Activated B cells also infiltrate into the rheumatoid synovium [26]. In this study, we found that the frequency of CD19+IgD+CD27− naive B cells in RA patients was significantly higher than that in the HC, while

the percentages of preswitch CD19+IgD+CD27+ B memory cells in RA patients were significantly lower than that in the HC. Our findings were consistent with a previous report that showed a higher frequency of naive B cells, but lower percentages of memory B cells in patients with new-onset RA [27]. Src inhibitor This suggests that antigen stimulation may promote the redistribution of naive B cells from lymph tissues to circulation. Souto-Carneiro et al. [28] found that the percentages of circulating preswitch CD19+IgD+CD27+ memory B cells decreased in RA patients, while the frequency of preswitch CD19+IgD+CD27+ memory B and post-switch CD19+IgD−CD27+ memory B cells increased in the synovial membrane. It is possible that circulating CD19+IgD+CD27+ B cells could migrate and accumulate in the synovium of RA patients. However, a previous study has suggested that there may be an accumulation of post-switch CD19+IgD−CD27+ memory B cells, whereas the CD19+IgD+CD27+ memory B cells are reported

in RA patients with long-standing disease [29]. The disparities between our data and the results of previous learn more studies may be due to a number of factors, including varying genetic backgrounds, disease duration, Rebamipide cohort size and therapy. Activated B cells increased the expression levels of certain activation markers, such as CD86 and CD95 [30, 31]. CD86 is a critical co-stimulatory molecule for B cell activation and CD95 is

associated with apoptosis. To assess activated B cells further in RA patients, we analysed the frequency of CD86+ or CD95+ B cells and found that the percentages of CD86+CD19+ and CD95+CD19+ B cells were significantly higher in the RA patients than that in the HC, consistent with a previous report [32, 33]. These data indicated more activated B cells in RA patients. Given that CD95 is a death receptor, the higher frequency of CD95+ B cells in RA patients suggests that those activated B cells may be susceptible to spontaneous apoptosis, diminishing the total number of activated B cells in RA patients. Moreover, it is possible that the relatively higher frequency of naive B cells may stem from high differentiation of bone marrow stem cells due to the continuous loss of memory B cells, and this feedback regulation will help in maintaining B cell homeostasis in RA patients. O’Neill et al. [34] found that the expression of CD80/CD86 co-stimulatory molecules on B cells was critical for inducing autoreactive T cell activation and autoimmunity during the development of arthritis. In our study the percentages of CD86+CD19+ B cells in the RA patients were correlated positively with the DAS28 scores, suggesting that activated B cells might be major players in the pathogenesis of RA.

The clinical and immunological patterns of this unique chronic infectious disease clearly demonstrate a continuous scale of changes in histological lesions. Disease classification is defined within two poles (tuberculoid to lepromatous) with transitions between these clinical forms. While typical epithelioid

macrophages predominate at the paucibacillary tuberculoid pole of the disease, inactivated foamy macrophages predominate at the lepromatous end [1]. In lepromatous leprosy (LL), the lack of systemic inflammatory signals and corresponding local ones strongly indicates that a complex anti-inflammatory network is at work. In this regard, neuroendocrine system involvement, in conjunction with the existence of multiple suppressive pathways under the control of the innate and adaptive immune Opaganib datasheet response, has been reported [2-7]. We have suggested that IDO may play a role in a hitherto unknown suppressive mechanism in leprosy [6]. It has also been reported that accumulated oxidized host phospholipids in lepromatous macrophages downregulate the innate immune response [8]. Foamy macrophages seem to sustain intracellular mycobacteria in a physiological state similar to a nonreplicating

vegetative one [9]. In this context, Montoya et al. [10] demonstrated that lepromatous macrophages SRT1720 exhibit a high expression of the cysteine-rich superfamily scavenger receptor (SRCR), which increases the phagocytic capacity of macrophages and leads to a reduction in bactericidal activity. CD163, a receptor only expressed in monocytes and macrophages, is a member of the class B SRCR superfamily with immunomodulatory medroxyprogesterone properties. Likewise, CD163 is a receptor of hemoglobin (Hb) and hemoglobin–haptoglobin (Hp, Hb–Hp) complexes. The metabolites resulting from intracellular Hb degradation exhibit potent antioxidative

and anti-inflammatory effects. It has been described that the binding of Hb to CD163 induces the release of IL-10 and other anti-inflammatory mediators from macrophages in vivo [11]. It has also been demonstrated that IL-10 enhances CD163 expression by creating a feedback arm of regulation [12, 13] and that the CD163 levels in plasma inversely correlate with the expression of CD163 in blood monocytes [14]. In addition, increased CD163 shedding seems to be associated with the immunosuppressive control of inflammation [15]. The role of CD163 as a bacterial sensor has also been proposed, raising the possibility that a different extracellular domain in this receptor is responsible for triggering proinflammatory cytokines, in contrast to what has been considered its traditional endocytic role [16]. Recent reports have demonstrated ongoing interaction between CD163 and IDO in bone marrow-derived dendritic cells (BMDCs), perhaps indicating that different CD163 signals lead to IDO expression [17].

Further comparison of thyroid function in patients with different genotypes showed that the frequency of the G-allele was significantly higher among hypothyroid patients (P < 0·05). Interestingly, among 25 hypothyroid patients NVP-AUY922 chemical structure with both elevated thyroid peroxidase antibody and thyroglobulin antibody concentrations, 14 presented with the AG genotype and 11 with the GG genotype, while no AA genotype was found in this group. Evaluating the independent effect of different genetic and non-genetic factors on thyroid function with multiple regression analysis, we established a strong contribution

of thyroid peroxidase antibodies (P < 0·0002) and an insignificant contribution of thyroglobulin antibodies, CT60 genotype, age, family history and smoking. After elimination of the thyroid autoantibody effect, the contribution of the CT60 genotype reached the level of significance (P < 0·05). This study of patients with two different forms of thyroid

autoimmune disease, HT and PPT, demonstrates a strong contribution of CT60 CTLA-4 SNP to thyroid autoantibody production. The significant increase of thyroid peroxidase antibody concentration and slight increase of thyroglobulin antibody concentration found in patients carrying the polymorphous CT60 CTLA-4 allele is consistent with our previous report on HT patients, where exon 1 and promoter CTLA-4 polymorphisms were studied [6]. Exon 1 SNP has also been shown to influence higher thyroid learn more autoantibody production in Graves’ disease [9]. Nevertheless, no data are available in the literature on association of TCL CT60 SNP with thyroid autoantibody production. Similarly, the data on genetic susceptibility in PPT are scarce in spite of the relatively high prevalence of 8% in the postpartum period [10]. A few earlier reports suggested an association with human leucocyte antigen (HLA) status, which was not confirmed afterwards [11]. The first report referring to the CTLA-4 gene in PPT

was published a decade ago, describing no association between PPT and microsatellite CTLA-4 polymorphism [12]. The second report was our recent case–control study, where we were not able to demonstrate a link between CT60 CTLA-4 SNP and PPT [13]. However, the strong influence of thyroid peroxidase antibodies on development, thyroid function and prognosis of PPT was reported, as patients with higher thyroid peroxidase antibodies in the postpartum period developed PPT more often, presented with hypothyroidism more often and developed permanent hypothyroidism more often [2,11,14,15]. The current study also showed that thyroid peroxidase antibody concentrations were significantly higher in the hypothyroid form of PPT and the frequency of patients positive for thyroid autoantibodies was also significantly higher among hypothyroid patients.

The published data also support the hypothesis that increased VLA-4 will allow for improved in vivo function and improved ability to accumulate within the granuloma. One could propose therefore that the level of nitric oxide within the lesional site can dramatically impact the local protective and immunopathological response by reducing accumulation of specific subsets of activated effector cells and by altering the potency of the lymphocytes with regard to accumulation within the lesion and cytokine production. By demonstrating the differential impact of nitric oxide on distinct buy Lumacaftor functional subsets of cells, we have identified a mechanism whereby

protection and pathology in mycobacterial disease are modulated by nitric oxide. The development of inflammation during mycobacterial infection is an important component of the disease process and is actively modulated by CD4+ T cells. Herein, we demonstrate that within the pool of effector T cells, there is an activated T-cell subset that is more HSP phosphorylation susceptible to the regulatory factors active within the granuloma. Defining the relative protective and pathological role of this activated T-cell subset (CD4+T-bet+CD69loVLA4hi) will allow for improved vaccination and immunotherapeutic intervention. All mice were bred

at the Trudeau Institute and were treated according to National Institutes of Health and Trudeau Institute Animal Care and Use Committee guidelines. All animal protocols used herein were approved by the Trudeau Institute Animal Care and Use Committee. C57BL/6 and B6.129P2-nos2tm1Lau (nos2−/−) (originally purchased from JAX Mice, Maine) Selleckchem Sorafenib were used in these experiments. Mice were infected with M. avium 25291 (ATTC) at a dose of 1 × 106 cfu by lateral tail vein injection. The level of bacteria in specific organs was determined by homogenizing the organs and plating on agar and counting colonies [48, 49]. Some infected WT mice were treated with aminoguanidine hemisulfate (Sigma-Aldrich) at 2.5 g/100 mL in the drinking water for defined periods of time; control mice received water without drug.

Liver sections were placed in 10% neutral-buffered formalin, blocked in paraffin, processed for light microscopy, and stained with hematoxylin and eosin to provide cell structure. For immunofluorescence staining, liver sections were harvested into cold HBSS and 3–4 mm sections cut with a scalpel. Sections were placed in 4% low-melt agarose (Lonza Seaplaque Agarose, Fisher Scientific) in HBSS. The solidified gel containing sections of liver was then sectioned using a vibrating microtome cooled to 4°C (Leica VT1000) and 200-micron sections were collected into 12-well plates containing HBSS, FcBlock, 5% normal mouse serum. Sections were stained with fluorescently labeled antibodies, anti-CD4 PE (RM4–5), anti-CD8 PE (clone 53–6.

Apoptosis of inflammatory cells and their phagocytic clearance by phagocytes are critical for the resolution of inflammation.7 LPS triggers inflammatory responses by inducing inflammatory cytokine

production and thus influences the rate of inflammatory cell apoptosis.9,21 In this study, we focused on the role of LPS and LPS-induced inflammatory modulators in regulating phagocytosis of apoptotic cells by macrophages. We demonstrated that LPS significantly inhibited phagocytosis of apoptotic neutrophils by mouse peritoneal macrophages via LPS-driven induction of TNF-α and suppression of Gas6 production. Macrophage phagocytosis prevents apoptotic cells from undergoing secondary necrosis and releasing https://www.selleckchem.com/products/AZD2281(Olaparib).html their histotoxic contents. As different macrophage subpopulations exhibit different phagocytic features, so macrophages at different stages of maturity.11,12,22 A recent study reported that LPS inhibits the ability of human monocyte-derived macrophages to ingest apoptotic neutrophils.13 In agreement with this report, the present study showed that LPS significantly inhibited phagocytosis of apoptotic neutrophils by mouse peritoneal macrophages. However, we found that the LPS inhibition of phagocytosis occurred Apitolisib at an earlier time-point (8 hr) after LPS treatment than that (96 hr) reported in the previous study.13 This discrepancy may be explained by the different macrophage

types used in the two studies. We have provided evidence for that LPS-mediated induction of TNF-α was partially responsible for LPS inhibition of phagocytosis. TNF-α can be rapidly released

by macrophages after stimulation with LPS, and is one of the most abundant inflammatory factors in inflamed sites.23 TNF-α is actively involved in the development of both chronic inflammation and autoimmune disease.24 Consequently, the blockade of TNF-α activity, using a neutralizing antibody or a soluble TNF-α receptor, has been shown to have a therapeutic benefit in the treatment of chronic inflammatory diseases.25 However, the mechanisms underlying the role of TNF-α in the development of chronic inflammation remain to be clarified. In the present study, we have provided convincing evidence that LPS-induced TNF-α inhibits the phagocytosis of apoptotic neutrophils by mouse peritoneal macrophages. This result suggests that excess TNF-α in inflamed tissue may result in inefficient removal of apoptotic cells. This would lead to secondary cell necrosis and damage of the surrounding tissue, which in turn will delay the resolution of inflammation. However, TNF-α does not sufficiently account or LPS inhibition of phagocytosis, because neutralization of TNF-α activity by antibodies did not completely reverse the LPS inhibitory effect. In addition, LPS inhibition of phagocytosis was also observed in TLR4−/− macrophages, which had no capacity to induce TNF-α.

The objective of this study was to assess whether peptidoglycan (PGN) derived from Gram-positive bacteria induces trophoblast stem (TS) cell death or alters TS cell cytokine

production. Method of study  Toll-like receptor (TLR) transcript expression was assessed by RT-PCR. Protein expression was determined by confocal microscopy or flow cytometry. 7-Aminoactinomycin D (7-AAD) staining was used to assess TS cell death. Morphological features of cell death were evaluated by transmission electron microscopy. The presence of cleaved caspase-3 and high mobility group box 1 (HMGB1) protein was examined by Western blot. Cytokine levels Ibrutinib price in cell supernatants were determined using a mouse cytokine 23-plex panel. Results  Toll-like receptor 2 and TLR4 protein was expressed from the 1-cell stage through the blastocyst stage of murine embryo development. Murine TS cells expressed TLR2 and TLR6 but not TLR1 or TLR4 RNA. Only TLR2 protein was detected at the plasma membrane of TS cells.

PGN induced TS cell death by a caspase-3-independent mechanism. The cell death pathway induced by PGN was morphologically consistent with necrosis. Finally, PGN induced HMGB1 release Deforolimus concentration and increased MIP-1β secretion while inhibiting the constitutive release of RANTES. Conclusion  Peptidoglycan-induced TS cell necrosis and the subsequent BCKDHB release of HMGB1 and MIP-1β may regulate an infection-induced inflammatory response at the maternal–fetal interface and thus may play a role in the pathogenesis of infection-associated pregnancy complications. “
“A good understanding of the immunological correlates of protective immunity is an important requirement for the development of effective vaccines against malaria. However,

this concern has received little attention even in the face of two decades of intensive vaccine research. Here, we review the immune response to blood-stage malaria, with a particular focus on the type of vaccine most likely to induce the kind of response required to give strong protection against infection. Malaria still causes serious illness and many deaths in some of the poorest countries in the world. Over 200–300 million new cases are reported each year with 1·2 million deaths, mainly of young children [1]. There is still no vaccine that confers strong protective immunity to infection. Gaps in our understanding both of putative vaccine antigens and of the nature of antimalarial immunity have held back the development of a protective vaccine. While some immunity is acquired to infection after several years of repeated exposure to malarial infection, it is never complete. Such partial immunity or naturally acquired immunity that does develop, in an age and exposure related manner, involves both antibody and cell-mediated immune responses.

The phylogenetic tree Selleckchem Ibrutinib also showed that three SLA-2-HB alleles were close to SLA-2*10es21, SLA-2*1001, SLA-2*10sk21 and SLA-2*10sm01

(Fig. 1) but far from, SLA-2*05sy01, SLA-2*0502 and SLA-2*w09pt22. However, all SLA-2 alleles were different from HLA-A2 with at least 0.336 distances. The SLA-2-HB alleles were aligned with representative rat and human MHC class I alleles and the main variable amino acids in their functional domains analyzed. The results are shown in Figure 2. In the signal peptide domain, the SLA-2-HB alleles differed from H-2K1, HLA-B15 and HLA-A2; the numbers of different amino acids were 14, 8 and 10, respectively. In the α1 and α2 domain in which the peptide-binding groove is located, SLA-2-HB retained all eight key amino acids that can bind Selleckchem Deforolimus peptides in human HLA-A2; that is Y7, Y59, Y84, T143, K146, W147, Y159 and Y171 (11). SLA-2-HB retained 14 of the 19 amino acids in the α1 and α2 domains of HLA-A2 that bind β2m. It was also found that the extracellular domain of SLA-2-HB contained three key amino acids, Gln115(Q), Asp122(D) and Glu128(E), that bind CD8 molecules (12). SLA-2-HB retained 18 of the CD8-binding amino acids at sites 199–223 of the α3 domain; seven amino acids had mutated, at 199(V/A), 207(G/S), 211(K/A), 214(S/T), 216(S/T), 220(E/D) and 222(Q/E) Comparing SLA-2-HB with H-2K1 and HLA-B15, the number of mutated amino acids was eight and six,

respectively. It has been reported that 199–205, 211 and 221 are the essential amino acid sites for binding CD8 molecules (13,14), and SLA-2-HB had mutated at 199(V/A) and 211(K/A). Compared with H-2K1, SLA-2-HB had mutated at site 211(K/A); compared with HLA-B15, the variable sites were 199(V/A) and 211(K/A). SLA-2-HB showed complete consistence with the amino acids that

bind β2m in the α3 domain of HLA-A2. SLA-2-HB displayed more variable amino acid sites with HLA-A2, H-2K1 and HLA-B-15 cytoplasmic and transmembrane domains than in other domains. The homology modeling of SLA-2-HB01 as well as SLA-2-HB02, SLA-2-HB03 and SLA-2-HB04 showed a very similar 3D structure, i.e, with two α-Helix structure and eight β-strain structure, BCKDHB which constituted an antigenic peptides groove of SLA-2 protein. Most of the 11 key variable amino acid sites were found in the antigenic peptides groove of SLA-2 protein. Among them, 73(N), 155(G), 156(E) sites were in α-helical regions while 23(F), 24(I), 95(I), 114(R), and 216(S) sites were all in β-strain regions, and only 43(A), 44(K), 50(Q), sites were outside of antigenic peptides groove of SLA-2 protein (Fig. 3). SLA-1, SLA-2 and SLA-3 are the three functional loci of the SLA-I molecule.

Using TEM, the number of neutrophils and MCs were counted on two intestinal grids for each infected fish. The number of each type of granulocyte was determined in an area measuring 1800 μm2 in close proximity to the point of cestode attachment (i.e. the interface region) and in a second area measuring 1800 μm2 at a distance of approximately 200 μm from the site of cestode attachment. Prior to analysis, the Gaussian distributions (i.e. normality) find more and the homogeneity of variances of the data were assessed; the data were subsequently square

root transformed to meet these assumptions. Using the software package Statistica 7, anovas (Statistica 7, Praha, Cech Republic) were performed to detect significant differences in the number of granulocytes determined from the uninfected and infected tench and in the abundance of neutrophils and MCs at the point of cestode attachment and then at a distance of 200 μm away. Bonferroni post hoc tests and a P < 0·01 level of

significance were used throughout. Fourteen (60·9%) of the 23 tench were parasitized with M. wageneri; identity of the cestodes was confirmed using morphology and standard taxonomic keys. The intensity of infection ranged from 3 to 130 worms per host (39·5 ± 47·7, mean ± SD). The anterior part of the intestine bore the heaviest infections with the vast majority of tapeworms still attached with their scolices embedded within the intestinal wall (Figure 1a). Upon dissection in situ, M. wageneri were noticed in groups of variable numbers and in some portion of the host intestine the presence of more than one foci was frequent (Figure 1a). In tench gut wall, at the site Pyruvate dehydrogenase lipoamide kinase isozyme 1 of M. wageneri attachment, CHIR-99021 in vitro a raised plaque-like formation or round nodule encircled the firmly attached scolex (Figure 1b). Histological sections revealed that specimen of M. wageneri had penetrated by means

of bluntly truncated scolex deep into the mucosa and submucosa (Figure 2a, b) and in some instances into the muscularis layer (Figure 2c). This parasite anchoring system provided a secure attachment to the tench intestine (Figures 1a, b and 2b). At the site of attachment, the tapeworms induced necrosis, degeneration and/or loss of the epithelium (Figure 2a). M. wageneri elicited intense immune cells and fibroblasts proliferation within the thickness of the tench gut wall (Figure 2b, c). Diffuse hyperplastic inflammation was noticed in tench with few M. wageneri as well as in those harbouring numerous tapeworms (Figure 2a–c). Within the submucosa layer, beneath the point of M. wageneri scolex insertion, numerous granulocytes (e.g. neutrophils, MCs) (Figure 2d), rodlet cells (Figure 2e) and collagenous fibres were observed. Degranulation of the granulocytes, which was visible by light microscopy (Figure 2d), was common in the submucosa. Parasitized intestines were determined to have a significantly higher number of granulocytes than those that were uninfected (Table 1; anova, P < 0·01).

2 × 105 cfu/mouse L. monocytogenes i.v. In conclusion, we found that that JWS 833 induces greater immune responses than LGG both in vitro and in vivo. Moreover, administration of Tyrosine Kinase Inhibitor Library ic50 E. faecium JWS

833, induces immune responses as well as reducing viable counts of L. monocytogenes in the livers of mice and increases the survival rate of mice after L. monocytogenes infection. Further studies are needed to validate using JWS 833 as a feed supplement to provide immune-enhancing effects in poultry and protection against bacterial infections. This work was supported by a research grant from Chungbuk National University in 2011. No authors have a relationship with any company whose product figures in the submitted manuscript, nor do they have any interest in manufacturing any product described in this manuscript. “
“Groups of 5-month-old lambs which had been trickle infected with Teladorsagia circumcincta for 8 weeks then drenched, and worm-free control lambs were challenged

Deforolimus clinical trial with 50 000 T. circumcincta L3s. From 10 days later fewer parasites were recovered from the previously infected sheep, and secondary cellular and humoral responses were observed in the gastric lymph. Increases in CD4+ and CD25+ T lymphoblast traffic on day 3, followed by CD21+ and IgA+ lymphoblasts on day 5, and an increase in total and parasite specific IgA concentrations peaking on day 6 were observed in previously infected lambs. Similar peaks in lymphoblast output were not observed until days 10–12 in the control lambs. This data was highly comparable with that obtained recently from yearling sheep subjected to an identical infection-challenge regime, and contrasted with that obtained from similar experiments in the 1980s when 41/2-month-old previously infected lambs were more susceptible to and had much weaker immune responses to challenge than 10-month-old sheep. The fact that 40% fewer larvae were given during the trickle infection regime in the four recent trials is offered as an explanation for this difference. Teladorsagia circumcincta is an abomasal nematode parasite of sheep, and is a serious problem in temperate areas both in terms of animal welfare

and economic loss. Current Methisazone control methods rely on the use of anthelmintic drugs; however, resistance to these drugs is wide-spread and increasing, and isolates of T. circumcincta have been identified which display phenotypic resistance to several classes of anthelmintic (1–3). Sheep which have been exposed to Teladorsagia can acquire protective immunity, so vaccination is viewed as a possible alternative method of control. Both cellular and humoral responses have been associated with protective immunity. Previously infected adult sheep undergo a local blast cell response in the first few days after challenge infection, and these cells adoptively transferred partial immunity to genetically identical parasite naïve recipients (4–6).

However, upon incubation of viable immature DC with apoptotic DC followed by LPS treatment, only

20–25% of viable immature DC become CD86+, which is in fact similar to the levels seen in viable immature DC without any LPS treatment (Fig. 4B and C). Furthermore, incubation of viable immature DC with apoptotic splenocytes also resulted in the suppression of LPS-induced subsequent DC maturation. However, the extent of immunosuppression MAPK inhibitor induced by apoptotic splenocytes was not as potent as apoptotic DC (Fig. 4B and C). These results indicate that uptake of apoptotic DC by viable immature DC prevents subsequent upregulation of CD86 in response to LPS. In the absence of inflammatory stimuli, viable immature DC do not produce any IL-12. However, in response to LPS, approximately 22% of cells become IL-12+ (Fig. 4D and E). Similarly, viable immature DC incubated with necrotic DC followed by treatment with LPS show similar proportion of IL-12+ DC. In contrast, viable DC incubated with apoptotic splenocytes followed by LPS treatment showed a slight reduction in IL-12 production, as only 8–11% of the cells became IL-12+. However, viable immature DC incubated with apoptotic DC followed by treatment with LPS failed to induce IL-12, as only 1–2% of DC become IL-12+ (Fig. 4D and E). The uptake of apoptotic

DC by viable immature DC is critically important for the suppression of CD86 upregulation, and IL-12 buy Ku-0059436 induction in response to LPS for no suppression is observed in response to LPS if apoptotic DC and viable DC are separated in culture via transwell (data not shown). In addition to IL-12, DC maturation is also characterized by the upregulation of Smoothened other inflammatory cytokines. In order to assess the effects of apoptotic or necrotic DC uptake by viable immature DC on induction of inflammatory cytokines in response to LPS, we looked at the mRNA expression levels of inflammatory cytokines, including IL-1β (Fig. 5A), IL-6 (Fig. 5B), TNF-α (Fig. 5C), IL-12p35 (Fig. 5D) and IL-12p40 (Fig. 5E). These inflammatory cytokines are expressed at very low levels in viable immature

DC at basal levels. However, in response to LPS, there is massive and rapid induction of these cytokines at mRNA levels (Fig. 5A–E). However, incubation of viable immature DC with apoptotic DC but not necrotic DC suppressed induction of the aforementioned inflammatory cytokines in response to LPS. These findings collectively indicate that the specific uptake of apoptotic DC converts viable immature DC into tolerogenic DC. Next, we looked at the ability of viable DC to prime OVA-specific T-cell proliferation upon apoptotic DC uptake (Fig. 5F). Viable immature DC were incubated with apoptotic or necrotic DC and then pulsed with OVA in the presence of LPS. Then, these were cultured with naïve T cells to assess their ability to induce OVA-specific T-cell proliferation.