brasiliensis, sets of mice from each study group were sacrificed see more at different times. After total RNA extraction from the NI-MG, ISSI-MG, CI-MG, and NbI-MG foot tissue samples, RT-PCR was performed to amplify fragments of the mRNA corresponding to the receptors, using the mRNA for β-actin as a control. All photographs were processed digitally to enhance their quality. In Fig. 1, the band intensities of the amplified fragments are shown. The intensity of the NI-MG band was considered to be the constitutive basal level for each receptor (T0). The intensity of the bands relative to that of β-actin was constant for all tested tissues at all different

times. The density of the band corresponding to the expression of TLR2 was more intense than that of the baseline band after 2 h. The maximum intensity was observed at 4 h, after which a slight decrease was observed; it then remained constant for the subsequent time points. The density of the band corresponding to the expression of

TLR4 remained similar to the baseline level after Belinostat cell line 2 and 4 h, but after 8 h, it showed decreasing intensity for the rest of the study. Figure 2 shows the clinical features of three representative times in the evolution of experimental actinomycetoma. A few minutes after inoculation with N. brasiliensis, a slight subcutaneous swelling was observed in the right foot pad (Fig. 2a, arrow). At 20 days PI, a large area of induration with notable erythema

had developed (Fig. 2b). At 6 months PI, numerous abscesses were observed under the skin and some sinus tracts extended to the surface, resulting in a necrotic area (Fig. 2c, arrow). In Fig. 3, the analysis of the densitometry values obtained for the intensity of the TLR2 and TLR4 bands in the three mouse groups is shown. Figure 3a shows that a significant increase in TLR2 expression was observed in the NbI-MG with respect to the baseline value (33.87±5.92 ng) at all assessed times, with the peak of expression at 4 h PI (73.84±11.82 ng). In the ISSI-MG (Fig. 3b), TLR2 expression decreased Morin Hydrate significantly at 2 h PI and returned to the baseline level after 4 h. In the CI-MG (Fig. 3c), the expression of TLR2 decreased significantly at 2, 4, and 8 h PI relative to healthy individuals; at subsequent times, the values showed a tendency to increase towards the baseline level. TLR4 showed high constitutive expression (93.49±20.7 ng). In the NbI-MG (Fig. 3d), the expression of this receptor showed a gradual decrease PI, with the lowest value occurring at 50 days PI (20.59±18.3 ng). A significant difference from the baseline levels was found at all times after 8 h PI. In the ISSI-MG (Fig. 3e), a nonsignificant decrease was observed 2 h PI, after which the values showed a tendency to return to the baseline level. In the CI-MG (Fig. 3f), TLR4 expression showed a pattern similar to that of TLR2 expression.

Rather, previous investigations have been largely restricted to endpoint susceptibility determinations in dispersed, pure cultures or have inferred effects from individuals with defined HDP deficiencies (Dale & Fredericks, 2005). The aim of the current investigation therefore was to evaluate the effect of representatives of the four classes of HDPs (HNP 1, HNP 2, hβD 1, hβD 2, hβD 3, His 5, His 8 and LL37), selected on the basis their in situ predominance, using a previously validated in vitro plaque ecosystem (Ledder & McBain, 2011). Since nascent plaque communities are arguably the dominant mode of bacterial growth in the mouth (Marsh & Martin, 1999) and

are more amenable to compositional modification than mature plaques (Pham selleck inhibitor et al.,

2006; Madhwani & McBain, 2011), salivary ecosystems were developed upon hydroxyapatite surfaces in the presence of various peptides. These were applied singly and in various combinations, and effects on consortial composition and bacterial aggregation, which is reportedly an important process in plaque development (Kolenbrander et al., 1989; Palmer et al., 2004), were assessed. Chemicals and formulated bacteriological media were obtained from Sigma (Dorset, UK) and Oxoid (Basingstoke, UK), respectively. Hydoxyapatite discs used for the establishment of in vitro plaques were obtained from Clarkson Chromatography Inc. (Philadelphia, PA). This was used to support oral bacteria in nutritional BEZ235 mw conditions similar to human saliva. Composition was as follows (g L−1 in distilled water): mucin (porcine type II), 2.5; tryptone, 2.0; bacteriological peptone, 2.0; yeast

extract, 1.0; NaCl, 0.35; KCl, 0.2; CaCl2 0.2; cysteine hydrochloride, 0.1; haemin, 0.001; Vitamin K1, 0.0002 (McBain et al., 2003). These were set up using 2-mm (diameter) hydroxyapatite discs. Double-strength Anidulafungin (LY303366) artificial saliva (100 μL) supplemented with 0.4% sucrose was added to each well of a 96-well microtitre plate. Physiological saline or a double-strength salivary HDP in saline (concentrations detailed in Table 1; 100 μL) was added to each well. Presterilized hydroxyapatite discs were transferred aseptically to each well of the plate which was then mounted on an orbital shaker (144 oscillations min−1) for 1 h to allow conditioning of the discs. For inoculation, unstimulated saliva samples (c. 5 mL) were obtained by expectoration from a healthy human donor who had no extant periodontal disease and who had not used antibiotics for at least 1 year. The transfer of endogenous HDPs from the salivary inoculum to the growing cultures was minimized by centrifugation (2 mL) at 13 000 g for 5 min. and resuspension in physiological saline (200 μL). This resuspended pellet (10 μL per well) was then used to inoculate the HDMs.

g. CD2 or CD28, with their ligands on APCs. During antigen-specific T-cell activation, these surface receptors, along with intracellular signaling or scaffolding proteins, organize in supramolecular

activation clusters (SMACs) and form an immunological synapse 1, 2. Functionally, this immune synapse provides a stop signal on APCs for migrating T cells 3 and is important for enhancing, directing or terminating T-cell immunity 4. Since the immune synapse has an important function in T-cell MLN8237 chemical structure activation, sustained signaling, and effector functions 4, 5, it is important to elucidate whether clinically used immunosuppressive drugs interfere with immune synapse formation or stabilization. Glucocorticoids are commonly used immunosuppressants in organ transplantation or the treatment of dermatitis, arthritis, or inflammatory bowel disease. The immunosuppressive action of glucocorticoids is thought to be mainly based on the inhibition of cytokine expression and dependent on the regulation of cytoplasmic glucocorticoid receptors (GRs). Whether glucocorticoids influence costimulatory signals required for immune synapse formation and the dynamic actin rearrangement of untransformed

human T cells was so far unexplored. It has been known for a long time that the formation and stabilization of the immune synapse requires dynamic rearrangements of the actin cytoskeleton as well as costimulation 6, 7. We have recently shown that expression of the actin-bundling protein L-plastin is crucial for actin polymerization after antigen encounter, immune synapse maturation, Doxorubicin mouse and sustained T-cell signaling 5. L-plastin is post-translationally regulated by phosphorylation on Ser5 and this phosphorylation is induced in primary human T cells via costimulation, i.e. TCR/CD3 plus CD28 or CD2 8, 9. This phosphorylation facilitates the surface transport of activation-induced receptors like CD69

8. Furthermore, it was demonstrated by others that phosphorylated L-plastin has a higher affinity toward F-actin in HEK293T cells 10. Although it is known that http://www.selleck.co.jp/products/AG-014699.html expression of L-plastin is mandatory for the maturation of the immune synapse 5, the role of L-plastin phosphorylation on Ser5 in that process remained as yet unclear. Moreover, it was unknown whether commonly used immunosuppressive drugs influence the actin regulatory functions of L-plastin required for the formation of the immune synapse upon antigen encounter. Here, we demonstrate that phosphorylation of the actin-bundling protein L-plastin is crucial for the formation of a stable immune synapse and the increased F-actin content in superantigen-stimulated untransformed human T cells. Interestingly, the immunosuppressive drug dexamethasone interferes with L-plastin phosphorylation and T-cell functions that rely on L-plastin phosphorylation, such as actin polymerization and immune synapse formation.

GRP-78 is a glucose-regulated protein belonging to the HSP-70 family, which is mainly present in the endoplasmic reticulum where it mediates several cellular processes as a chaperon, including protein folding, degradation of misfolded proteins, regulation of calcium homeostatis and sensing the endoplasmic reticulum stress.[32, 37-41] Recent studies indicate that a fraction of GRP-78 is also translocated to the cell surface in many cell types,[41] wherein it acts as the receptor mediating penetration and damage of endothelial cells by Mucorales, leading to the observed angioinvasion.[32] Mice with diabetic ketoacidosis

have an increased expression of GRP-78 in sinus, lungs CCI-779 in vivo and brain, and anti-GRP-78 serum can protect such mice from mucormycosis, indicating a plausible role of GRP-78 overexpression in susceptibility of diabetics

to this disease.[32, 39] It is generally believed that distinct clinical presentations of mucormycosis are associated with specific underlying risk factors, with ROC, pulmonary, gastrointestinal and cutaneous types occur in patients with diabetes, haematological malignancies or neutropaenia, severe malnutrition, and trauma or burns respectively.[1, 4-7] However, uncontrolled diabetes has been found as the major factor in all types of mucormycosis in India except the isolated renal form, although ROC manifestation remains the most common clinical type and is significantly associated with uncontrolled diabetes.[1, 4-7, C1GALT1 20, 21] As the selleck chemicals llc majority of Indian patients have diabetes and metabolic acidosis as the major risk factors, the principal management modalities in such cases include a control of hyperglycaemia and prompt reversal of ketoacidosis, along with surgical debridement and amphotericin B therapy.[3] It is hypothesised that a decrease in diabetes-associated mucormycosis in USA in recent years may be attributed to an increased use of statins

in diabetic patients and the inhibitory action of statins against mucoralean agents.[42] Although statins are regularly prescribed in Indian patients with diabetes, no fall in the number of diabetes-associated mucormycosis cases has been reported from this country.[3] Therefore, a detailed study is required for assessing the role of statins against mucormycosis. Among the different clinical types of mucormycosis, cutaneous and rhino-cerebral types have a better survival rate due to possibility of an early diagnosis. Though majority of the Indian patients have rhino-cerebral presentation, the mortality rate of mucormycosis remains high (nearly 50%) in India.[4] This is largely due to a delay in seeking medical attention, diagnosis and therapy.[3] Apart from the common clinical types, isolated renal mucormycosis in apparently healthy hosts is being reported as a new clinical entity in India.[4-6, 43] Although the kidney is involved in nearly 22% cases of disseminated mucormycosis,[44] isolated renal mucormycosis is described rarely in literature.

Depletion of dendritic cells from CD3-activated PBMC or from unstimulated PBMC reduced cancer cell destruction by approximately 50%. It has been reported that signals from activated CD4+ T cells enable dendritic cells to instruct bystander dendritic cells to prime naïve CD4+ T cells [50, 51]. However, CD3-activated T cells could not initiate this dendritic circuit without monocytes; furthermore, monocytes were required in unstimulated PBMC cultures that were added to CD3-activated PBMC. Depletion of monocytes from CAPRI cells immediately before their coculture with cancer cells did not significantly reduce lysis. However,

depletion of dendritic cells decreased cancer cell destruction by 50% (Fig. 5A, B). This suggests that dendritic cells may provide a continuous flow of cytokines CP-690550 mouse and/or of tumour-immunogenic information by building an information bridge between cancer cells and effector T cells to maintain cancer cell destruction by T effector

cells. Supplementary professional antigen presentation by activated dendritic cells may prevent rudimentary TCR signalling by cancer cells leading to multiple immunosuppressive effects, such as default secretion of IL-10 by Th1 cells [52]. Taken together, optimal priming for cancer destruction required cell-mediated bidirectional cooperation among a cellular quartet consisting of CD14+ monocytes, CD14−CD1a+CD83+ dendritic Nintedanib (BIBF 1120) cells, CD4+ T cells and CD8+ T cells, whereas

a cellular trio comprising dendritic cells, helper T PD0325901 in vitro cells and cytotoxic T cells achieved optimal cancer cell lysis without monocytes. Carcinomas often escape from recognition by downregulating their own HLA expression [32, 33]. Increased HLA expression of cancer cells correlates with increased survival of patients [53–56]. Could CAPRI cells, which lyse HLA-restricted tumour cells, influence the HLA expression of cancer cells? Examination of CFSE-stained carcinoma cells showed that cocultured CAPRI cells did indeed increase the expression of HLA class I and class II molecules in autologous cancer cells (Fig. 3), and they most likely do so in many cancer types lysed by CAPRI cells (listed in Table 3, lysis not shown). Of particular note was the successful CAPRI cell-mediated lysis of carcinoma cells of Bowen’s disease. These intraepidermally growing carcinoma in situ cells are commonly recalcitrant to therapy because they are enveloped by fibroblasts. Less than 1% of Bowen’s cancer cells bound keratinocyte antibodies in cytospins (not shown). This cancer is an excellent example of the proposed inhibitory role of tumour stroma, as this stroma can prevent direct lysis by T cells [57].

Total Pexidartinib RNA was extracted from cells or tissues using Isogen (Nippon

Gene, Tokyo, Japan). Single-strand cDNA was synthesized using ExScript RT reagent kits (Takara, Otsu, Japan). Real-time RT–PCR was performed using an ABI PRISM 7500 Sequence Detection System (Applied Biosystems, Foster City, CA, USA), with primers described in Table 1. Amplifications were performed in duplicate with SYBR Premix Ex Taq (Takara), according to the manufacturer’s instructions. Target mRNA levels were normalized against β-actin mRNA. Bone marrow dendritic cells (BMDC) were obtained from WT or FcγRIIb-deficient mice according to the method described previously [18]. The bone marrow cells were cultured at 1 × 106 cells/ml in the presence of 20 ng/ml CHIR 99021 murine granulocyte–macrophage colony-stimulating factor (GM-CSF). The medium was replaced with a GM-CSF-containing medium on day 4 of culture. On day 6 of culture, BMDCs were collected and CD11c+ BMDCs were purified using the autoMACS system. Sensitized FcγRIIb-deficient mice were injected i.v. with 1 × 106 CD11c+ BMDCs 24 h before i.v. administration of IgG and challenged with OVA for 3 days. All results are expressed as mean ± standard deviation. A t-test was conducted

to determine differences between two groups. As measured values were not distributed normally and the sample size was small, non-parametric analysis using a Mann–Whitney U-test confirmed that differences remained significant, even if the

underlying distribution was uncertain. The P-values for significance were set at 0·05 for all tests. To estimate the effects of IVIgG on bronchial asthma, rabbit IgG was administered intravenously to the murine allergic airway inflammation model. OVA sensitization and challenge induced a substantial increase see more in total cells in BALF. This was due largely to increased eosinophil numbers, which is one of the characteristics of eosinophilic airway inflammation in bronchial asthma. Administration of 1 mg of rabbit IgG before airway challenge markedly decreased the number of total cells and eosinophils in BALF (Fig. 1a) in a dose-dependent manner. The treatment, such as the same amount of IgM or F(ab′)2, did not influence significantly the BALF cell counts, nor did administration of 1 mg of mouse IgG influence cell counts. In the IVIgG experiment after challenge, rabbit IgG administration after OVA challenge for 3 days also reduced the number of total cells and eosinophils significantly compared with PBS-treated mouse (Fig. 1b). Because 1 mg of rabbit IgG suppressed airway inflammation sufficiently, we used this dose to analyse the role of IVIgG before OVA challenge in our subsequent experiments. Plasma OVA-IgE levels were also elevated in challenged mice. This effect was suppressed by rabbit IgG administration (Fig. 1c). Next, to assess the effect of IVIgG on AHR, the relative increase of Penh in response to methacholine inhalation was evaluated.

On the other hand, in the present study, there was no significant difference

in the gB antibody-positive rate between gH-m+ and gH-m− recipients with acute rejection (Table 3), suggesting that presence of antibodies against gB is a risk factor irrespective of gH serological matching. Many studies have reported a relationship between CMV and allograft rejection FK228 order in renal transplant recipients. Previously, we reported that mismatch of gH antibody types between donors and recipients of renal transplantation in a D + /R+ setting, which probably indicates reinfection with a strain different from the original CMV strain, is associated with acute rejection after transplantation [15]. In this study, we revisited the risk of acute rejection in the same cases and found that 23 of the 27 recipients who experienced biopsy-proven acute

rejection during the 6 months follow up after transplantation had antibodies against CMV gB AD2, indicating that the presence of antibodies against the gB AD2 may be a good predictor of rejection in recipients in a D + /R+ setting. About 30–70% of CMV positive subjects have antibodies against gB AD2 [9, 17], which is one of the major epitopes for neutralizing antibodies [9, 11]. That the prevalence of antibodies against gB is similar in gH-matched and -mismatched recipients with acute rejection, suggests that the presence of gB antibodies is a risk factor, independent of mismatch of gH serotypes. Because of the limited DMXAA mw number of recipients with acute rejection, further study of a larger patient group is required to confirm this finding. Nevertheless, we postulate that immune responses against CMV gB, which our ELISA system detected, may be associated with acute rejection. Although CMV-specific cellular immunity provides protection by limiting

CMV reactivation and replication, it is plausible that acute rejection is a consequence of strong cell-mediated responses against ongoing CMV activity. Because gB is one of the significant targets for CMV-specific CD8+ and CD4+ T-cell immunity [10, 18], it would be interesting to ascertain (-)-p-Bromotetramisole Oxalate whether CMV-specific T-cell activity against CMV-gB correlates with the outcome of our ELISA findings concerning gB AD2. Endogenous CMV-gB is presented efficiently by MHC Class II molecules of endothelial, epithelial and glial cells and can promote CD4+ T-cell recognition [19]. In conclusion, this study, which reevaluated a previous study, indicates that the presence of antibodies against gB in transplantation recipients may be a good indicator of possible acute rejection. Further study are needed to evaluate the association between antibody responses against gB and cellular immune responses in renal transplant recipients. We thank all the subjects who participated in this study. This work was supported by a Grant-in-Aid for Scientific Research from the Japan Society for the Promotion of Science (No. 16591609). No authors have any conflicts of interest to declare.

Further details of the methodology, including illustrations of typical staining can be found in Alkazmi, 2004 (30). Sixty hamsters were allocated randomly to five experimental treatment groups, as shown in Table 1, and with the exception of a few values for measured parameters (see legends to figures for exact details), were CX-5461 mostly based on five animals from relevant treatment groups at each time point. Initially three groups (2, 3 and 5) were infected orally with 50 infective larvae

of A. ceylanicum on day 0 and all animals were confirmed as infected by faecal egg counts after day 17 post-infection (p.i.). Five weeks after this primary or immunizing infection, Groups 3 and 5 were treated with ivermectin to remove RAD001 concentration all the worms. Faecal egg counts carried out on days after treatment confirmed that these animals no longer passed hookworm eggs. Group 4 animals, as the challenge control group (secondary infection only), were also treated in case there was a residual effect against the subsequent infection. Groups 4 and 5 received 50L3 on day 63 of the experiment, 28 days after the anthelmintic treatment. Five hamsters from all groups were killed on days 73 and 94 of the experiment (corresponding to days 10 and

31 after the second infection), but in addition five hamsters from Group 5 (primary + secondary infections) were also culled on days 80 and 87. Group 1 animals were age and sex-matched naïve controls that provided baseline values for all parameters. Group 2 hamsters (primary continuous infection) carried worms from the original primary (immunizing) infection throughout the experiment. Group 3 animals (primary abbreviated infection) experienced an original SPTLC1 five-week primary infection that would have stimulated a potent mucosal response, and after removal of their worms provided information for comparison with

Group 5 on the extent to which parameters of the response had/had not returned to baseline values. Group 4 hamsters (secondary infection only) acted as the challenge control group, enabling comparison between primary and secondary responses. Group 5 hamsters (primary + secondary infections) were the key group, that had experienced the abbreviated primary infection, followed by 4 weeks without infection, and were then challenged. Animals were weighted weekly for 2 weeks before the initial infections and then twice weekly thereafter to enable animals suffering distress to be identified and culled. Although there was some weight loss amongst infected animals that did not exceed 10% of body weight and none were culled (data not shown). Differences between groups in worm burdens were examined using a 2-way nonparametric anova as described by Barnard et al. (31), based on Meddis (32), employing bespoke software.

B cell developmental subsets specified by the staining pattern

are indicated below each column with corresponding gates. The percentage of cells within the identified gates is shown for representative animals. FIGURE S2. Summary of data obtained for Fig. 1C and for analysis of T cell populations in the spleen thymus and lymph node. (A) Summary of data obtained for Fig. 1C in bar graph format. (B) Lymphocyte-gated cells CP-690550 ic50 prepared from WT or dnRAG1 spleen, thymus, and lymph node (LN) were analyzed for the expression of CD4 and CD8. (C) Summary of data obtained for Fig. S1B in bar graph format. Significance was determined from post-hoc analysis following one-way ANOVA (*, p<0.05; **, p<0.01; ***, p<0.005). FIGURE S3. Comparison of cell cycle status and apoptosis levels between sorted CD19+B220hi and CD19+B220lo B cells purified from WT and dnRAG1 mice. (A) Sorted CD19+B220hi and CD19+B220lo B cells purified from WT and dnRAG1 mice were incubated with Vindelov’s reagent and propidium iodide (PI) staining was analyzed by flow cytometry. The percentage of cells in the G1, S, and G2 phase of the cell cycle were determined using the ModFit software (upper panels). Statistical analysis of data obtained from n≥3 animals displayed in bar graph format (lower panels). (B) Sorted CD19+B220hi and CD19+B220lo B cells beta-catenin inhibitor purified from WT and dnRAG1 mice were incubated with Annexin V (AV)

and PI and analyzed by flow cytometry. The percentage of cells in each quadrant was determined using the FloJo software (upper panels). Statistical analysis of data obtained from n≥3 animals presented as in (A) (lower panels). Significance was determined from post-hoc analysis following one-way ANOVA (*, p<0.05; many **, p<0.01; ***, p<0.005). FIGURE S4. Flow cytometric analysis comparing surface expression levels of B220 versus CD43 on BM B cells, and AA4.1 versus B220, IgMa versus IgMb and Igκ vs Igλ on splenic B cells from WT, dnRAG1, 56Rki, and DTG mice. (A) Cells prepared from WT, dnRAG1, 56Rki, and DTG bone marrow or spleen and identified by the gating parameters shown above each row were analyzed

for the expression of B220, CD43, and AA4.1. B cell developmental subsets specified by the staining pattern are indicated below each column with corresponding gates. The percentage of cells within the identified gates is shown for representative animals. (B) Cells prepared from WT, dnRAG1, 56Rki, and DTG spleen and identified by the gating parameters shown above each row were analyzed for the expression of IgMa, IgMb, Igκ and Igλ. The percentage of cells within the identified gates is shown for representative animals. The absolute number of cells in each population is shown in the lower panel (***, p<0.005). "
“HFE, an MHC class Ib molecule that controls iron metabolism, can be directly targeted by cytotoxic TCR αβ T lymphocytes.

In both cases, CD161 expression levels appeared lower in NK cells from individuals with symptomatic HCMV infection, an effect that was not perceived when groups were compared (Fig. 1). The NKR distribution pattern associated to HCMV infection in T lymphocytes resembled only partially that observed in NK cells (Fig. 2). Overall, the absolute numbers of NKR+ T cells were increased in HCMV+ children, particularly in the congenital symptomatic group. In fact, the proportions of

NKG2C+, LILRB1+, and CD161+ T cells were significantly higher in congenitally infected than in noninfected children. In addition, NKG2A+ T cells appeared also higher in children with congenital symptomatic infection, at variance with the reduced proportions of NKG2A+ NK cells in the same group. Altogether, these results point LY294002 research buy out that marked changes in NKR distribution, particularly an increase of NKG2C+ and LILRB1+ NK cells, are associated with congenital symptomatic HCMV infection. The putative implications of the NKG2C deletion on the response to HCMV infection are uncertain. On that basis, a genotypic analysis of NKG2C was conducted in children with symptomatic (n = 15) and asymptomatic (n = 11) congenital infection, as well

as in a control group including children with postnatal infection (n Daporinad research buy = 11) and noninfected (n = 19). The homozygous NKG2C deletion was found in a single uninfected control individual. In addition, no significant differences were found between the frequencies Ketotifen of the heterozygous NKG2C+/− genotype detected in uninfected controls and children with congenital infection (42.1% versus 34.6%; p = 0.61). Altogether these results argue against a direct relation of the NKG2C deletion with the incidence of congenital HCMV infection in newborns. In line with previous reports [26, 27, 32], individual differences in NKG2C surface staining intensity were noticed (Supporting Information Fig. 1). The NKG2Cbright/intermediate expression pattern was generally

associated to HCMV infection, whereas all noninfected and ∼43% of infected children displayed a predominant NKG2Cdim phenotype. The proportions of NKG2C+ cells correlated significantly (r = 0.74; p < 0.001) with the KLR surface expression levels (MFI). The possibility that NKG2C copy number might influence the expansion of NKG2C+ cells and/or the expression levels of the receptor was addressed. To this end, the proportions and absolute numbers of NK cells bearing NKG2C, as well as its surface staining intensity, were compared after stratification for HCMV infection and the NKG2C genotype. As expected, increased proportions of NKG2C+ NK cells and higher surface levels of the KLR were detected in HCMV-positive children (Table 3); though less marked, a significant association of both parameters with the NKG2C genotype was also noticed.