEI-CHUAN3,6, HUANG CHIA-TSUAN1,2, CHEN HUNG-CHUN3,6 1Department of Family Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan; 2Department of Pediatrics, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan; 3Division of Nephrology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan; 4Department of Public Health, Kaohsiung Medical University, Kaohsiung, Taiwan; 5Graduate Institute of Medicine,

College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; 6Faculty of Renal Care, College of Medicine, Kaohsiung Medical University, buy PS-341 Kaohsiung, Taiwan Introduction: Chronic obstructive pulmonary disease (COPD) increase all-cause of mortality and cardiovascular events in general population. This population-based cohort study aimed to investigate the mortality and cardiovascular risks of COPD among end-stage renal disease (ESRD) patients receiving hemodialysis. Methods: From the Taiwan National Health Insurance Research Database,

83,509 Taiwanese hemodialysis patients were screened for eligibility between January 1, 1998 and December 31, 2006. COPD was defined by a specific diagnosis code and COPD-related medications. After excluding RGFP966 mouse patients age less than 40 year-old and receiving renal transplantation before and after enrollment, we included a total of 13,592 patients who were diagnosed COPD, and matched them 1:1 with 13,592 controls by age,

gender, urbanization, and economic Neratinib purchase status. Participants were followed up for the occurrence of death, acute coronary syndrome (ACS), and ischemic stroke, or until 2008. Results: From 1998 to 2008, the 10-year cumulative incidences of death in the COPD and comparison cohorts were 33.74% and 33.84%, as Incidence rate ratio (IRR) 0.969 (95% confidence interval [CI], 0.930–1.009); those of ACS were 20.63% and 6.45%, as IRR 3.013 (95% CI, 2.793–3.251); and those for ischemic stroke were 7.98% and 3.18%, as IRR 2.410 (95% CI, 2.156–2.694). As compared with the comparison cohort, hemodialysis patients with COPD was associated with multivariate-adjusted hazard ratios of 1.050 (95% CI, 0.969–1.137) for death, 1.183 (95% CI, 1.041–1.345) for ACS, and 1.217 (95% CI, 1.013–1.463) for ischemic stroke after adjusting comorbid disorders and drugs prescription during follow up. Conclusion: Hemodialysis patients with COPD are associated with increased cardiovascular risks but not all-cause of mortality.

[10] The discovery that the mechanism of action of FTY720 occurs via S1PR modulation[11] spurred interest in immunological functions of S1P signalling. Later studies demonstrated amelioration of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, with low-dose FTY720,[12] which has since been approved as a first-line oral agent for treatment of relapsing–remitting multiple sclerosis.[13-15] The pharmacology and biology of FTY720 are covered in great depth by other reviews.[16, 17] Studies to characterize the mechanisms underlying the induction of lymphopenia by FTY720 paved the

way to better buy Deforolimus understanding of the basic biological principles of lymphocyte circulation and revealed the importance of S1P1 in this process[4] (Fig. 1a). Using fetal liver from S1pr1−/− embryos to create bone marrow chimeric mice, Matloubian, et al. demonstrated that egress of lymphocytes from thymus and secondary lymphoid organs did not occur in the absence of S1P signalling, establishing

a requirement for S1P–S1P1 interaction in regulating lymphocyte egress. Additional FK228 nmr studies established that S1P1 expression was temporally regulated during T-cell development, culminating in high expression by mature single-positive CD4 or CD8 thymocytes and that conditional deletion of S1pr1 in T cells alone was sufficient to block their egress from the thymus. As S1P1 provides a critical chemotactic cue, and levels of S1P are high in the blood and lymph and low in most tissues,[7] it was postulated that this

‘S1P gradient’ would play a role in lymphocyte egress. Indeed, disruption of the S1P gradient by 2-acetyl-4-tetrahydroxyimidazole, an inhibitor of the S1P degradative enzyme S1P lyase, led to lymphopenia and blocked T-cell egress from the thymus.[18] This effect was mediated by increases in tissue concentrations of S1P and S1P-mediated down-regulation of surface S1P1, so impairing chemotactic responses.[18] Studies using conditional deletion of the S1P biosynthetic enzymes, sphingosine kinases 1 and 2 (Sphk1/2) demonstrated that an almost complete loss of S1P in the blood and lymph correlated with high cell surface expression Adenosine of S1P1 on naive T cells in the circulation. Lymphopenia was also evident, but infusion of S1P (in the form of S1P-producing erythrocytes) into sphingosine kinase-deficient mice, led to the release of lymphocytes into the blood concomitant with decreased cell surface expression of S1P1.[19] Mutant mice that express an internalization-defective S1P1 that is signalling competent have delayed lymphopenia kinetics in response to FTY720 or 2-acetyl-4-tetrahydroxyimidazole treatment, further supporting the premise that cell surface residency of S1P1 is a primary determinant of lymphocyte egress.[20] These observations combine to create a model whereby high concentrations of ligand lead to S1P1 surface down-regulation and so to non-responsiveness to S1P chemotactic cues.

Finally, these biochemical markers can only be useful to patients if interpreted in the context of the clinical history and GSK126 cell line examination and a consideration of what management is appropriate for the specific patient, and if a cardiovascular therapy that is effective in this population is identified or developed. MAR is supported by an NHMRC Training

Fellowship (628902). Key messages regarding troponin testing in dialysis patients with acute cardiac symptoms: The pre-test probability of cardiovascular disease is high “
“Date written: June 2007 Final submission: October 2008 a.  The best designed randomised controlled trial demonstrates no advantage of donor-specific transfusions (DSTs) in graft survival at 2 years or in the incidence of acute rejection. (Level II evidence) (Suggestions are based on Level III and IV evidence) The high risk BGJ398 solubility dmso of sensitisation does not justify the routine use of DSTs (Level III evidence) No recommendation. Maximising graft survival from living donors is a major goal in transplantation given the mismatch between the number of available donors and the ever-increasing number of recipients. Blood transfusion from living donors to the recipient prior to kidney transplantation

was introduced several decades ago with the aim of improving graft outcome. However, with reduced acute rejection rates associated with newer immunosuppressive agents and recombinant erythropoietin use, DST is rarely practised. Nevertheless, modulating the immune response

to the donor and inducing ‘pseudo-tolerance’ without having to rely heavily on immunosuppression continues to be a goal of transplantation medicine. When reviewing the evidence, it needs to be recognized that there may be fundamental differences between early reports of DST use and the DST of today; red blood cells are now washed and are essentially free of white blood cells – which may have been an important mediator of the observed effects. Furthermore, more recent literature suggests that the beneficial effect of tolerance develops only if the blood donor and recipient have one HLA haplotype or at least one HLA-B and one HLA-DR Adenosine antigen in common.1 Many of the studies reviewed below do not specify these details. The purpose of these guidelines is to review the evidence on DST in living kidney donation (LKD) and to provide recommendations on when and whether its use is warranted. Databases searched: MeSH terms and text words for kidney transplantation and living donor were combined with MeSH terms and text words for blood transfusion. The search was carried out in Medline (1966 – September Week 2, 2006). The Cochrane Renal Group Trials Register was also searched for trials not indexed in Medline. Date of search: 26 September 2006.

92 Moreover, polymorphisms in not only STAT3, but also in IL23R

and JAK2 loci, correlate with Crohn’s disease.93–95 Therefore, appropriate activation of the STAT proteins is clearly required for the development of a healthy immune response. Interestingly, several studies show abnormal expression of SOCS proteins in autoimmune diseases. In particular, SOCS1 mRNA is elevated in patients who present with systemic lupus erythematosus96 and rheumatoid arthritis,97 and single nucleotide polymorphisms in SOCS1 are associated with multiple sclerosis98 and coeliac disease.99 All of these autoimmune pathologies are characterized by increased IL-17 secretion, which would be consistent with the fact that SOCS1 promotes the development of Th17 cells. Compellingly, selleck inhibitor the correlation between SOCS3 expression and the severity of atopy is also apparent in patients. Markedly buy PXD101 elevated SOCS3 expression is observed in skin samples from patients suffering from severe atopic dermatitis (AD) when compared with individuals with normal skin or with the Th1-mediated condition psoriasis.100 Furthermore, specific haplotypes of the SOCS3 gene have been linked with AD in two independent Swedish childhood cohorts

and SOCS3 mRNA is more highly expressed in AD skin.101 The detection of elevated SOCS3 expression in peripheral T cells and in AD skin may be of particular relevance because the SOCS3 gene is located on chromosome 17q25, one of the established AD genetic loci.102 Similarly, SOCS3 expression in T cells positively correlates with the severity of asthma and AD,33 whereas elevated SOCS3 mRNA levels and polymorphisms within second the SOCS3 locus are found in patients with AD.101 Asthmatics also present with polymorphisms within the SOCS1 promoter, consistent with the fact that SOCS3 and SOCS1 regulate Th2 differentiation.103

The correlation between elevated SOCS1 expression and asthma severity in patients suggests that SOCS1 may inhibit IFN-γ-dependent Th1 differentiation, thereby enhancing Th2-mediated pathology.104 Of note, disruption of SOCS2 expression increases murine susceptibility to atopy but whether this is of relevance in patients has yet to be determined.59 Taken together, these different studies confirm the importance of SOCS proteins in the regulation of human pathogenic immune responses. Clearly, both STATs and SOCS are key regulators of lineage commitment and collaborate to tightly regulate CD4+ T-cell polarization. As with STATs, SOCS often exert opposing effects and may cross-regulate one another,59,61,105,106 and although murine null models exemplify this cross-compensation, this may well reflect reality because SOCS proteins are differentially expressed in individual CD4+ lineages.

“
“Here, we tested the hypothesis that

glial responses via the production of cytokines such as transforming growth factor-beta 1 (TGFβ1) and tumour necrosis factor alpha (TNFα), which play important roles in neurodegenerative diseases, are correlated with the severity of congenital hydrocephalus in the hyh mouse model. We also searched for evidence of this association in human cases of primary hydrocephalus. Hyh mice, which exhibit either severe or compensated long-lasting forms of hydrocephalus, were examined and compared with wild-type mice. TGFβ1, TNFα and TNFαR1 mRNA levels were quantified using real-time PCR. TNFα and TNFαR1 were immunolocalized in the brain tissues of hyh mice and four hydrocephalic human foetuses relative to astroglial and microglial reactions. The TGFβ1 mRNA levels were not significantly different between hyh mice exhibiting severe or compensated hydrocephalus and normal Idasanutlin mice. In contrast, severely hydrocephalic mice exhibited four- and two-fold increases in the mean levels of TNFα and TNFαR1, respectively, Bortezomib cost compared with normal mice. In the hyh mouse, TNFα and TNFαR1 immunoreactivity was preferentially detected in astrocytes that form a particular periventricular reaction characteristic of hydrocephalus. However, these proteins were rarely detected in microglia, which did not appear to be activated.

TNFα immunoreactivity was also detected in the glial reaction in the small group of human foetuses exhibiting hydrocephalus that were examined. In the hyh mouse model of congenital hydrocephalus, TNFα and

TNFαR1 appear to be associated with the severity of the disease, probably mediating the astrocyte reaction, neurodegenerative processes and ischaemia. “
“Frontotemporal lobar degeneration (FTLD) is classified mainly into FTLD-tau and FTLD-TDP according to the protein present within inclusion bodies. While such a classification implies only a single type of protein should be present, recent studies have demonstrated dual tau and TDP-43 proteinopathy can occur, particularly in inherited FTLD. We therefore investigated 33 patients with FTLD-tau (including 9 with PRKD3 MAPT mutation) for TDP-43 pathological changes, and 45 patients with FTLD-TDP (including 12 with hexanucleotide expansion in C9ORF72 and 12 with GRN mutation), and 23 patients with motor neurone disease (3 with hexanucleotide expansion in C9ORF72), for tauopathy. TDP-43 pathological changes, of the kind seen in many elderly individuals with Alzheimer’s disease, were seen in only two FTLD-tau cases – a 70-year-old male with exon 10 + 13 mutation in MAPT, and a 73-year-old female with corticobasal degeneration. Such changes were considered to be secondary and probably reflective of advanced age. Conversely, there was generally only scant tau pathology, usually only within hippocampus and/or entorhinal cortex, in most patients with FTLD-TDP or MND.

They could additionally damage myocardial tissue, because MHC class I proteins

disappeared in the central infarction sites, whereas their expression was conserved, but weaker in the surrounding peri-necrotic zones of the MI 1 week after an acute coronary event when compared to myocardial tissue sections of persons who died 5 weeks after an acute coronary event. It ICG-001 ic50 suggests susceptibility of peri-infarction zones for NK cell killing mediated by cytotoxic mediators. GNLY+ CD3+ cells and rarely GNLY+ CD56+ cells reach the apoptotic APAF-1+ cardiomyocytes in the border infiltration zone of persons who died 1 week after the acute coronary event and could participate in the apoptosis of these cells. Accordingly, apoptotic single-stranded DNA–positive cells were found in the border zones and granulation tissue cells in the infarct region by Akasaka et al. [7]. But, it is unlikely that GNLY+ cells cause significant cardiomyocytes apoptosis because of their small

numbers. In addition, later after the MI, the APAF-1+ apoptotic myocardial cells are found without close contact with GNLY+ cells, suggesting implementation of GNLY-independent mechanism of cellular loss. A formation of apoptosome after the binding of APAF-1 protein with cytochrome C could induce caspase 9 dimerization and autocatalysis [32]. Indeed, apoptotic markers (caspase 3 and apoptotic bodies) are present in the surviving zone of the heart, remote from the infarct region, as early as day 1 after MI and persist for up to 1 month

[3, 33]. Additionally, many learn more on day 7 after an acute coronary event, the significant increase in the percentage of peripheral blood GNLY+ NK cells enables GNLY-mediated K-562 apoptosis, as the mechanism attributed to perforin-mediated cytotoxicity [31]. GNLY probably accesses the K562 target cell cytoplasm through perforin pores or by other mechanisms that involve sublytic perforin concentrations in agreement with Lettau et al. [18], because an additive effect between GNLY- and perforin-mediated cytotoxicity has not been found. This suggests that they probably use the same mechanism for entering cells. On day 14, in patients with NSTEMI, GNLY expression, as well as perforin expression [31], in all peripheral blood lymphocyte subpopulations was the lowest and it was reflected in negligible NK cell apoptotic activity against K-562 cells. The lower percentage of GNLY-positive NK cells in patients with NSTEMI on day 21 as compared to day 7, correlated well with mostly perforin-mediated NK cell killing as a redundant apoptotic mechanism [27]. At the end of a 1-month rehabilitation period in patients with NSTEMI, we again found significant participation of GNLY in K562 apoptosis as a result of restored GNLY expression in peripheral blood NK cells.

Despite the importance of TEC to the immune system, fundamental questions regarding their differentiation, turnover, and function throughout life remain unanswered. This knowledge gap is largely due to technical difficulties in isolating, quantifying, and purifying this rare cell type. Here, we describe methods for the enzymatic digestion of the thymus to obtain single-cell suspensions of TEC, their analysis by flow cytometry, enrichment using

magnetic beads, and purification for a variety of downstream applications. © 2014 by John Wiley & Sons, Inc. “
“Kawasaki disease (KD) is an acute vasculitis syndrome of unknown aetiology in children. The administration of Candida cell wall antigens induced KD-like coronary vasculitis in mice. However, the responses of KD patients to Candida cell wall antigen are unknown. In this study, we examined the response of KD patients to β-glucan (BG), one of the Selleck X-396 major fungal cell wall antigens, by measuring the anti-BG titre. In KD patients, the anti-C. albicans cell wall BG titre was higher than that in normal children. The anti-BG titre was also higher in KD patients compared to children who find more served as control subjects. The efficacy of intravenous immunoglobulin (IVIG)

therapy in KD is well established. We categorized the KD patients into three groups according to the therapeutic efficacy of intravenous immunoglobulin (IVIG) and compared the anti-BG titre among these groups. Anti-BG titres were similar in the control group and the non-responsive group. In the fully responsive group, the anti-BG titre showed higher values

than those in the normal children. This study demonstrated clinically that KD patients have high antibody titres to Candida cell wall BG, and suggested the involvement of Candida cell wall BG in the pathogenesis of KD. The relationship between IVIG therapy and anti-BG titre was also Cediranib (AZD2171) shown. These results provide valuable insights into the therapy and diagnosis of KD. “
“Citation Rozner AE, Dambaeva SV, Drenzek JG, Durning M, Golos TG. Modulation of cytokine and chemokine secretions in rhesus monkey trophoblast co-culture with decidual but not peripheral blood monocyte–derived macrophages. Am J Reprod Immunol 2011; 66: 115–127 Problem  Decidual macrophages are thought to promote pregnancy success, in part through interactions with invading trophoblast cells in hemochorial placentation. However, the factors that constitute this regulatory cross talk are not well understood. Method of study  Rhesus monkey decidual and peripheral blood–derived macrophages were co-cultured with primary Rhesus trophoblasts. Macrophage functions including cell-surface marker expression, antigen uptake and processing, in vitro migration, and cytokine and chemokine secretions were evaluated.

Idiopathic thrombocytopenia purpura (ITP), a disease associated with low platelet counts and mucocutaneous bleeding, is driven primarily by antibodies. In a historical experiment, Harrington demonstrated, by injecting himself with the blood from an ITP patient, that a serum factor

was responsible for ITP [2]. Within a few hours after the administration of the blood from the ITP patient, Harrington reported a rapid drop in his blood platelet counts [2]. Patients with antibody deficiencies are highly susceptible to microbial infections [3], and paradoxically are also more prone to ITP or autoimmune hemolytic anemia than the general population [4]. find more These diseases are caused by autoantibodies directed against platelets or RBCs, respectively, and can be treated by the administration of high doses of intravenous immunoglobulin (IVIg).

IVIg is increasingly used to treat autoimmune diseases, yet the suppression of such diseases by the injection of serum Ig remains poorly understood. STA-9090 concentration In this issue of the European Journal of Immunology, Schwab et al. [5] report important new findings on the molecular pathways involved in neutralizing the pathogenic functions of autoantibodies by such Ig preparations. IVIg was initially developed for the treatment of immunodeficiencies. The first treatment of an autoimmune disease by IVIg was reported in 1981 by Imbach et al. [6], who observed that administration of large doses of IVIgs led to a rapid rise in platelet counts in children with ITP. IVIg consists of polyclonal preparations of human Igs obtained by pooling plasma from large numbers (usually more than 3000) of donors. These preparations consist predominantly of intact IgG with a distribution of isotype subclasses corresponding to that found in normal serum [7]. IVIg also contains small amounts of IgA, and IgM, as well as traces

of cytokines [8]. The utilization of IVIg to treat immunodeficiencies or autoimmune disorders has increased steadily Thalidomide over recent years, and its worldwide consumption nearly tripled during the period 1992–2004 [9]. Application of IVIg in the clinic is currently limited by availability and elevated production costs. There is therefore considerable interest in identifying the active components mediating the anti-inflammatory effects of IVIg because this might guide the development of alternatives suitable for broader utilization. There is evidence that both the antibody variable region (Fab fragments) and the constant crystalizable domain (Fc fragment) can contribute to the anti-inflammatory effects of IVIg [10, 11]. Nonetheless, the beneficial effects of IVIg could be recapitulated in children with acute ITP using only the Fc fragments from IgG antibodies [11].