B-1 cells were identified by flow cytometry as live, CD3/4/8− F4/80−, GR-1−, CD19hi IgM-a+ IgD-alo CD43+ CD5+/− cells. A total of 2 mg AF6-78.2.5 antibody was given

for six weeks by bi-weekly injections, after which time allotype chimeras Napabucasin were maintained for at least two additional months before conducting experiments. To generate B-2-derived plasma cells, BALB/c mice were infected with influenza A/Mem/71 for 10 days as described previously 27. For reconstitution of RAG-1−/− mice, mice were irradiated with 850 rd full body γ-irradiation and reconstituted 16 h later with 2×106 total BM, or BM depleted of IgM+ cells via magnetic cell depletion using an auto-MACS (Miltenyi Biotec, Auburn, CA, USA). Mice were bled 6 weeks after reconstitution for analysis of serum IgM levels. Single-cell suspensions from spleen, peritoneal cavity wash out, BM and peripheral (pooled inguinal and axillares) LNs of individual mice were cultured in the absence of further stimuli in complete RPMI 1640 media (RPMI 1640, 2 mM L-glutamine, 100 μg/mL of penicillin and streptomycin, 10% heat-inactivated

fetal calf serum, and 50 μM 2-ME) at 37°C, 5% CO2 to assess spontaneous IgM secretion. Supernatants Rucaparib were harvested after 16–18 h and analyzed by ELISA for presence of total and influenza virus-binding IgM. Total and virus-specific IgM secreting antibody-forming cells were enumerated by ELISPOT as previously described 56. B-1 and B-2 cell-derived IgM antibody-producing foci (AFC) were determined using Ig-allotype-specific monoclonal antibodies. Briefly, 5 μg/mL of anti-IgM (331, (-)-p-Bromotetramisole Oxalate not allotype-specific) or 1000 HAU/mL of purified A/Mem/71 were coated onto 96-well plates (Multi-Screen HA Filtration, Millipore, Bedford, MA, USA). After plates were blocked (PBS with 4% bovine serum albumin (BSA)), 2-fold serially diluted single-cell suspensions from various tissues were prepared and incubated overnight in complete RPMI 1640 media at 37°C, 5% CO2 chamber. Binding was revealed with in-house biotinylated allotype-specific anti-IgM (DS-1.1 for IgMa and AF6-78.2.5 for IgMb) followed by SA-HRP (Vector Labs, Burlingame,

CA, USA). Spots were developed with 3-amino-9-ethylcarbazole (Sigma Aldrich, St. Louis, MO, USA) and counted with the help of a stereomicroscope. Data are expressed as the number of IgM-secreting AFC per input cells. IgM production was quantified by sandwich ELISA as described previously 56. Briefly, 5 μg/mL of anti-IgM (331) antibody was coated onto 96-well plates (Maxisorb, Nalgene Nunc, Rochester, NY, USA). After blocking non-specific protein binding, serially diluted culture media was added to plates. Binding was revealed with biotinylated anti-IgM antibodies. The levels of total IgM production (μg/ml) were calculated using purified IgM as the standard. Single-cell suspensions from peritoneal cavity wash outs (PerC), spleen and BM were stained with the following antibody conjugates at predetermined optimal concentrations.

Table 1 provides a summary of the relationships among the levels of various inflammatory mediators throughout the protocol. The results demonstrated significant correlations among selected mediators, with CRP levels being independent of the other inflammatory biomarkers. However, the acute phase reactants, BPI and LBP, showed the most consistent relationship as markers of systemic inflammation throughout the pregnancy and ligature-induced disease. Table 2 provides a similar assessment see more in relating the inflammatory mediators to serum antibody levels to oral bacteria at baseline, mid-pregnancy and delivery.

Using a forward stepwise regression to assess the level of antibody specificity that best predicted the individual systemic inflammatory analyte levels, the results provided some interesting outcomes. Generally PGE2, RANTES and BPI levels were unrelated to the antibody responses. CRP, IL-8, MCP-1 and LBP showed significant relationships to Panobinostat antibody response profiles at baseline. IL-8 and MCP-1 levels maintained a relationship to

specific antibody profiles through mid-pregnancy, including both antibody specificities and direction. IL-6 levels were related to specific antibody patterns at mid-pregnancy and delivery. Examination of the overall systemic antibody responses indicated that responses to F. nucleatum, P. gingivalis, A. actinomycetemcomitans and C. rectus were associated most frequently with variations in inflammatory mediator levels. Finally, we attempted to model the oral clinical disease expression via a specific profile of systemic inflammatory responses. The results in Table 3 provide a summary of these analyses. Levels

of IL-6, IL-8 and LBP demonstrated a significant profile across the entire population irrespective of the sampling interval. Separating these comparisons into the individual sampling times demonstrated that none of the analytes profiled the oral clinical presentation at baseline. However, at mid-pregnancy, PGE2 and RANTES were related significantly to the oral disease, with only PAK5 BPI levels as a significant correlation of oral disease at delivery. Interestingly, throughout the experimental protocol, the profiles of serum mediators were less dependent upon the sampling interval, and patterned more closely the actual clinical presentation of the animals throughout the course of the study (Table 3). As more attention is being directed towards chronic diseases in the human population, new concepts of aetiology and resulting loss of tissue/organ function continue to develop. Many of these chronic diseases have been identified to have components of chronic inflammation, both locally and systemically, that contribute to inducing collateral damage of the host resulting in the clinical symptoms.

The relationship between enteroviruses, especially type B Coxsackieviruses (CV-B) and T1D, in genetically predisposed individuals has been highlighted largely through epidemiological studies [7–11]. Several mechanisms Z VAD FMK not mutually exclusive have been suggested to elucidate the viral pathogenesis of T1D [11,12]. One of the possible mechanisms is the disturbance of central tolerance

as a result of the infection of thymus with viruses. Clinical evidence and experimental findings show that viral infections are responsible for thymus abnormalities and dysfunctions, although in some cases the organ has not been reached selleck chemical by the infectious agent. HIV, belonging to the Retroviridae family, is the virus that has been associated most frequently with thymus disorders in the literature. HIV has been detected in thymuses of infected individuals [13–16]. In addition, human intrathymic T cell precursors and their progeny, representing many stages of T cell ontogeny, have been demonstrated to be susceptible to HIV-1 infection in vitro[17]. The chimeric severe combined immunodeficiency–human (SCID-hu) xenograft mouse model (bearing human T cells derived from transplantation of human thymic fragments

and liver tissue under the renal capsule) showed that human thymocytes are also susceptible to HIV

infection in vivo[18,19]. Moreover, it is likely that HIV infects the thymic microenvironment, as marked disruptions and significant viral loads have been observed in the thymic compartment in HIV-infected SCID-hu mice [19], a finding that was confirmed later by the demonstration of infected thymic dendritic cells [20]. Whether or not the thymic epithelium is also infected by this virus is an issue that deserves further investigation. Indeed, thymic epithelial cells (TEC) were shown previously to contain HIV RNA in human autopsy samples and also in the SCID-hu mouse model, GNAT2 although productive infection of these cells could not be demonstrated definitively [14,19]. Furthermore, the same SCID-hu mouse model showed degenerating TEC even without detection of HIV in these cells [19]. The relevance of TEC infection lies in the fact that these cells play a critical role in the differentiation of T cell precursors, providing a microenvironment with a unique capacity to generate functional and self-tolerant T cells [21,22]. HIV infection is generally accompanied by several cytological and histological abnormalities in the thymus network.

No microbubble coalescence and no increased size were observed. Adhesion of some microbubbles to leukocytes was observed in various microcirculation models. Microbubbles are captured by Kupffer cells in the liver. Targeted microbubbles were shown to adhere specifically Selleck Ceritinib to endothelial receptors without compromising local blood flow. Conclusion:  These results support the safety of both targeted and nontargeted UCAs as no microvascular flow alteration or plugging of microvessels were observed. They confirm that binding

observed with targeted microbubbles are due to the binding of these microbubbles to specific endothelial receptors. “
“Microcirculation (2010) 17, 348–357. doi: 10.1111/j.1549-8719.2010.00036.x Objective:  The canonical Wnt signaling pathway, heavily studied in development and cancer, has recently been implicated in microvascular growth with the use of developmental and in vitro models. To date, however, no study exists showing the effects of perturbing the canonical Wnt pathway in a complete microvascular network undergoing physiological remodeling in vivo. Our objective was to investigate the effects of canonical Wnt inhibition on the microvascular remodeling of adult rats. Methods:  Canonical Wnt inhibitor

DKK-1, Wnt inhibitor sFRP-1, BSA or saline was superfused onto the exteriorized mesenteric windows HM781-36B chemical structure of 300 g adult female Sprague-Dawley rats for 20 minutes. Three days following surgery, mesenteric windows were imaged intravitally and

harvested for immunofluorescence staining with smooth muscle alpha-actin and BRDU. Results:  We not observed prominent differences in the response of the mesenteric microvasculature amongst the various treatment groups. Significant increases in hemorrhage area, vascular density, and draining vessel diameter were observed in windows treated with Wnt inhibitors as compared to control-treated windows. Additionally, confocal imaging analysis showed significant increases in proliferating cells as well as evidence of proliferating smooth muscle cells along venules. Conclusions:  Together, our results suggest that canonical Wnt inhibition plays an important role in microvascular remodeling, specifically venular remodeling. “
“Please cite this paper as: Sundd, Gutierrez, Petrich, Ginsberg, Groisman, and Ley (2011). Live Cell Imaging of Paxillin in Rolling Neutrophils by Dual-Color Quantitative Dynamic Footprinting. Microcirculation 18(5), 361–372. Objective:  Neutrophil recruitment to sites of inflammation involves P-selectin-dependent rolling. qDF is a useful tool to visualize the topography of the neutrophil footprint as it interacts with the substrate. However, elucidating the role of specific proteins in addition to topography requires simultaneous visualization of two fluorochromes. Methods:  To validate DqDF, mouse neutrophils were labeled with the membrane dyes DiO and DiI and perfused into microchannels coated with P-selectin–Fc.

001). Levels amongst all hypertensive pregnancies (GH-1287, EH-881 and PE-817 pmol/L) were lower than NP-1715 pmol/L (P < 0.05). this website ACE2 levels

were higher in NP-276 mU/L v C-119 mU/L (P < 0.001), however NP levels did not differ from hypertensive pregnancies (GH-305, EH-296, PE-332 mU/L). Similarly Angiotensin II was higher in NP-114 pg/mL vs C-56 pg/mL (P < 0.001), with no difference between NP and hypertensive's (GH-121 pg/mL, EH-92 pg/mL, PE-89 pg/mL). Neither Ang (1–7) nor ACE levels differed amongst groups. Conclusions: Activity of the ACE2 enzyme is higher in normal pregnancy than in controls; however we were unable to find a difference between NP and pregnancies complicated by PE. 184 A CHRONIC KIDNEY DISEASE MODEL OF CARE – 4 YEAR REVIEW OF A NURSE PRACTITIONER ROLE C STONE1, A BONNER2,4, A SALISBURY3,4, Z WANG3,4, W HOY3,4 1Queensland Health; 2School of Nursing, Queensland Tamoxifen research buy University of Technology; 3Centre

of Chronic Disease, University of Queensland; 4CKD.QLD, Australia Aim: To describe the Nurse Practitioner (NP) chronic kidney disease (CKD) model of care (MOC) in a large Queensland metropolitan Hospital and Health Service, including patient characteristics and outcomes, over a four-year period. Background: There are increasing numbers of CKD NPs in Australia with the milestone of 1,000 NPs (all disciplines) registered with AHPRA in 2014. This reflects the growing international evidence that NPs are effective in achieving patient outcomes in a variety of chronic disease contexts. Methods: Longitudinal patient data was recorded from commencement of this MOC in 2009. Data was reviewed on referral and at 12, 24, 36 and 48 months and included eGFR, proteinuria, blood pressure, HbA1c, lipids, Ca, phosphate, PTH and BMI against renal key performance indicators. Results: 217 patients were referred to the NP – 132 women and 85 men. Mean age on referral was 68.9 and 68.0 years respectively. CKD stages on referral were stage 1 and 2 (19.9%), stage 3A (29.2%), stage 3B (42.1%), stage 4 (7.9%) and stage 5

(0.9%). Primary renal very diagnosis was overtly diabetic nephropathy (42.9%) and renovascular (37.3%), with GN (all) 4.1%, single kidney 3.2% and uncertain 2.3%. The service increased from 41 active patients in 2009 to 93 in 2013, with patient movement from the MOC including discharge (54), transfer (70) and death (6). 30% of patients had improvement in eGFR, 50% were “stable”, and 20% progressed. Conclusions: This analysis provides information that enables reporting and review of components in CKD patient care, including longitudinal outcomes, and supports benchmarking of an NP MOC against national and international targets. This process provides NP MOC evidence to patients, families and to health service providers.

The amounts of IL-2, IL-4, IL-10 and IFN-γ were determined by indirect ELISA according to the manufacturer’s instructions (Jiamay Biotech, Beijing, China). Fourteen days after the final vaccination, eight BALB/c mice were selected randomly from each group and challenged intraperitoneally with 500 tachyzoites of the Selleckchem Omipalisib highly virulent T. gondii RH strain. All mice were observed twice daily, and the survival times were recorded. Those mice that were alive 2 weeks after the challenge

were considered to have survived. Statistical analysis was performed using SPSS 14·0 software for variance (anova) and Duncan’s multiple ranges. P < 0·05 was considered to be statistically significant. The coding region of TgCyP was amplified by RT-PCR and combined with the eukaryotic expression vector pVAX1. The constructed plasmid pVAX1-TgCyP, which carried the TgCyP insert, was verified by sequencing. Forty-eight hours after HeLa cells were transfected with the recombinant plasmid pVAX1-TgCyP, the recombinant CyP protein (green fluorescence) was found to be significantly expressed by immune-fluorescence staining. There was no signal in the pVAX1 vector-transfected cells. These results indicated that the recombinant plasmid was successfully

constructed and expressed in vitro (Figure 1). A specific antibody response against https://www.selleckchem.com/products/SP600125.html T. gondii tachyzoites was detected in the pVAX1-TgCyP vaccinated BALB/c mice. Two weeks after the final immunization, the antibody level of the pVAX1-TgCyP group was significantly higher than control groups, which were immunized with pVAX1 or PBS (P < 0·05). This result was shown in Figure 2. Splenocytes collected 2 Y-27632 2HCl weeks after the final vaccination were stimulated with TLA, and a significant increase in splenocyte proliferation was detected in the pVAX1-TgCyP group (Table 1) (P < 0·05). The production of IFN-γ and IL-2 was highly elevated in splenocytes after stimulation with TgCyP in the pVAX1-TgCyP-vaccinated BALB/c mice (Figure 3) (P < 0·05). Nevertheless, a slight difference was observed

in PBS- and pVAX1-immunized mice. No significant difference was observed in IL-4 or IL-10 release among all of the study groups. Two weeks after the last vaccination, all of the mice were challenged intraperitoneally with 500 tachyzoites of the T. gondii RH strain. There was no significant difference in the protection levels between the pVAX1- and PBS-immunized groups (P > 0·05). In comparison to the control groups, significantly higher protection was observed in the pVAX1–TgCyP vaccinated group with a survival rate of 37·5% (P < 0·05) (Figure 4). Overall, the TgCyP DNA vaccine produced significant protection in BALB/c mice. In this study, the protection efficacy of the T. gondii vaccine candidate TgCyP was determined in BALB/c mice.

endogenous H2O2, localization, and concentrations). Several studies have proposed that H2O2 is an EDHF [52,53,58,59,77]. H2O2 produces vasorelaxation in various murine, porcine, and human vessels via either endothelium-dependent or endothelium-independent mechanisms [3,5,6,24,37,44,47,75,98,99] but in some studies H2O2 causes vasoconstriction [26,38,47,68,73,83,100]. H2O2 is required for flow-induced increases of NO• [40] and flow-mediated dilation [58]. Overexpression of NAD(P)H oxidase in transgenic mice predominately increases H2O2 levels and exerts beneficial effects on vasodilator function and blood pressure due to H2O2 production [72]. In coronary ischemia/reperfusion

injury endogenous H2O2 contributes in vivo to coronary vasodilation to compensate for the loss of NO• and plays a cardioprotective role, particularly in microvessels [97]. H2O2 that functions in AZD8055 endothelial signaling may be derived from several sources, depending on physiological conditions. In skeletal muscle arterioles exposed to intraluminal flow, both age and exercise training increased

eNOS-derived O2•− selleck screening library signaling; this elevation in eNOS-derived O2•− was accompanied by an increase in catalase-sensitive vasodilation, suggesting that eNOS-derived O2•− constituted the source of vasodilatory H2O2 [78]. In contrast, in skeletal muscle arterioles from both young and old rats, stimulation with acetylcholine produces catalase-sensitive vasodilation that is abolished by treatment with either apocynin or an inhibitor of gp91phox (Sindler, unless A.L., Muller-Delp, J.M, unpublished observations). In cerebral

arterioles of aged rats, both p67phox and gp91phox proteins increased, with accompanying impairment of endothelial function, suggesting that NAD(P)H-derived O2•− is not transformed to vasodilatory H2O2 [55]. In the aged myocardium, H2O2 is generated by the electron transport chain of myocytes, and because it is freely diffusible, produces metabolic vasodilation of coronary arterioles [48]. Thus, the cellular sources of H2O2 vary between arterioles from distinct vascular beds. In future work, identifying the sources of ROS generation may provide insight into therapeutic targets for prevention and/or remediation of age-related vascular dysfunction. SOD reduces oxidant stress by dismutating O2•− into H2O2; however, in the presence of catalytic transition metals, SOD can rapidly form HO• [67]. H2O2 generates HO• through metal-catalyzed reactions, such as the Fenton reaction as follows: H2O2 + Fe2+ Fe3+ + HO• + OH−. The formation of HO• is further promoted by the presence of O2•−, which reacts with Fe3+ to produce Fe2+ through the Haber–Weiss reaction [29,70]. The net effect of SOD is the dismutation of O2•− to produce either the vasodilatory H2O2, or in the presence of Fe2+, HO•. This production of HO• may occur more readily if the production of H2O2 exceeds the enzymatic capacity of endogenous catalase or peroxidases.

Previous reports 20–23 questioning the role of Fas in CD4+ T-cell-induced autoimmune diabetes studies rely on a single CD4+ T-cell specificity, using a TCR transgenic model. We propose that these monoclonal cells probably overrepresent one effector mechanism rather than the panoply of mechanisms involved in the overall in vivo scenario when a polyclonal population of effector cells, composed of several CD4+ T-cell clones, mediate diabetes. Therefore, our study suggests that see more the diabetogenic

action of NOD CD4+ T lymphocytes is very probably dependent on Fas expression on target cells. Our results indicate that diabetogenic CD4+ T cells may have an impaired ability to transfer diabetes into NOD/SCID recipients which over-express FasL on β cells compared to transgene-negative recipients. This could indicate immune privilege acquired by β cells as a consequence of the expression of FasL on their surface when they encounter activated, diabetogenic CD4+ T cells.

These data seem to be in apparent contradiction to that reported previously 14, in which overexpression of FasL in WT NOD mice accelerates diabetes onset. This paradox of FasL Talazoparib order expression on β cells could imply that expression of FasL on β cells favors an autoaggressive repertoire while the immune repertoire is maturing. In NOD/SCID mice, however, T- and B-cell subsets are missing, which might otherwise contribute to that final configuration of the immune repertoire in the islet. Last but not least, β-cell-specific transferred T cells are mostly activated, and hence, expressing Fas on their surface. Nevertheless, further work should be done to resolve this paradox. Here, we report that IL-1β does not play an essential role in spontaneous autoimmune diabetes although progression to diabetes is slower in NOD/IL-1R KO mice 34; the overall impact on the disease is not remarkable. Thus, caution should be exercised when translating in vitro studies in which islets or β-cell

lines are exposed to IL-1β since the results may not necessarily correspond to what is actually taking place in vivo during disease progression. Although IL-1β seems to play a crucial role in β-cell destruction in islet transplantation models 35–38, it does not do so in the NOD Phosphoprotein phosphatase model of spontaneous diabetes. This may be explained by the fact that during transplantation, the immune system is activated because of a strong inflammatory environment developing in and around the entire graft. However, in spontaneous T1D the immune response is cell-targeted and the pro-inflammatory environment is mostly limited to the islet. Therefore, IL-1β may help to exacerbate the spontaneous β-cell attack, but in its absence, other mechanisms may replace it (e.g. IFN-γ and/or TNF-α). Therefore, diabetogenic CD4+ T cells do not require Il-1β to mediate Fas-dependent β-cell death.

RNA samples were resuspended in diethylpyrocarbonate-treated water and stored at −70 °C. The RNA concentration was determined

from the optical density using a micro-volume spectrophotometer (Nanodrop 1000, Nanodrop Technologies LLC, Wilmington, NC, USA). Real-time PCR reactions.  Reverse transcription total RNA was DNase treated (Turbo DNA-frees, Ambion Inc., Austin, TX, USA), and 1 μg was used for cDNA synthesis. The reaction was carried out using the First-Strand cDNA synthesis kit (Fermentas, Glen Burnie, MD, USA), following the manufacturer’s recommendations. Primer design.  Primers were designed using the Primer JAK pathway Express 3.0 probe design software (Applied Biosystem, Foster City, CA, USA). The primer sequences are presented in Table 1. PCR Reactions.  Quantitative real-time polymerase chain reaction (qPCR) was performed in the 7300 Real Time PCR (Applied Biosystem) using the SYBR Green PCR Master Mix (Fermentas). The reaction product was quantified with the Relative Quantification tool, using GAPDH as the reference

gene. Negative controls with SYBR Green PCR Master Mix and water were performed for all reactions. Statistical analysis.  The statistical analysis was performed using a software program (GraphPad Prism 4.0, La Jolla, CA, USA). Data were first examined for normality by the Kolmogorov-Smirnov check details test and, since the data achieved normality, parametric method was employed. The percentages of sites with visible plaque accumulation, BoP, SUP, the means PD, CAL were

computed for all teeth. Clinical parameters, mRNA data, the levels of cytokines and IgA were averaged into both groups. The differences in clinical parameters, age, mRNA levels, IgA, and cytokines levels between groups were compared using Student’s t-test. The level of significance was set at 5%. Table 2 summarizes the demographic characteristics and the clinical parameters of the study population. There Alanine-glyoxylate transaminase were no differences in the mean age and gender distribution between groups (p > 0.05). As expected, the levels of all periodontal parameters were lower in the control group when compared to chronic periodontitis group considering full-mouth and the teeth selected for gingival biopsies levels (P < 0.05). Salivary levels of antibody were normalized by comparing the IgA antibody in ELISA to the total protein (Bradford method) found in the saliva. The mean level of total protein found in the saliva of the periodontal disease individuals was 1471.60 ± 438.09 μg/ml, and from healthy individuals was 1056.79 ± 381.13 μg/ml. The normalized mean levels of IgA (pg/ml) in total saliva are presented in Figure 1. The total IgA antibody levels were significantly higher in the chronic periodontitis group compared to periodontally healthy ones (P < 0.05). As observed in Fig. 2A, the gingival mRNA levels for IL-21 was significantly higher (P < 0.05) in the chronic periodontitis group when compared to the healthy group.

IL-9 exerts

pleiotropic activities on T and B lymphocytes, mast cells, monocytes and haematopoietic progenitors [54,55]. IL-15 and TNF-α are known to prime T lymphocytes and NK cells when secreted by DCs [56] and to induce anti-tumour immune responses [57]. Eotaxin is known to selectively recruit eosinophils also contributing to anti-tumour effects [58,59], and MIP-1β is a chemoattractant for NK cells, monocytes and a variety of other immune cells [60]. In addition, serum levels of arginase tended to decrease after DC transfer. Because serum arginase activity reflects the numbers of MDSCs that inhibit T lymphocyte responses in cancer patients [36], the patients treated with OK432-stimulated DCs might have developed lower levels of suppressor cells. Collectively, the results suggest that infusion of OK432-stimulated DCs may orchestrate the immune environment in the whole body that Epigenetics inhibitor could enhance learn more beneficial anti-tumour effects, although the precise molecular and cellular mechanisms associated with the actions of these cytokines and chemokines were not defined clearly in the current analysis. The authors thank Kazumi Fushimi and Mariko Katsuda for technical assistance. We also thank the patients for participating in this trial. This work was supported in part by research grants from the Ministry of Education, Culture, Sports, Science, and Technology of Japan, the Ministry of Health, Labour and Welfare of Japan and the Japanese

Society of Gastroenterology. The authors have declared that no conflict of interest exists.

“
“Human Thy-1 (CD90) has been shown to mediate adhesion of inflammatory cells 3-mercaptopyruvate sulfurtransferase to activated microvascular endothelial cells via interaction with Mac-1 (CD11b/CD18) in vitro. Since there are no data showing the physiological relevance of Thy-1 for the recruitment of inflammatory cells in vivo, different inflammation models were investigated in Thy-1-deficient mice and littermate controls. In thioglycollate-induced peritonitis, the number of neutrophils and monocytes was significantly diminished in Thy-1-deficient mice. During acute lung inflammation, the extravasation of eosinophils and monocytes into the lung was significantly reduced in Thy-1-deficient mice. Moreover, during chronic lung inflammation, the influx of eosinophils and monocytes was also strongly decreased. These effects were independent of Thy-1 expression on T cells, as shown by the transplantation of WT BM into the Thy-1-deficient mice. In spite of the strong Thy-1 expression on T cells in the chimeric mice, the extravasation of the inflammatory cells in these mice was significantly diminished, compared to control mice. Finally, the altered number and composition of infiltrating leukocytes in Thy-1-deficient mice modified the chemokine/cytokine and protease expression at the site of inflammation. In conclusion, Thy-1 is involved in the control of inflammatory cell recruitment and, thus, also in conditioning the inflammatory microenvironment.