Retinal microvascular changes are known to be affected by inflammatory factors [26], and may be another biologic mechanism through which diet mediates microvascular caliber.

Selleck Talazoparib Although the mechanisms underlying the above associations may not be completely understood, this data supports the vascular-protective effects of increased dietary fish, fiber, and low GI food consumption. Sedentary behavior, low levels of physical activity, and low cardiorespiratory fitness are all well-established risk factors for atherosclerosis and CVD [34]. Recent research has also shown that the adverse effects of lack of physical activity and low fitness extends to changes in microvascular structure [3,4,15,16,55]. Sedentary behavior, indicated by time spent watching TV and lower levels of physical activity, assessed via self-report, were found to be associated with retinal venular caliber [3,4,55], suggesting a possible deleterious

effect of decreased levels of physical activity and increased sedentary behavior on the microvasculature. In addition, the impact of physical activity on the retinal microvasculature was also observed in a cohort of 6-year children. In the study by Gopinath et al., children who spent more time in outdoor sporting activities had wider mean retinal arteriolar caliber [15], but those who spent more time watching TV had narrower mean retinal arteriolar HDAC inhibitor caliber. More importantly, for each hour of daily television viewing time, Thymidylate synthase similar retinal arteriolar changes are associated with a 10 mmHg increase in systolic blood pressure [15]. Recently, there is also evidence showing the relationship between higher levels of physical fitness and retinal microvascular structure [16]. Higher cardiovascular fitness, as assessed by individual anaerobic threshold, was found to be related to retinal arteriolar dilation and higher retinal

AVR [16]. Moreover, 10 weeks of exercise training was also shown to induce arteriolar dilatation in obese individuals and increased AVR in both obese and lean individuals [16]. Conflicting results were found in a study of older women with type 2 diabetes in which no training-induced improvements in retinal vessel caliber were found after 12-weeks of moderate-intensity exercise. In this cohort, however, increased retinal microvascular density, shown by increased Df was associated with increased time to exhaustion during peak exercise testing, a measure of physical fitness. Observed associations between physical activity and changes in the retinal microvasculature may provide in vivo evidence regarding the effect of physical activity on the systemic circulation. Although the exact pathophysiologic mechanisms behind these relationships is not know, recent research suggests that moderators of vascular tone, specifically NO and ADMA, may play a significant role.

In support of this hypothesis, they found that stimulation of DCs with MSU caused upregulation of p21, which is protective against p53-driven cell death in Nlrp3−/− cells, but not WT DCs. Furthermore, WT DCs

exhibited a significant increase in MSU-induced cell death, as measured by propidium iodide staining and lactate dehydrogenase release, with decreased expression of the prosurvival genes Xiap and Birc3, when compared with those in Nlrp3−/− DCs. Although the authors assert that this form of programed cell death is pyroptosis, the data do not confirm caspase-1 dependence and the lack of proinflammatory cytokines in the model precludes that label as yet. Thus, these data represent a novel mechanism by which the NLRP3 inflammasome, together with the Ibrutinib p53 pathway, restricts DNA repair and promotes cell death following oxidative and genotoxic stress. That the novel NLRP3 inflammasome

pathway described by Licandro et al. proceeds independently of IL-1β and IL-18 is intriguing considering the glut of literature on the topic asserting that proinflammatory cytokine production is the main means by which the inflammasome exerts its effector function. Although infrequent, other reports proposing noncanonical pathways for caspase-1 exist. For example, Shao et al. [17] identified glycolytic enzymes as additional substrates for caspase-1, demonstrating that caspase-1 causes a reduction in the cellular glycolytic rate during conditions of endotoxic Deforolimus mw shock or infection with Salmonella typhimurium, which contributes to pyroptosis. Of particular interest for future studies is the connection between the NLRP3 inflammasome and the tumor suppressor

BCKDHB p53, which is thought to be mutated in greater than 50% of human cancers [18]. The authors propose that the NLRP3 inflammasome and the p53 pathway might intersect at the inflammasome adaptor molecule ASC, as it has been shown to colocalize at the mitochondria with apoptosis-inducing molecule, Bax [19]. The data presented by Licandro et al., taken together with the widely accepted concept of inflammation as a hallmark of cancer [20], are certain to inspire exciting
s of investigation. Indeed, a few studies have begun to look into the relationship between NLRP3 inflammasome-driven inflammation and cancer, however the results are conflicting at present [21-25]. Further exploration into the molecular interactions between these two networks will yield a better understanding of the maintenance of homeostasis following assaults on genomic integrity. NIH grants R01 AI087630 (F.S.S.) and T32 AI007511 (S.H.) supported this work. The authors declare no financial or commercial conflict of interest. “
“The goal of this study was to investigate the phenotype and functional responsiveness of CD4+ and CD8+ T-cells in the upper reproductive tract of healthy premenopausal women.

Unused tumour samples were also minced to small pieces and cryopreserved in DMSO, like PBMC [21]. The

establishment of cell lines that divided at least 20 times was successful only with samples from patients who had not yet received chemotherapy or radiation therapy. All cell lines originated from Caucasian patients. Isolation of immune cells.  PBMC were isolated from venous blood puncture or leukapheresis samples by density gradient centrifugation as described previously [21] using lymphocyte separation medium (LSM; PAA). Immune cells were either BMN 673 molecular weight used immediately or cryopreserved and stored in the nitrogen gas phase. Isolation, cryopreservation and thawing procedures as well as the use of optimized culture conditions (38.5 °C, 6.5% CO2) have been described in detail [21]. Activation of T cells in PBMC bulk cultures: CD3 activation and CAPRI cell generation.  Both methods started with the activation of T cells in PBMC bulk cultures using the CD3 monoclonal antibody OKT3 (Orthoclone; Cilag, Sulzbach/Taunus, Germany), which

binds to signaling pathway the non-polymorphic ε-chain of the CD3 molecule, and the addition of interleukin 2 (IL-2; Proleukin; Chiron, Ratingen, Germany). CD3 antibodies were immobilized at a concentration of 1 μg/ml in 0.05 M borate buffer pH 8.6 and distributed in 50-ml tissue culture flasks (Greiner cAMP Bio-One, Frickenhausen, Germany). Coated flasks were kept at 4 °C at least overnight and washed twice with phosphate-buffered saline prior to incubation with

PBMC. PBMC were added at a concentration of 2 × 106 cells/ml in a total volume of 10 ml, and IL-2 was added within 2–12 h at a concentration of 20 U/ml. CD3-activated cells were expanded on day 4 with IL-2 (20 U/ml) and harvested on day 7 for immediate use or cryopreservation. For the generation of CAPRI cells, CD3-activated PBMC were removed from the flask after 4–6 h, washed and then cocultured in a second CD3 ‘antibody-free’ flask with an equal number of unstimulated autologous PBMC, which contained naïve/resting T cells, at a concentration of 2 × 106/ml in a total volume of 10 ml. Cells were expanded on day 1 with IL-2 (20 U/ml) and harvested on day 4. Microscopic classification, preparation of tumour target cells and quantification of cancer cell destruction using the Cr51-release assay.  Cancer cells were removed from flasks by trypsinization, resuspended in culture medium (RPMI 1640 with l-glutamine; PAA) supplemented with 10% FCS and washed twice. Cancer cells were counted and distributed in different concentrations into 96-well flat-bottom culture plates (Falcon; Becton Dickinson, Heidelberg, Germany) either for microscopic evaluation of lysis or for the Cr51-release assay.

Upon TLR stimulation, NF-κB and activator protein-1 are activated and subsequently the secretion of SEAP is promoted. THP-1 XBlue cells were stimulated with LPS 100 ng/ml or h-S100A9 20 μg/ml for 4 hr or 48 hr at 37°. Levels of SEAP were detected spectrophotometrically (optical density at 650 nm; SpectraMax340pc; Molecular Devices, Sunnyvale, CA) after 4 hr incubation of supernatants with Quanti-Blue medium (InvivoGen, Vienna, Austria).

In some experiments, THP-1 XBlue cells were treated with 50 μg/ml polymyxin B together with S100A9 Selleckchem AZD6738 or LPS at the concentration stated above. Cytokine concentration in culture supernatants was determined using a Human and Mouse inflammatory cytokine CBA kit (BD Bioscience, San Jose, CA) for simultaneous detection of six cytokines in human THP-1 cells [interleukin-1β (IL-1β), IL-6, IL-8, IL-10, IL-12p70, tumour necrosis factor-α (TNF-α)] and three cytokines in mouse BM-DC (IL-6, IL-1β, TNF-α) according to the manufacturer’s instructions. Data were acquired with a BD FACS LSRII flow cytometer (BD Bioscience). In some

experiments THP-1 cells were pre-incubated with proper inhibitors for 30 min at 37° and thereafter stimulated as indicated. Measurements of TNF-α secretion were performed as described above. The following inhibitors were Tanespimycin datasheet purchased from Merck (Darmstadt, Germany) and used at the indicated concentrations: 10 μm BAY11-7082, 1 μm SB203580, 5 μm MG132, 5 μm PD98059, 10 μm chloroquine. The final concentration of DMSO present in the cultures was < 0·05% of the total culture volume for each inhibitor. Supernatants were

collected, and nitrite content was determined as follows: cell culture supernatants or sodium nitrite standards (0–100 nm) were mixed with an equal volume of freshly prepared Griess reagent (a mixture of 0·1% (weight/volume) N-(1-naphthyl)-ethylenediamine dihydrochloride and 1% (weight/volume) sulphanilamide in 5% (volume/volume) phosphoric acid). After 30 min incubation at room temperature, the absorbance at 550 nm was measured using a plate reader (Spectramax340pc; Molecular Devices). Cells were collected and cytoplasmic/nuclear extracts were isolated as follow: cells were washed twice in TBS (50 mm Tris–HCl pH 7·4, 150 mm NaCl) and incubated for 15 min on ice Rucaparib with buffer A (10 mm HEPES pH 7·9, 10 mm KCl, 0·1 mm EDTA, 0·1 mm EGTA, 1 mm DTT, protease inhibitor cocktail Complete; Roche). Then, 1% NP-40 was added to each sample and the samples were centrifuged briefly. Supernatants were collected (cytoplasmic extract), the pellet was incubated in buffer C (20 mm HEPES pH 7·9, 400 mm NaCl, 1 mm EGTA, 1 mm EDTA, 1 mm DTT, protease inhibitor cocktail Complete), shaken vigorously for 15 min at 4° and thereafter briefly centrifuged. Supernatants were collected, divided into aliquots and stored at −80° (nuclear extract).

The results demonstrated significant differences in selected serum inflammatory mediators during the ligation phase of the study related to the time-point PD-0332991 nmr of the study and associated with ligation of teeth in two quadrants (MP) or four quadrants (D). Interestingly, the profile of inflammatory mediators at the various time-points of disease was not associated consistently with increasing disease, with only IL-6 levels demonstrating a significant increase after 6 months of periodontal disease. The results suggested that although there were variations in systemic analyte measures related to periodontitis, individual

variation in the clinical responses of the animals may have a substantial impact upon interpreting the direct link between oral disease and systemic responses. PD0325901 clinical trial Moreover, while previous studies in human periodontitis have suggested local involvement of a range of mediators, including IL-1β and TNF-α, expression of these proinflammatory response molecules were not observed in the systemic responses of the baboons to periodontal disease progression. This is consistent with differences in local versus systemic cytokine/chemokine response profiles observed with this disease in humans [13]. Therefore, we evaluated changes in the inflammatory mediators through the 6-month ligation in subsets of the animals based upon clinical presentation

at baseline. These results demonstrated consistent patterns of systemic

inflammation related to progressing periodontitis. PGE2 levels increased significantly by MP and remained elevated throughout the entire pregnancy. Similarly, BPI levels were also increased significantly by MP in most of the animals and generally decreased substantially by delivery. LBP levels were elevated generally at baseline and decreased significantly throughout the disease process. As was noted with the population as a whole, IL-6 levels were increased significantly by delivery, irrespective of the baseline clinical characteristics of the animals. Both IL-8 and Resveratrol MCP-1 decreased from baseline throughout the study, with the lowest levels of IL-8 in serum samples obtained at delivery, unrelated to the clinical presentation of the animals at baseline. A summary of these outcomes was that the clinical presentation at baseline had less impact on the systemic inflammatory mediator levels than the effect of the continued disease over 6 months induced by ligation and creation of chronic periodontitis in the animals. Finally, based upon these findings, we evaluated response differences in subsets of animals as they progressed through the experimental challenge during pregnancy. Thus, at baseline, stratification of the animals related to naturally occurring oral health/disease showed some distinct differences in serum inflammatory mediators that differentiated the healthy from gingivitis from the periodontitis groups.

As an example of that, single-walled carbon nanotubes (SWNTs) were reported to have strong antimicrobial activities against microbes (Vecitis et al., 2010). Electrospun polymer mats with incorporated narrow diameter SWNTs were found to significantly reduce bacterial colonization and subsequent biofilm formation (Schiffman & Elimelech, 2011). Besides microbicidal agents, non-microbicidal agents are also used to block microbial attachment. For example, pathogens often bind human cell surface through pili and

form biofilm in vivo (Tsui et al., 2003; Okahashi et al., 2011). A 12-mer peptide (RQERSSLSKPVV), which binds to the structural protein PilS of the type IVB pili of Salmonella Typhi, was isolated by using a ribosome display system and shown to inhibit adhesion to or invasion of human monocytic THP-1 cells by piliated S. Typhi (Wu et al., 2005). This group also identified high-affinity this website single-stranded RNA aptamer [S-PS(8.4)] as a type IVB pilus-specific ligand and further showed that the aptamer [S-PS(8.4)] could significantly inhibit the entry of the piliated S. Typhi into human THP-1 cells (Pan et al., 2005).

Bovine lactoferrin was also shown to interact with cable pili of Burkholderia cenocepacia and efficiently inhibit invasion of alveolar epithelial cells by free-living bacteria or biofilm (Ammendolia et al., 2010). Increasing efforts have been put on development of modified surfaces with anti-adhesive properties by means of physicochemistry. For example, electropolished stainless steel was shown to significantly reduce attachment Selleck FK506 and biofilm formation by bacterial cells than the sand-blasted and sanded stainless steel surfaces (Arnold & Bailey, 2000). Raulio et al. (2008) reported that hydrophilic

or hydrophobic coated stainless steel by diamond-like carbon or certain fluoropolymers could reduce or almost eliminate adhesion and biofilm formation by Staphylococcus epidermidis, Deinococcus geothermalis, Methamphetamine Meiothermus silvanus and Pseudoxanthomonas taiwanensis (Raulio et al., 2008). A robust peptide-based coating technology for modifying the surface of titanium (Ti) metal through non-covalent binding was introduced by Khoo et al. (2009). In their study, a short HKH tripeptide motif containing peptide (e.g. SHKHGGHKHGSSGK) possessing affinity for Ti was identified by means of a phage display based screening and amino acid substitution study. Based on this peptide, a PEGylated analogue was found to rapidly coat Ti and efficiently block the adsorption of fibronectin and attachment of S. aureus (Khoo et al., 2009). Anti-adhesive properties and microbicidal properties are combined by researchers when designing novel surfaces. In a recent study, Yuan et al. (2011) immobilized lysozyme to the chain ends of poly(ethylene glycol) branches of the grafted poly(ethylene glycol) monomethacrylate (PEGMA) polymer after PEGMA was coated to stainless steel surfaces (Yuan et al., 2011).

Thus, transcriptome profiles, TCR repertoire analysis, as well as analysis of neuropilin-1 expression, indicate that Treg cells in the gut are quite different compared with Treg cells at other sites, and, in particular, the gut Treg-cell population is comprised of substantial numbers of iTreg cells besides nTreg cells. It is tempting to speculate that a higher prevalence of iTreg cells in the gut might be due

to the particular intense contact with foreign antigen in that location and, in fact, Treg cells in the LP have been noted to encode TCRs directed against the intestinal microbiota [16]; however, this seemingly straightforward correlation between antigen load and iTreg-cell numbers needs to be tempered by considering the total number of Treg cells in the gut. Although Foxp3+ cells are abundant

in CH5424802 the gut LP, they are still less frequent as compared with macrophages, plasma cells, and some other T-cell subsets. By carefully counting the number of Treg cells in longitudinal 7 μm ileum cryosections for mice we observed, on average, 0.35 cells per villus (O. Pabst, unpublished observation). We expect this number might vary depending on the housing conditions and intestinal microbiota composition, as both are Vadimezan known to skew the Treg-cell pool in the gut [17, 18]. In any case, the actual number of Treg cells per villus seems too limited, rendering it unlikely that the Treg-cell pool with its TCR specificities might fully cover the complexity of the total antigen load. It is therefore possible that the antigen-driven generation of iTreg cells

does not account for immunoregulation covering the full antigen load but might rather constitute a sophisticated pathway to deal with particularly “problematic” antigens. In vitro, TGF-β and IL-2 are sufficient to induce expression of Foxp3 in a substantial Urease fraction of activated CD4+ T cells [19] and this fraction can be further increased by the addition of retinoic acid (RA) [20]. TGF-β and RA have also been suggested to enable iTreg-cell generation following antigen administration through the oral route [21, 22]. One commonly used experimental setup to quantify Treg-cell conversion in the intestinal immune system involves the adoptive transfer of TCR-transgenic Foxp3− T cells to recipient mice. Subsequent antigen feeding results in T-cell activation and proliferation, and the formation of a sizable number of Foxp3+ T cells (Fig. 1) [3, 21, 23]. In the gut-draining mesenteric lymph nodes (mLNs), this frequency is considerably higher as compared with that of other lymphoid compartments. Such a high capacity to generate iTreg cells could be recapitulated in vitro by stimulating Foxp3− cells via “intestinal” DCs, that is, DCs isolated from mLNs or intestinal LP, but not those from pLNs or splenic DCs [21, 24].

The resulting supernatant was resuspended in 10 μL of Solution A. The protein concentration of the nuclear and mitochondria/cytoplasm fractions was determined using the Biorad Protein Assay. These procedures were done as previously described 20. Quantitation of the Western blots was performed using Adobe Photoshop CS3 as described (http://lukemiller.org/journal/2007/08/quantifying-western-blots-without.html).

Briefly, the Adobe Photoshop lasso tool was used to outline each protein band and a background region on the membrane. The mean gray value and the pixel value were multiplied to determine the absolute intensity of the band. When no band was visible, the outlined region was made equal in pixel number to that of the NSC 683864 supplier background region. The background to be subtracted from a given band was determined by multiplying the mean gray value of the outlined background region by the pixel

measurement for the corresponding band. The authors thank Victor E. Marquez for his generous gift of HK434 and Yuefang Sun for taking care of the mouse colonies. JAK inhibitor This study was supported by a grant from the National Institute of Health (to A. W.) and the Research Supplement for underrepresented minorities from the National Cancer Institute (to J. T.). Conflict of interest: The authors Rho declare no financial or commercial conflict of interest. “
“Monocytes are blood leukocytes that can differentiate into several phagocytic cell types, including DCs, which are instrumental to the inflammatory response and host defence against

microbes. A study published in this issue of the European Journal of Immunology by Balboa et al. [Eur. J. Immunol. 2013. 43: 335-347] suggests that a shift of the CD16− monocyte population toward a CD16+ subpopulation may represent an immune evasion strategy that ultimately favors persistence of Mycobacterium tuberculosis. Together with other recent reports, the article by Balboa et al. sheds new light on the function of CD16+ monocytes in health and disease; in this commentary, we discuss the implications stemming from these findings. Immunity to pathogens and inflammatory reactions relies on the coordinated action of several immune cell populations including lymphoid cells and monocyte-derived phagocytes, such as macrophages and DCs. Monocytes are generated in the marrow and circulate in the blood where they can patrol the whole body for signs of infection or inflammation, and migrate to injured tissues upon attraction by several chemokines and microbial ligands. Monocytes exhibit high plasticity and can differentiate into a variety of cell subsets depending on their microenvironment in infected or inflamed tissues [1, 2].

However, it is also being shown that the recovered immune function in these natural revertants might be very variable, suggesting that the effects of ERT might be unique to each patient. In this report, we describe the molecular and immunologic abnormalities associated with ADA deficiency in a child selleck inhibitor diagnosed at the age of 1 month with T-B- SCID, in whom low numbers of PB T lymphocytes were found later at the age of 23 months and became normal by 50 months of age. This was associated initially

with homozygosity for a mutation that later resulted in a mosaic because of a monoallelic reversion of this mutation documented in his T cells. As this child was not eligible for HSCT or GT, he was placed on ERT, and we describe the molecular and immunologic changes due to partial immune reconstitution and the clinical outcome after 17 months of ERT. Patient and control subjects.  Our patient was a boy diagnosed with ADA-SCID at the Primary Immunodeficiencies Clinic in the University of Antioquia in Medellin (Colombia), that we followed until the age 67 months. NVP-AUY922 purchase Written informed consent approved by the IRB at the University of Antioquia was obtained from both parents and healthy age- and sex-matched controls. Immunophenotyping of peripheral blood lymphocytes.  Peripheral blood lymphocytes (PBL) from EDTA

whole blood were stained with different combinations of fluorochrome-conjugated monoclonal antibodies against CD3, CD4, CD8, CD19, CD21, CD27, IgD, CD16, CD56, TCRαβ, TCRγδ, CD45RA and CD45RO (eBioscience

Inc, San Diego, CA, USA and BD Biosciences, San Jose, CA, USA) for 30 min at room temperature, followed by treatment with lysing solution (BD FACS Lysing Solution®; BD Biosciences) for 10 min to remove RBC. After this, the cells were washed twice in PBS (Dulbecco’s phosphate-buffered saline; Sigma Aldrich, Saint Louis, MO, USA), fixed in 200 μl of 2% formaldehyde and read on a FACScan Flow Cytometer equipped with a 388-nm laser (Becton Dickinson, San Jose, CA, USA). Files were analysed using the software FlowJo v8.2 (TreeStar Inc, Ashland, OR, USA), and the results were compared with the controls as indicated [15]. Mutation analysis.  Genomic DNA from the patient Edoxaban and controls was extracted from whole blood, PBL and buccal epithelial cells as well as from negatively enriched CD3+ T cells using a DNA Purification Kit (Puregene, Gentra Systems, Minneapolis, MN, USA). Primers and PCR conditions used for the amplification of all ADA exons have been described previously [5, 16]. The nucleotide sequences were determined using the genetic analyzer ABI-PRISM 3100 (AB Applied Biosystems, Foster City, CA, USA) and analysed using the Sequencher software v. 4.8 (Gene Codes Corporation, MI, USA). ADA activity and adenine nucleotide content in RBC.

This divergence probably results from the different infectious disease challenges associated with the respective ecological niches that Anti-infection Compound Library screening these two species inhabit. Unfortunately, these differences between the mouse and human immune systems also result in dissimilar inflammatory responses to burns, trauma, and endotoxemia at the gene expression level, such as integrin, ICOS-ICOSL, CD28, and PKCΘ signaling [3]. Therefore, alternatives to classical mouse models, which more closely model human immune system behavior during infection

in vivo, would be of significant benefit for the development of immunomodulatory treatments. The category of new models, which comes closest to achieving this goal, is mice with reconstituted human immune system components. These mice are mainly generated by neonatal injection of human hematopoietic progenitor cells in mice that lack murine innate and adaptive lymphocytes, namely NOD-scid γc−/− (NSG), NOD-scid γctm1sug, NOD Rag1−/− γc−/−, or BALB/c Rag2−/− γc−/− (BRG) mice [4] (Fig. 1). For some studies, a fetal organoid of liver and thymic tissue is implanted under the kidney capsule, which together with the i.v. injection of human hematopoietic progenitor cells generates BM liver thymic mice [5]. In

all of these models, cellular components of the human immune system develop over several months, BVD-523 nmr including human T cells, B cells, natural killer (NK) cells, monocytes, macrophages, and dendritic cells (DCs) [6-8]. However, the degree of human immune system component reconstitution differs significantly between these mouse strains, with 60% of mononuclear cells being of human origin in the spleen and blood of NSG, NOD-scid γctm1sug, and NOD Rag1−/− γc−/− mice 3 months after

human hematopoietic progenitor cell transfer, while in BRG mice only 20% are of human origin at this time point [9, 10]. This difference in the proportion of mononuclear Carbohydrate cells of human origin among the various mouse models results at least in part from the polymorphism among mouse strains in signal regulatory protein-α (SIRP-α), an inhibitory receptor on mouse myeloid cells. This receptor recognizes human CD47 in the NOD mouse background and thereby prevents phagocytosis of human cells by the mouse myeloid compartments, which are still intact in all these mouse backgrounds [11]. Indeed, when human or NOD-mouse signal regulatory protein-α is transgenically introduced into BRG mice, or when BRG mice are reconstitute with human hematopoietic progenitor cells that are transduced to express mouse CD47, human immune system reconstitution is similar to that in NSG mice [12, 13]. In particular, human T-cell and NK-cell reconstitution is very sensitive to optimal reconstitution of the other human immune compartments, such as dendritic cells, but comprise up to 60 and 5% of human CD45-positive cells, respectively [9, 14, 15].