Viruses and bacteria use chimerism and horizontal gene transfer to pick up genes from their hosts, and adopting cytokine genes Temsirolimus is perfectly possible; many pathogens contain host genes such as cytokines [118, 119]. A strictly instructive model for phenotype decisions would require hard-coded programs that deal with all pathogens in the appropriate way. Consequently, a single mistake in Th-cell phenotype would jeopardize survival of

the host if Th-cell phenotype decision-making relied exclusively on instruction. Given the fact that organisms are constantly combatting fast(er)-evolving pathogens, it is hard to see how this model could lead to durable protection of the host. Furthermore, the concept of immunological memory seems redundant in a system relying largely on instructive signals – making adaptive immune responses little different from the innate immunity. Indeed, how can a correct

Th-cell phenotype be chosen? Due to stochasticity, all possible Th-cell phenotypes tend to be generated in a response to any type of infection, and instructive signals seem to be easily subverted by pathogens in a number of ways. Generating a proper response in the presence of such inconsistent signals is challenging. One solution to this conundrum is to utilize the effectiveness of an immune response to choose the correct phenotype, that is, ‘success-driven feedback [120]. This hypothesis states that Th cells have some way find more Tau-protein kinase to judge their success in combatting a pathogen. A success-driven

feedback mechanism would allow incorrect phenotypes to be shut down, while correct phenotypes are propagated. Such a mechanism would resemble quorum sensing that limits Th-cell expansion as discussed earlier, but then in a phenotype-specific manner. In that sense, the success-driven feedback concept is a specific type of immune homoeostasis [121, 122]. Although success-driven feedback is an attractive concept, there is little evidence for it and its mechanisms remain to be elucidated. The most obvious parameter for evaluation success is antigen clearance. If the antigen is cleared, the response is successful; if not, this particular phenotype is apparently not appropriate and should be shut down. There are several potential mechanisms that could effectuate this type of feedback. For instance, IL10 expression by cells that are activated for longer periods of time could be one such mechanism (Figure 3). If IL10 expression by Th cells were in some way antigen dependent, this could function as a success-driven feedback, although this would require IL10 to function in a mostly autocrine fashion.

The candidacidal mechanism of 3M-003-activated macrophages was investigated. MMA was used to test for 3M-003 induction of inducible nitric oxide synthase (iNOS) and its effect on candidacidal activity. We found that MMA at 0.2 mM significantly reduced the candidacidal activity of 3M-003 (10 and 100 μg mL−1)-activated macrophages from 40% and 44% to 28%

and 23%, respectively (P<0.05 for both) (Fig. 2b). Moreover, the candidacidal activity of IFN-γ-activated macrophages (51%) was reduced to 36% by 0.2 mM MMA. These findings were reproduced in a second experiment with 3M-003 100 μg mL−1 and IFN-γ 1000 U mL−1. These results indicate that iNOS induced by 3M-003 or IFN-γ can be inhibited by MMA, resulting in decreased killing Wnt activity of C. albicans. Monocytes had low candidacidal activity (0–10%

in various experiments), and treatment with 3M-003 did not significantly Quizartinib in vitro enhance candidacidal activity (maximum, 14%) (Fig. 3a). On the other hand, IFN-γ at 250 U mL−1 significantly (P<0.05) increased monocyte candidacidal activity to 28% (Fig. 3a). IFN-γ concentrations of 500 or 1000 U mL−1 did not prove superior to 250 mL−1. In another experiment where the challenge time was 2 h instead of 4 h, similar results were obtained, for example IFN-γ at 250 U mL−1, but not 3M-003, significantly (P<0.05) increased the candidacidal activity of monocytes compared with the candidacidal activity of monocytes cultured in CTCM. Neutrophils cultured in CTCM had significant candidacidal activity (46%). Treatment of neutrophils with 3M-003 (0.1–10 μg mL−1) did not significantly increase killing of C. albicans (51%) compared with neutrophils treated with CTCM (Fig. 3b). By contrast, neutrophils treated

with IFN-γ (1000 U mL−1) significantly (P<0.01) increased killing of C. albicans (to 82%) compared with killing by control neutrophils (Fig. 3b). Similar data were obtained at E : T of 50 : 1. In another experiment where the E : T ratio was 10 : 1, killing by control (CTCM) neutrophils (25%) was not significantly different from 22% to 32% killing by 3M-003 (1 μg mL−1)-treated neutrophils; however, killing Etomidate by IFN-γ-treated neutrophils was significantly (P<0.01) increased to 54%. When the supernatants from PBMC cultures stimulated by 3M-003 were tested for cytokines by ELISA, high levels of TNF-α and IL-12 were found (Table 1). 3M-003 at 1 μM appeared to be optimal for the production of these proinflammatory cytokines. It can be noted that IL-10 production was increased twofold above the background (Table 1). On the other hand, 3M-003 stimulation of PBMC did not induce IFN-γ production above the background (data not shown). Splenocyte preparations from macerated mouse spleens produced lower amounts of cytokines after stimulation with 3M-003 than did PBMC (data not shown).

Another effect mediated by Ab–FcR interactions is the induction of reactive oxygen and nitrogen species in macrophages, neutrophils, and other phagocytic cells. The resulting oxidative burst, mediated by these short-lived molecular species, plays an important role in the control of viruses, bacteria, and parasites 10. Ab–FcR interactions have a number of additional functions such as cell activation, the induction of cytokine production, receptor-mediated endocytosis, targeting Cell Cycle inhibitor of immune complexes for degradation, storage of immune complexes in germinal centers

of secondary lymphoid organs, and the augmentation of MHC-restricted Ag presentation. In this review, we will focus on the role TSA HDAC in vivo of these functions in immune responses against intracellular bacteria and parasites, and in invasive fungal infections. Four different classes of FcγRs have been identified

in mammals, known as FcγRI (CD64), FcγRII (CD32), FcγRIII (CD16), and FcγRIV, which bind the different IgG subclasses with varying affinity and specificity. Functionally, FcγRs can be divided into activating (FcγRI, FcγRIIA/C, FcγRIII, and FcγRIV) and inhibitory (FcγRIIB) receptors, which transmit signals via immunoreceptor tyrosine-based activation (ITAM) or inhibitory motifs (ITIM), respectively. Activating signals through ITAM-containing FcRs involve a number of kinases and ultimately lead to a large variety of effector responses in innate immune effector cells, such as oxidative burst, cytokine release, phagocytosis, ADCC, and the degranulation of mast cells. On the contrary, the inhibitory receptor FcγRIIB acts as a negative regulator of immune complex-triggered activation as it counteracts effector cell functions either triggered through activating receptors. It also plays an important role in the selection of affinity-matured B cells and the modulation of Ab production 11. Most cell types express activating as well as inhibitory

FcγRs and simultaneous engagement sets thresholds for cell activation and ensures a balanced immune response 12. In contrast to FcR-independent phagocytosis involving interactions between the cell-surface receptors and the corresponding ligands on a particulate Ag, FcR-mediated phagocytosis involves FcR activation and downstream ITAM signaling 13. The ratio of local concentrations of activating to inhibitory FcγRs recruited during phagocytosis determines whether an IgG-opsonized particle is ultimately taken up or not, and differential recruitment of FcγRs is mainly achieved by their different affinities for IgG subclasses 14. Furthermore, the density of IgG on the particle correlates with the magnitude of early FcR signals and results in an all or none response of uptake 15.

Of these, 14 were patient samples from the clinical unit with raised MCT and no apparent mastocytosis, 24 samples from patients with anaphylaxis and 13 samples from patients with mastocytosis. Five of 20 (25%) samples from the raised RF group (no prior knowledge of MCT) had raised MCT. Twenty-seven of 83 (33%) samples were RF-positive (Fig. 1). TSA HDAC purchase One of the WHO criteria for systemic mastocytosis is MCT > 20 µg/l. There were 51 of 83 patients with MCT > 20 µg/l. Five of these became MCT < 20 µg/l after HBT treatment. Toorenenbergen

et al. [6] used a value of 12% (four times the within-run CV%) to indicate any significant change in tryptase following treatment with the HBT tubes. However, in the samples with no detectable levels of RF (<9·8 IU/ml), a change in tryptase level (both positive and negative) of up to 17% (independent of baseline tryptase levels) was seen following HBT treatment. This suggested that there was a wide range of non-specific blocking taking place and/or a number of summative

errors within the analytical technique itself. A value of 17% was therefore chosen as the cut-off level above which any change was attributed to heterophile activity. Clearly, this may underestimate the true contribution of heterophilic antibodies to observed assay values. Of the samples, 14% ABT-263 cell line had false-positive MCT results – eight of 56 (14%) had raised levels pre-HBT which became normal following HBT blocking; these samples were deemed to be falsely elevated due to assay interference. Almost half the RF factor-positive patients had raised tryptase: 27 of 83 (32%) patients were RF-positive with a range of 15·3 to 4690 IU/ml; 12 of 27 (44%) RF-positive patients had raised tryptase values (>14 µg/l). Half the tryptase values in RF-positive sera showed evidence of heterophile antibody interference: 14 of 27 (52%) RF-positive patients had a decrease (>17%) in their tryptase concentration following

treatment with the HBT. In the RF-negative cohort only one sample Phloretin had >17% reduction. Of the raised tryptases in the RF-positive cohort, 57% were false positives: eight of 14 (57%) RF-positive samples had raised MCT levels (>14 µg/l) pre-HBT which became normal (<14 µg/l) post-block (false positives). Six of 14 RF-positive samples had a reduction of >17% in their MCT value but the pre- and post-tryptase values were <14 µg/l and so remained within the normal range at all times, even though there was evidence of heterophilic interference. The IgM RF concentrations were also variably reduced by up to 75% (Table 1). A significant association was observed between the presence of the IgM RF and heterophile interference. A χ2 test (Table 2) was performed and gave a value of 30·84 (P < 0·0001), suggesting a significant relationship between changes in tryptase level and the presence of RF in the patients’ serum, but clearly not all RF isotypes are bound by the HBT treatment and a perfect correlation would not be expected.

Thymus transplantation is a promising therapy for the treatment

of DiGeorge syndrome-associated immunodeficiency [16], and a recent check details report, using postnatal allograft transplantation, hinted at the role of K14+ and human cTEC-marker CDR2-positive epithelial cells in the reconstitution of the thymus allograft [17]. Certainly, the next step would be the identification of the progenitor markers in the adult thymus as this would have practical implications for human thymus transplantation and for the restoration of T-cell immunocompetence. Despite the fact that the thymus starts involution soon after birth and becomes atrophic with age [18], the adult thymic epithelium is constantly regenerated from a pool of adult progenitor cells, albeit with decreasing PF-01367338 mw efficiency [7]. Thus, the capacity for renewed thymopoiesis is not lost with aging and could be restored therapeutically [19]. Different treatment strategies with growth factors (growth hormone, IGF-1, and FGF-7), IL-7 or sex steroids have been already applied in

diverse experimental systems to improve age-related loss of thymic function (reviewed in [20]). The differentiation of thymic epithelium shares features and markers with other epithelial tissues, including skin or mammary epithelial cells [21-23]. In this respect, lineage-tracing analysis of progenitor cells from mammary epithelium with cytokeratin promoters, has revealed the existence of a K14+ multi-potent progenitor at an early embryonic stage,

whereas postnatal and adult development are ensured by K14/K5+ and K8/K18+ unipotent stem cells that differentiate into myoepithelial and luminal lineages, respectively, and are no longer maintained by Tacrolimus (FK506) rare multi-potent progenitors [24]. The shift from bipotent stem cell prevalence at embryonic stage to unipotent or compartment-specific progenitors at postnatal and adult tissues may well take place in thymus too—the rapid turnover and the capacity to regenerate after the selective ablation indicate the potency of cTEC and mTEC lineage-specific progenitors in the postnatal and adult thymus [25, 26]. The study by Baik et al. [1] raises unanswered questions, namely the persistence of embryonic bipotent TEPCs and the relation of these TEPCs to the bi- or unipotent progenitors in the adult thymus. The cTEC/mTEC marker pattern, identified here, should be useful for further isolation and then characterization of the progenitors. Finally, the bipotent TEPC (and possible cTEC lineage progenitor) specificity for CD205, an endocytic C-type lectin-like molecule with a role in the recognition of apoptotic cells for antigen uptake and processing [27] warrants further characterization. The authors thank the European Regional Fund/Archimedes Foundation and the Estonian Research Council funding IUT2–2 for their support. The authors declare no financial or commercial conflict of interest.

Several research groups are studying ICG-001 purchase donor treatment and it may be applied clinically in the near future. However, our experimental model could not be transferred directly to a cadaveric donor transplant model, because brain death of the donor has not been considered. Brain death is a strong proinflammatory event that results in the activation of several pathways [54].

However, we believe that the model could be clinically useful for those patients with living donors who require prolonged bench surgery, or for those patients included in donor pair programmes requiring a longer time of cold ischaemia. As there is no evidence of immunosuppression to donors in living donors, this issue should be debated within a bioethical framework. To our knowledge, this is one of the few studies showing evidence of a lower I/R injury with combined immunosuppressive treatment of donors using a syngeneic rat model. The use of immunosuppressive drugs administered PD0325901 to donors has attenuated

the I/R injury process and this was demonstrated by a marked necrosis and apoptosis decrease in renal tubular epithelial cells. Further studies based on this exploratory study would describe the use of immunosuppressive treatment to the donor to improve the quality of the organ to be transplanted. The authors thank Professor Dr Enrique Portiansky for his assistance in the quantification of optical densities and areas of IHC. The authors of this manuscript have no conflicts Chloroambucil of interest to disclose. “
“Secretory proteins of Mycobacterium tuberculosis are the major immunomodulators of the host immune response. Open reading frame (ORF) Rv2626c, encoding a conserved hypothetical protein eliciting a strong humoral immune response in patients with tuberculosis (TB), was shown to be up-regulated upon infection in mice under hypoxic conditions. We now show that recombinant Rv2626c protein (rRv2626c) can bind to the surface of murine macrophages and elicit the type-1 immune response, as manifested by nitric oxide (NO) secretion and expression of inducible nitric oxide synthase (iNOS). Significant induction of pro-inflammatory

cytokines [interleukin (IL)-12 and tumour necrosis factor (TNF)-α] was evident upon stimulation of murine macrophages, as well as peripheral blood mononuclear cells (PBMCs) isolated from patients with active TB disease, with rRv2626c. Stimulation with rRv2626c also enhanced the expression of costimulatory molecules such as B7-1, B7-2 and CD40 on murine macrophages. We further show that the production of NO and pro-inflammatory cytokines in response to rRv2626c is mediated by the transcription factor nuclear factor (NF)-κB, and this was further confirmed using pyrrolidine dithiocarbamate (PDTC), a specific pharmacological inhibitor of NF-κB. Rv2626c therefore appears to modulate macrophage effector functions by eliciting both innate and adaptive immune responses, suggesting its possible use as a vaccine candidate.

epidermidis

spx mutant strain. We followed the same allelic exchange strategy (Bruckner, 1997) as that used in the construction of an S. epidermidis clpP mutant strain (Wang et al., 2007). More than 2000 clones were screened, but the desired double-crossover strain in which spx is replaced by an erythromycin-resistance cassette was not found, although we indentified single-crossover strains as determined by PCR amplifying the spx bordering regions (data not shown). The attempt to construct an spx mutant stain with a high-efficiency system through pKOR1 (Bae & Schneewind, 2006) also failed (data not shown). We further used a molecular epidemiological approach to examine the existence of spx in a collection of 80 S. epidermidis (Li et al., 2009) clinical isolates. All tested strains harbor the spx gene, indicating find more the possibility that spx could be an

essential gene (data not shown). Instead, we constructed an spx antisense knockdown plasmid PQG56 coding reversed spx mRNA to downregulate the expression of Spx. In a previous study, Nakano et al. (2003a) overexpressed Spx in B. subtilis to study its regulatory functions. Because the construction of an S. epidermidis spx mutant strain failed, we attempted to overexpress Spx in S. epidermidis to study its regulatory effect on biofilm formation. Attempts to overexpress Spx in B. subtilis were at first unsuccessful due to the rapid degradation of the protein by ClpP protease. Luminespib ic50 Successful overexpression of Spx was achieved when an spx mutant allele that codes for a protease-resistant form of Spx (C-terminal mutant) was constructed

and expressed in B. subtilis (Zuber, 2004). Thus, in addition to the expression plasmid pQG54, which carries a WT spx, we constructed another expression vector (PQG55) with an altered spx allele, with a substitution from Ala and Asn codons in the C-terminal to two Asp condons to encode a mutated DOCK10 SsrA peptide, in order to avoid the SsrA peptide-tagged proteolysis by ClpXP. These three plasmids were transformed into S. epidermidis. To prevent the resistance from being degraded, we compared the expression level of Spx in strains carrying PQG53, PQG54 and PQG 55 separately. As a result, little Spx protein was detected in the vector control stain harboring PQG53 and the WT expression allele harboring PQG54, whereas Spx accumulated in the strain harboring PQG55 (Fig. 1). Biofilm formations of S. epidermidis strains harboring different plasmids were compared using semi-quantitative assays. Biofilm formation of the strain harboring pQG54 was comparable with that of the vector control strain harboring pQG53, whereas biofilm formation of the strain harboring pQG55 decreased drastically (Fig. 2). The Spx levels in these strains were examined by Western blot. The result that Spx accumulated in the strain harboring pQG55, but not in the strain harboring pQG54, indicates that Spx had a negative effect on the biofilm formation of S. epidermidis.

[1, 4, 5] Sequencing of PCR products is a very powerful method for the correct typing of dermatophytes but, unfortunately,

it is not convenient for the processing large numbers of samples.[13, 14] Real-time PCR proved valuable in the identification of dermatophytes because of its high sensitivity and rapidity, but it is costly.[10, 11] This study aimed at evaluating a MX PCR technique based on the amplification of the CHSI gene and the ITS region which are the most widely used targets in the https://www.selleckchem.com/products/r428.html molecular diagnosis of dermatophytic onychomycosis in humans.[8, 17, 21, 23] On the other hand, MX PCR was shown to be a powerful tool for the characterisation of dermatophytes when DNA extracted from clinical specimens is used.[1, 6, 7, 9, 17] We were only interested in T. rubrum and T. mentagrophytes complex because they are the most frequent among the species isolated in our region.[14, 23] In addition, previous reports on PCR assays that allow distinguishing TR and TM are very few.[9] In this study, MX PCR was applied to a collection of culture samples (standards and controls) of dermatophytes and non-dermatophytes fungi, and to nail specimens obtained from patients with dermatophytic onychomycosis previously confirmed by mycological examination. The analysis of our results showed that the specificity of the

technique was excellent as none of the non-dermatophytic fungal specimens and none of the uninfected nails yielded positive results in MX PCR. Our results PLX3397 cell line are in agreement with most previously studies.[4, 6, 7, 11, 16, 17, 25] As far as sensitivity is considered, MX PCR may be considered very satisfactory as 100% of controls and 97% of nail specimens yielded positive results. Sensitivity values reported in previous studies using different PCR methods and primers ranged between 51% and 94.8%.[1, 4, 6, 7, 11, 17, 19, 21] On the other hand, our results showed the PCR to be more sensitive than mycological examination (97% vs. 81.1%). This finding is in accordance with most previously reported studies.[5, 7, 9, 13, 19, 20, 25] In contrast, in some reports, results of PCR and mycological examination were nearly similar

in terms of sensitivity.[3, 12, 15] The threshold of DNA detection in MX PCR was 50 pg of DNA per reaction. This value is similar to that reported in Candida and Aspergillus Pyruvate dehydrogenase systemic infections.[15, 16] In contrast, it is much higher than the threshold reported in MX PCR for the detection of other non-dermatophyte fungi.[19] The limited existing genomic data on dermatophytes and the close ITS gene sequence similarity between related dermatophyte species (e.g. T. rubrum and T. violaceum on one hand, and T. mentagrophytes, T. schoenleinii and T. tonsurans on the other hand) impede designing specific primers for all known dermatophyte species. Indeed, ITS region primer pair TR was found to cross-react with T. violaceum, and TM with T. tonsurans, T. equinum and T. schoenleinii.

This work was supported by the National Institutes of Health (NIH) grant P01 AI080192-01 (to R.A.), grant R37 AI30048-17 (to R.A.), grant AHMED05GCGH0 (to R.A.), Center for HIV/AIDS Vaccine Immunology and Immunogen Discovery UM1AI100663 (to R.A.), and post-doctoral fellowship F32 A1096709-01A1 (to J.S.H.). The authors have no conflicts of interest to disclose. Crizotinib molecular weight “
“Given the ability of erythrocytes to bind immune complexes (ICs), we postulated that they can serve a dual role during inflammatory or infectious processes. Erythrocytes could restrict stimulation of macrophages by free ICs by binding

C3b-opsonized ICs via their complement receptor 1 (CR1). Conversely, IC-loaded erythrocytes could stimulate macrophages to produce proinflammatory cytokines such as tumour necrosis factor (TNF)-α. To test our hypothesis we selected 72 individuals with low, medium or high red cell

CR1 expression and determined their IC binding capacity. We tested the in vitro ability of red cells to selleck chemicals inhibit IC-mediated stimulation of TNF-α production by macrophages or to stimulate TNF-α production when loaded with ICs. Plain erythrocytes inhibited IC-induced TNF-α production by macrophages and low CR1 expressors showed the lowest inhibitory capacity. IC-loaded erythrocytes stimulated macrophages to release TNF-α, but the effect was not proportional to the CR1 level. These data support our hypothesis that erythrocytes can serve a dual role

in regulation of cytokine responses in a setting of IC formation. Our findings suggest that individuals with low CR1 expression are ill-equipped to clear ICs and prevent IC-mediated stimulation of macrophages. In addition, IC-loaded red cells in areas Tyrosine-protein kinase BLK of sluggish circulation such as in the spleen or in brain capillaries blocked by sequestered malaria-infected red cells may induce inflammation by stimulating monocytes and macrophages, the latter leading to the development of cerebral malaria. Complement receptor type 1 (CR1/CD35) is a complement regulatory protein found on primate red cells [1] and most leucocytes [2]. It functions as a co-factor in the factor I-mediated cleavage of C3b to C3bi and C3dg [3,4]. Although red cells have relatively few copies of CR1 (average 600) [5] compared to an average of 5000 on white cells [6], due to the fact that they are the most numerous cells in the bloodstream, they account for most of the CR1 mass in the body. Red cells, by virtue of their CR1, bind C3b-opsonized ICs which are removed by macrophages during passage through the liver and spleen [1,7]. ICs are formed when antibodies encounter their target antigens in the circulation. These antigens can be derived from infectious agents or from self, the latter as a result of autoimmune disorders.

The NKp30-expressing NK-cell number was lower in the presence of the viruses in each independent experiment (although not significant)

as well as after TLR7 stimulation whereas it was increased by IL-2/PHA stimulation (Fig. 1A). The expression of other activating (NKp44, NKp46, and NKG2D) and inhibitory (KIR2DL2/3) NK-cell receptors was not modified by contact with LASV or MOPV and no NK-cell proliferation was observed either (data not shown). CXCR3 is the receptor for CXC chemokines and is involved in chemotaxis. The presence of replicative or inactivated LASV and, Selleck AZD4547 to a lesser extent, MOPV, upregulated CXCR3 expression at the surface of NK cells whereas TLR7 stimulation induced a downregulation of CXCR3 (Fig. 1B). No difference in the CXCR3 mRNA level was observed between mock and infected

cultures (data not shown). Unlike PMA/ionomycin stimulation, LASV and MOPV did not induce IFN-γ gene expression by NK cells (Fig. 1C). The proportion of NK cells expressing the lytic molecule granzyme B (GrzB) was neither modified by LASV and MOPV nor by TLR stimulation, and the cytotoxic effects of NK cells on K562 targets (lacking MHC-I molecules) were also unaffected (Fig. 1D). Thus, LASV and MOPV can neither infect NK cells nor activate these cells, induce proliferation or modify their effector properties. However, the expression of CXCR3 at the surface of NK cells was increased by LASV and, to a lesser extent, by MOPV, and NKp30 also appeared

to be slightly downregulated. Nutlin-3 research buy Unlike DCs, MΦs have been reported to be activated early in infection with MOPV and, to a lesser extent, with LASV [6, 8]. In our model, DCs and MΦs were infected with LASV or MOPV and co-cultured with autologous NK cells. Cells were analyzed 3 days after to study the activation of infected APCs cocultured with NK cells and to determine whether they could mediate NK-cell activation and proliferation. As a positive control, NK cells were activated directly with IL-2/PHA and APC-mediated NK-cell activation was performed with LPS-matured DCs and MΦs. Infected DCs were not activated in the absence or presence of autologous Suplatast tosilate NK cells (data not shown). Consistent with our previous studies, the expression of CD40 and CD80 at the surface of MΦs was increased by MOPV infection only and CD86 was upregulated in the presence of both viruses (Fig. 2A). The analysis of NK/MΦ cocultures revealed an increase in the proportion of CD40-, CD80-, and CD86-expressing MΦs in the presence of both viruses. Moreover, the activation of infected MΦs was substantially improved in the presence of autologous NK cells. No change in the expression of CD69, activating (NKp30, NKp44, NKp46, and NKG2D) or inhibitory (KIR2DL2/3) NK-cell receptors and CXCR3 was observed in the presence of LASV- or MOPV-infected DCs (Fig. 2B and data not shown).