7-Aminoactinomycin D (7-AAD), anti-human leucocyte antigen DR (HLA-DR)-allophycocyanin (APC), CD3-peridinin chlorophyll (PerCP), CD4-PerCP, CD45RO-APC, CD56-FITC, p-S6-Pacific blue, CD3-horizon V500, CD8-Pacific blue,

CD25-PE and CD14-PE mAb were obtained from BD Biosciences (Erembodegem, Belgium). CD19-PE, CD45RA-FITC, CD38-FITC, CD45-FITC, CD80-FITC and CD123-PE mAb were purchased from Beckman Coulter (Immunotech, Marseille, France) and CD40-APC, CD45RA-PE, immunoglobulin (Ig)G1-FITC, IgG2a-FITC, CD8-APC, anti-IFN-γ-PECy7, IL-17-PE, CD4-APC-eFluor780, anti-FoxP3-APC (clone: 236A/E7), functional grade IgG2a isotype control mAb and IFN-α, IL-6, IL-10 and TNF-α enzyme-linked immunosorbent assay (ELISA) Romidepsin chemical structure kits were obtained from eBiosciences

(Vienna, Austria). CD86-APC, anti-HLA-ABC-FITC, anti-IL-10-APC and IgG1-APC were obtained from Biolegend (London, UK). cytosine–phosphate–dinucleotide (CpG) A oligodeoxynucleotide buy GS-1101 (ODN) 2336 and loxoribine (LOX) were purchased from InVivogen (San Diego, CA, USA). Anti-LAG3-PE and IL-17 ELISA kit were purchased from R&D Systems (Abingdon, UK). IFN-γ, IL-4 and CXCL-10 (IP-10) ELISA kits and 5,6 carboxy-succinimidyl-fluorescein ester (CFSE) were purchased from Life Technologies (Bleiswijk, the Netherlands). Neutralizing IFN-αReceptor2 mAb was obtained from Merck Millipore (Amsterdam, the Netherlands). Rabbit anti-phosphorylated S6 antibody was from Cell Signaling Technology (Danvers, MA, USA) and mouse-anti-β-actin

antibody from SantaCruz Technology Tyrosine-protein kinase BLK (Heidelberg, Germany). Granulocyte–macrophage colony-stimulating factor (GM-CSF) was a kind gift of Schering-Plough (Kenilworth, NJ, USA) and neutralizing CD80 mAb B7-24 [21] was a kind gift of M. de Boer (Tanox Pharma BV, Amsterdam, the Netherlands), phytohaemagglutinin (PHA) was obtained from Murex (Paris, France). Rapamycin was purchased from Merck (Schiphol-Rijk, the Netherlands) and phosphatase and tensin homologue (PTEN)-inhibitor VO-OHpic trihydrate, PMA, ionomycin and brefeldin A from Sigma-Aldrich (St Louis, MO, USA). The Fix&perm cell permeabilization kit was obtained from An der Grub (Vienna, Austria). PBMC were isolated from buffy coats of healthy blood-bank donors by Ficoll density centrifugation. For isolation of PDC, PBMC were incubated with anti-BDCA4-PE mAb, washed and incubated with anti-PE microbeads. After a second wash, PDC were isolated in two rounds of separation over MS columns. Alternatively, BDCA-4-labelled PDC were isolated by enrichment over an LS-column, followed by flow cytometric sorting on a FacsAria II cellsorter. The purity of isolated PDC, as determined by staining with anti-BDCA2-FITC and flow cytometry, was > 94%. T cells were purified from PBMC by negative selection upon labelling with PE-conjugated antibodies against BDCA1, CD14, CD19, CD56 and CD123 as well as CD15 and CD235 microbeads followed by incubation with anti-PE microbeads.

[18, 31] Studies have demonstrated

dynamic changes in the ultrastructural features of the cell wall during morphogenic transformation to germ tubes, and have shown that the cell wall of germ tubes possesses www.selleckchem.com/products/INCB18424.html stratification comparable to that of the blastospore wall.[32] Other studies have shown internally collapsed cells with an intact cell wall leaving ‘ghosts-like’ cells and deflated Candida cells following exposure to subcidal concentrations of nystatin.[23] Therefore, it is not surprising that nystatin-induced changes in the cell wall structure of C. dubliniensis isolates would affect active budding and multiplication, thus suppressing its growth resulting in a PAFE of nearly 2 h in addition to subduing its adhesion to BEC as well as GT formation even after a brief exposure to nystatin. Microbial structures that contribute to the CSH include outer membrane protein, Selleckchem Dabrafenib lipoprotein, phospholipid, lipopolysaccharide and fimbriae.[28] Thus, drugs that modify these structural features have shown to reduce the CSH of microbes.[29] In the case of C. albicans, it has been shown that the CSH correlates with the concentration of fibrils in the exterior layer of the cell wall. As C. dubliniensis isolates are phenotypically similar to C. albicans isolates, the observed suppression of CSH elicited by nystatin (approximately 35% reduction) on

C. dubliniensis though very much less than the other two adhesion attributes observed in the current investigation (mean reduction of 34.81% for CSH vs. 74.45% for adhesion to BEC and 95.92% for GT formation), it too may be related to the aforementioned pharmacodynamics of the nystatin on the cell wall of C. dubliniensis.[18, 31] Therefore, it is reasonable to speculate that by affecting the cell wall structure, nystatin may be capable of suppressing the CSH of this Candida species. Analysis of the variation between the impact that nystatin had on the three pathogenic attributes revealed

that there was a significant positive relationship between the Glycogen branching enzyme suppressive effect of the drug on adhesion to BEC and GT formation by C. dublinienis isolates (P = 0.046), whereas the effect elicited by nystatin on CSH did not have a positive relationship with the clampdown of adhesion to BEC and GT formation. Relative CSH is considered as a non-biological physical force related to adhesion whereas adhesion to BEC and GT formation by Candida are direct biological traits pertaining to adhesion. Hence, this difference in the relationship on the impact of nystatin on adhesion attributes of C. dubliniensis, which has not been documented hitherto, may be due to the difference in biological and non-biological forces involved in the adhesion process. Notwithstanding these differences, nystain was capable of suppressing both biological and non-biological adhesion attributes of C. dubliniensis as seen in this study.

Serum or antibody diluted in 50 μl 5% non-fat milk containing 0.05% Tween-20 was added and incubated 1 h at

37 °C. For competition ELISA, serum or antibody premixed with serial concentrations of D-mannose (Sunshine Biotechnology, Nanjing, China) in 50 μl 5% non-fat Pirfenidone chemical structure milk containing 0.05% Tween-20 was added and incubated 1 hour at 37 °C. The plates were then washed five times and incubated with AP-conjugated goat anti-human antibody (Zymed, San Diego, CA, USA) in 50 μl 5% non-fat milk containing 0.05% Tween-20 for 1 h at 37 °C. Colour reaction was developed by adding 50 μl pNPP (Sigma), and the optical density at 405 nm was determined. Antibody depletion analysis was performed as described previously [19] with modifications. Briefly, 0.66 g cyanogens bromide-activated Sepharose 4B beads (GE

Healthcare) were hydrated and washed extensively with 100 ml 1 mm HCl, then with 30 ml coupling buffer (0.1 m NaHCO3, 0.5 m NaCl, pH 8.3) and resuspended in 2.3 ml coupling buffer to form ~50% slurry. The slurry was divided into four equal portions Everolimus and incubated overnight at 4 °C with coupling buffer only (blank), BSA (1 mg), gp120AE (0.5 mg) or V1V2BAL (0.5 mg), respectively. The beads were then washed extensively in coupling buffer and blocked in 0.1 m Tris-HCl (pH 8) for 3 h at room temperature. Any uncoupled proteins were removed by washing first in 0.1 m sodium Pregnenolone acetate-0.5 m NaCl (pH 4) and then in Tris-salt buffer (0.1 m Tris-HCl, .5 m NaCl, pH 8). 150 μl serum samples were diluted in Tris-salt buffer and added to sterile filtration

tubes containing ~200 μl 50% slurry for overnight incubation at 4 °C. The treated serum was recollected by low-speed centrifugation (100 g, 3 min). A panel of 80 sera, collected from HIV-1-infected Chinese patients, were initially analysed for their neutralizing activities against a minipanel of pseudoviruses consisting of five different isolates belonging to four subtypes (Table 2). The five isolates exhibited differential sensitivities to neutralization by a panel of well-characterized monoclonal antibodies (mAbs) (Table 2), with CNE40 the most sensitive and CNE55 the most resistant isolates, respectively. Virus pseudotyped with the envelope of Moloney murine leukaemia virus (MuLV) was used as a negative control for non-specific neutralization. Because some of the patients received HAART therapy, the MuLV enveloped pseudovirus would also serve as an indicator for the residual drug activity in the sera. Only the sera with neutralization activity against HIV-1 pseudoviruses but not MuLV (ID50 < 20) were chosen for further analysis. Serum 29, which showed HIV-1 neutralizing activity and moderate inhibitory activity against MuLV, was also chosen because the purified IgG (CNIgG29) showed no effect on MuLV infection, but still retained its neutralizing activity against HIV-1 pseudoviruses.

This case presentation will discuss the journey of a female patient from her initial admission to the paediatric renal unit at age ten, her transition to the adult transplant unit and return to

renal replacement therapy (RRT) under the care of the adult renal unit. Jane was KPT-330 purchase admitted to the paediatric renal unit with nephrotic syndrome associated with microscopic haematuria, proteinuria, hypertension and hypoalbuminaemia. A renal biopsy two weeks later revealed sclerosed glomeruli which confirmed the diagnosis of FSGS. Her renal function deteriorated over the next twelve months and despite second and third line therapies she commenced RRT. Twelve months later she received a renal transplant from her mother which Cobimetinib was complicated by the recurrence of the disease within forty eight hours. She was treated with

plasmapheresis initially three times a week. Gradually the frequency was reduced according to her proteinuria. Plasmapheresis was finally ceased twelve months post transplant and she maintained good graft function.Jane managed to complete her secondary school education and achieved results that enabled her to commence her higher education in general nurse training. During her first year of training she was transitioned to the care of the adult transplant unit at nineteen years of age marking the next phase of her journey. She enjoyed another two years of good renal function before the recurrence of proteinuria. Plasmapheresis was commenced and frequency of treatment was managed according to her proteinuria. Jane completed her general nurse training and had secured a graduate nurse position when her renal function deteriorated further. Unfortunately, Jane had to face the next phase of her journey, to recommence RRT. Conclusion: The management of FSGS is extremely challenging. However, effective management

by the specialist medical and nursing staff, along with the support of the multidisciplinary team, allowed Jane to have treatment choices. Despite starting RRT, the team supported Jane on her choice of modality, increasing her independence and maintaining her social, family and Tau-protein kinase working life. It certainly was a rewarding experience caring for Jane on her journey from childhood to adulthood. ISHIZUKA KIYONOBU1, HARITA YUTAKA2, KAJIHO YUKO2, TSURUMI HARUKO2, ASANO TATSUO1, NISHIYAMA KEI1, SUGAWARA NORIKO1, CHIKAMOTO HIROKO1, AKIOKA YUKO1, YAMAGUCHI YUTAKA3, IGARASHI TAKASHI2, HATTORI MOTOSHI1 1Department of Pediatric Nephrology, Tokyo Women’s Medical University, School of Medicine, Tokyo, Japan; 2Department of Pediatrics, Graduate School of Medicine, University of Tokyo, Tokyo, Japan; 3Yamaguchi’s Pathology Laboratory, Matsudo, Chiba, Japan Introduction: The post-transplant recurrence of FSGS occurs about 30%, and impact on the graft survival.

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, 5-Fluoracil mw 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 Opaganib datasheet 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 DCLK1 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.

This knowledge is stored in antigen-specific helper T cells with a particular phenotype that is characterized by the production of a specific set of effector selleck products cytokines. Upon re-encounter of the same antigen, be it food items, airborne particles or invading pathogens, the host readily knows how to respond and will have a large number of effector cells with a correct phenotype in its repertoire to mount the most appropriate response. Lifelong immunity therefore also harbours a qualitative – non-antigen-related – component, being the Th-cell phenotype of response or effector cytokine that is generated

against a pathogen. Given the importance of helper T-cell phenotypes for an effective immune response, it is striking to notice the amount of heterogeneity that is generated during the induction of Th cells. Interactions within the microenvironment and feedback in time allow for error correction and ensure that an appropriate response is raised. Furthermore, plasticity allows for Th

cell to be corrected even when a suboptimal phenotype has been induced initially. selleck chemicals Th cells receive signals from pathogens, the local tissue environment and the innate immune system that provides cues as to the phenotype that is required. Success-driven feedback that promotes appropriate responses would allow the Th cell to correctly choose its phenotype, but there is little direct proof for this hypothesis. Spatial segregation of Th responses is a key requirement for this model to work. In addition to Th cells, several other lymphocyte subsets have been reported to have similar properties. Generally speaking, these cells lack the exquisite antigen specificity as Th cells, but are capable of producing cytokines. For instance, gamma–delta T cells are less specific than normal Th (alpha–beta) cells, but do produce regulating cytokines.

Cytokine-producing NK and NKT cells are considered to be innate immune cells, but display a number of adaptive-like characteristics such as memory formation. Furthermore, innate-type lymphoid cells (ILCs) do not have T-cell receptors, but do appear to produce some of the regulating cytokines that are secreted by particular Miconazole Th-cell phenotypes. It is important that the role of these other lymphocyte subsets in immunity will be further elucidated. Deep sequencing can now be used to perform cell lineage tracing and can be combined with measuring cytokine expression. Recent deep sequencing data suggest that different T cells of the same clone, that is, those carrying the same TCR, may adopt different phenotypes [131]. A significant proportion of TCR sequences shared between Th1, Th2 and Treg phenotypes have been found, possibly reflecting the stochastic nature of Th-cell phenotype development.

31–33 Interestingly, ICCs in the lamina propria respond to ATP but not to muscarinic agonist carbachol, MK 1775 while ICCs in the detrusor respond to carbachol via M3 receptor, indicating a parasympathetic control of ICCs in the detrusor.34 This implies the two types of ICCs have different functional

roles in the bladder physiology. Spontaneous electrical activity and Ca2+-transients in the ICCs and close structural connections with nerves and SMCs26,35 have suggested that the ICCs may be pacemaking cells of SCs in the bladder. Indeed, the c-Kit tyrosine kinase inhibitor imatinib mesylate inhibited SCs.36,37 However, the frequency of spontaneous Ca2+-transients differed between the ICCs and neighboring SMCs.38 This evidence contradicts the notion that ICCs in the bladder function as pacemakers. ICCs in the detrusor are positive for cyclooxygenase XL765 datasheet related to prostaglandins synthesis,39,40 and a recent study showed that ICCs in the detrusor have numerous vesicles, indicating a secretory function.41 Therefore, ICCs

may control the SMC activity by releasing a modulator. This is an attractive hypothesis. There are at least three factors that may contribute to changes in the SCs due to SCI or BOO: myogenic alterations, local mediators in the detrusor and urotheliogenic modulation (Table 1). SMCs have spontaneous electrical and contractile activity. However, electrical coupling is normally limited to some neighboring cells, and action potentials may spread through gap junctional intercellular communication.42 In BOO, cell-to-cell communication between primary cultured SMCs of bladders stained with a fluorescent dye was enhanced in SMCs from rats with BOO compared with those from control rats.43 This enhancement was inhibited by a gap-junction inhibitor. Enhanced cell-to-cell communication may, therefore, contribute to the enhanced SCs associated with BOO. The expression of

connexin 43 gap junctions between SMCs is increased in the human bladder with DO mainly due to SCI.44 This implies that intercellular communication between SMCs is enhanced and may result in enhanced SCs in SCI. Alterations in ion channel activity may be involved in the generation of enhanced SCs pentoxifylline in BOO. Downregulation of large and small conductance calcium-activated potassium channels and the TREK-1 potassium channel, and upregulation of calcium-activated chloride channels may cause enhanced SCs.45–47 However, there have been contradictory findings, namely, upregulated expression of potassium channels has also been identified in bladders with BOO.22 The reason for this contradiction is unknown. Further studies of alterations to potassium channels are required. There is an intracellular signal transduction mechanism that can increase the contractile ability of SMCs, that is, calcium sensitization that involves the rhoA/rho-kinase pathway.48 The expression of rhoA and rho-kinase was upregulated in obstructed rat bladders.

Although the relation of elicited play to verbal IQ and its constituent subtests fell short of statistical significance, elicited play predicted poorer verbal working memory on the Digit Span test, confirming that this measure of the development of symbolic play competence in infancy may provide Selleckchem ICG-001 an early indicator of verbal working memory ability or early

executive function. The relation of symbolic play in infancy to FASD diagnosis at 5 years was examined using analysis of variance (Table 7). Whereas spontaneous play was unrelated to diagnosis, mean elicited play levels were lower for infants subsequently diagnosed with FAS/PFAS and also for the nonsyndromal heavily exposed infants when contrasted

to the abstainers/light drinkers. Post hoc tests showed that elicited play scores click here were lower for both the FAS/PFAS (p < .01) and other heavy exposed (p < .025) infants compared with abstainers/light drinkers. This study confirms the association between fetal alcohol exposure and elicited play in this heavily exposed Cape-Colored population that was first reported in a moderately exposed, inner city African American cohort in Detroit. In both the Cape Town and Detroit cohorts, the observed relation of prenatal alcohol exposure to spontaneous play was attributable to being reared in a less optimal social environment. In contrast, in both cohorts the association with elicited play remained significant after controlling for these influences, BTK inhibitor indicating an impact of prenatal alcohol that is independent of the adverse effects associated with being raised

in a less optimal social environment. The effect of prenatal alcohol exposure on elicited play suggests that this exposure is associated with a delay in the development of competence as the infant proceeds through the stages of mastering symbolic play. Alternatively, prenatal alcohol exposure may interfere specifically with the child’s ability to model his/her behavior to that demonstrated by the examiner, a capacity that plays an important role throughout early cognitive development. The replication of these findings in a sample of children whose ethnic and sociocultural background differs markedly from the original Detroit cohort and the distinct effects of alcohol exposure and environment on these two forms of symbolic play attest to the robustness of these effects. These data also demonstrate that the social environment plays a critical role in the rate at which the infant progresses through the stages of both performance and underlying competence in mastering symbolic play, as indicated by both the spontaneous and elicited play measures. Bradley et al. (1989) distinguish between process and status environmental factors in relation to mental development.

Haemodialysis, including

anticoagulation, is prescribed by dialysis doctors but delivered by dialysis nurses. The main agents used in clinical practice for anticoagulation during haemodialysis are unfractionated heparin (UF heparin) and low-molecular-weight heparin (LMWH). LMWH has a number of potential advantages, apart from cost. One of the most serious complications of the use of any form of heparin is heparin-induced thrombocytopaenia (HIT) Type II, which occurs more commonly with UF heparin than LMWH. HIT Type II Selleckchem Opaganib risks severe morbidity and mortality and is challenging to treat successfully in both the acute and chronic phase. In HIT Type II anticoagulation must be delivered without heparin. A wide array of newer anticoagulants are becoming progressively available, each with unique advantages and disadvantages. In maintenance haemodialysis patients with an increased risk of bleeding, a ‘no heparin’ dialysis may be undertaken, or regional anticoagulation considered. Because this aspect of dialysis is so important to the safe and effective delivery of haemodialysis therapy, dialysis clinicians need to review and update their

knowledge of dialysis anticoagulation on a regular basis. The coagulation cascade is complex, multiply redundant and includes intricate checks and balances. While the complexity of the coagulation cascade has been well studied, most schemas simplify the cascade into two arms – the intrinsic pathway and the extrinsic pathway, meeting at factor X which is activated to Xa to

trigger the subsequent activation of prothrombin (factor II) to thrombin (factor PI3K inhibitor IIa), leading to the formation of fibrin from fibrinogen in the final common pathway.1 The intrinsic pathway is activated by damaged or negatively charged surfaces and the accumulation of kininogen and kallikrein. The activated partial thromboplastin time (APTT) tends to reflect changes in the intrinsic pathway. The extrinsic pathway is triggered by trauma or injury, which releases tissue factor. The extrinsic pathway is measured by the prothrombin test. Haemodialysis involves the circulation of whole blood through a dialysis circuit and artificial kidney (dialyser) both of which have the tendency to activate coagulation pathways. The dialyser is generally constructed of synthetic microfibres with narrow lumen, lacking endothelial Quisqualic acid lining and experiencing disordered flow – including both shear and turbulence. Factors that determine the thrombogenicity of different dialysis membranes include chemical composition, charge, ability to adhere or activate circulating cellular elements (including platelets) and other characteristics which activate thrombotic pathways.2 Studies suggest that cuprophane membranes may be more thrombogenic than polyacrylonitrile, which is more thrombogenic than polysulphone membranes and haemophan, with the least thrombogenic possibly being polyamide.

2). At this point, the infection is established systemically and comes under immunological control click here in Fiebig Stage IV. It remains under control until accumulated damage to lymphoid architecture leads to failure of lymphocyte homeostasis and AIDS. Now that the key immunological and virological milestones during HIV acquisition and post-infection control have been laid out, the evidence implicating Fc-mediated effector function in protection in each of these phases will be considered. Although acquisition must occur first for there to be post-infection control, the discussion will begin with post-infection control because it provides the earliest and

the most comprehensive indication that Fc-mediated effector function contributes to protective

immunity to HIV. Details of Fc-receptor expression on various effector populations and binding to distinct IgG subclasses will not be discussed except in the context of specific examples because several excellent reviews deal with these subjects.[47-49] Instead, the primary focus will be on the evidence that Fc-mediated effector function contributes buy 3-deazaneplanocin A to blocking acquisition or post-infection control of viraemia. The first point at which Fc-mediated effector function might contribute to post-infection control is around day 8 post-T0 when immune complexes of HIV with IgM and IgG appear in the circulation.[29] The coincident appearance of IgM and IgG antibodies in immune complexes so early after infection is surprising. Either immunoglobulin class switching is occurring rapidly or the immune complexes are between virions and naturally occurring ‘innate’ antibodies specific for HIV.[50] Regardless of how the antibodies arise, there is evidence that naturally occurring IgM can neutralize

HIV, although this does not require Fc-mediated effector function.[50] There is also evidence that both neutralizing and non-neutralizing IgG can inhibit infection of macrophages (Mph) and immature monocyte-derived Pyruvate dehydrogenase dendritic cells by an Fc-receptor dependent mechanism.[51-53] Inhibition of macrophage infection was mediated by FcγR1,[51, 52] whereas inhibition of immature monocyte-derived dendritic cell infection was mediated by FcγRIIa.[53] It is not clear the degree to which this inhibition involves phagocytosis (reviewed in refs [54, 55]), but phagocytosis has been implicated indirectly in the passive protection of rhesus macaques against a vaginal challenge with SHIV162p3.[17] It is possible that it is responsible for the disappearance of virion–antibody complexes from the circulation around day 20 post-T0. If so, it will occur at systemic sites because HIV has spread to secondary lymphoid tissues by this time (Fig. 3).