Finally, we questioned if the above changes in epitope-specific CTL would also be associated with changes in immunity to LCMV infections. We performed virus titration from the spleens at different days p.i. after initializing first cross-priming in the same protocol as shown in Fig. 7A. The data in Fig. 7B demonstrate that immunization with ADC encoding LCMV proteins caused significant reduction in virus titers 4 days p.i. with LCMV compared control mice. By day 7, this effect was unambiguous with no detectable virus in the cross-priming condition. These results suggest that initial cross-priming of LCMV proteins

prior to viral infection can enhance anti-viral immunity due to increased frequencies of CTL as shown in Fig. 7A. Induction of protective immune responses against viruses or tumors can be achieved via cross-priming 4–6. In this study, we employed the LCMV infection model ITF2357 ic50 to study how cross-presentation selleck chemical of multiple epitopes translates when studying cross-priming. We used LyUV treatment of the ADC because it fully inactivated the virus and allowed for efficient NP396 cross-presentation similar to HEK-NP cells 7, 8. We initially expected that GP33 would fail to cross-present because it is located in the signal peptide

of LCMV-GP 12, but it was cross-presented with low efficiency, probably due to its exceptional long half-life of 6 h 15. Although NP396, located in the long-lived nucleoprotein 21, was efficient at cross-presentation, NP205 was poor, possibly due to inefficient processing by the phagosomal/proteasomal machineries. GP276 is another epitope that cross-presented with low efficiency, probably due to its low binding affinity to MHC 22, which could be critical when the antigen supply is limited. Immunoproteasomes, which have been implicated in cross-presentation 23, could Thiamet G also account for GP276 poor cross-presentation since it can downregulate GP276 presentation 24. We have

detected LMP7 expression in DC2.4 (unpublished data), which concurs with the previous data showing that immunoproteasomes are expressed in DC irrespective of their maturation states 25. Considering the direct presentation of the NP and GP-derived epitopes, it has been shown that NP epitopes can be detected as early as 2 h p.i., whereas GP epitopes were detected 4–6 h p.i. 20. Our results show that infected ADC can provide antigens for cross-presentation in a comparable time frame. Such kinetics would probably be dependent on the stress status of the infected cell 26 and would be sufficient to supply antigens for cross-presentation before the completion of the replication cycle. Thus far, one would expect that during cross-priming, NP396 will dominate the CTL response in vivo.

All variants followed the Hardy–Weinberg equilibrium (P > 0·05). The case series comprised 612 T1AD patients (of whom 81·9% were of European ancestry) who were treated with two or more injections of insulin per day, and 792 healthy individuals (of whom 65·4% were of European ancestry) without any family history of types 1 or 2 diabetes or autoimmune diseases and normal glucose and HbA1c levels. A heterozygous allelic variant (g.-241 T > A) was found

in the 5′-proximal region of the IL-21 gene in only one patient. This patient was female, aged 30 years, at the onset of disease. She was found to be positive for GAD65 autoantibody (22·8 U/ml) and IA-2 autoantibody (36·9 U/ml). This allelic variant was not found in the other 497 individuals (308 T1AD patients and 189 healthy controls). Although the CT and TT genotypes at this locus could be distinguished, Maraviroc cell line only two individuals with the TT genotype were found in this sample (one in the T1AD group and one in the control group). The CT and TT genotypes were pooled into a single class for statistical analyses to avoid classes with very small numbers, referred to as CT/TT. The CT/TT genotype frequency was 18·7% in the T1AD patients and 10·6% in the healthy controls [odds ratio (OR) = 1·94; confidence interval (CI): 1·37–2·73; P < 0·001; Table 1]. The distribution was similar in males

(12·7%) and females (14·9%), Selleckchem CHIR99021 but was more frequent in individuals of European ancestry (15·4 versus 9·6%; P = 0·0116). When the sample was analysed separately for ancestry, the CT/TT genotype was found to be associated with T1AD risk only in the cohort of European ancestry (OR = 1·811; P = 0·0046). The C1858T PTPN22 polymorphism was

not associated with the age of diabetes onset (11·6 ± 6·9 CT/TT versus 11·1 ± 7·3 CC; P = 0·5). The following islet and extra-pancreatic autoantibodies were analysed: anti-insulin (IAA), anti-glutamic acid decarboxylase (GAD65), anti-tyrosine phosphatase (IA2), anti-21-hydroxylase (21-OH), anti-thyroid peroxidase (TPO), anti-thyroglobulin (TG) antibodies, Selleck Forskolin anti-nuclear antibody (ANA), anti-liver/kidney microsomal type (LKM1), anti-smooth muscle (ASM), rheumatoid factor (RF) and TSH receptor antibody (TRAb). With the exception of anti-LKM1 (which was very rare in both the groups) and RF, all other autoantibodies were significantly more frequent in T1AD patients than in the healthy controls (P < 0·001). Islet autoantibodies were the most frequent in T1AD, followed by thyroid autoantibodies and ANA (Table 2; Fig. 1). The C1858T polymorphism was associated with a higher frequency of GAD65 (26·5% versus 15·9%; OR = 1·891; CI: 1·254–2·853; P = 0·003) and TG autoantibodies (22·2% versus 12·4%; OR = 2·023; CI: 1·164–3·513; P = 0·02) in the whole group (T1AD patients plus healthy controls). A subset of T1D patients who had had the disease for more than 10 years showed that this variant was not associated with persistent islet autoantibodies.

She otherwise had normal growth and development of the right leg. No recurrence was found at 12-year follow-up. Although slight contour asymmetry persists, the bone flap has grown much like the native mandible and the patient has no trismus or difficulties with mastication (Figs. 5A–5C). Melanotic neuroectodermal tumor is a rare entity, with sporadic case reports and series in the literature. Less than 400 cases have been reported to date. First described

in 1918, 90% of the cases are seen Torin 1 in vivo in the head and neck region, with the maxilla being the most affected (68.8%). It is accepted to be of neuroectodermal origin, and as a melanin producing tumor, it produces a blue or black, solid, rapidly growing mass, firmly adhered to the bone. Local excision, with total removal of the mass and curettage of the cavity is the adequate treatment of this benign tumor, but a 10–15% recurrency rate and a 3.2% risk of malignancy have been reported in the literature.[2, 3] In the case reported here, the mass was proportionally large, and a complete resection of the affected bone was preferred for adequate treatment. The feasibility of microsurgical reconstruction in children is no longer a discussion, and although technically challenging, the debate has shifted to evaluating the functional outcome of the reconstructed segment.[4, 5] One particular

concern with these complex reconstructions is how the transplanted tissue will respond to the continuous growth GDC-0199 order of the surrounding structures. We were successful in obtaining near normal growth of the neo-mandible in this case. In adults, the harvest of a fibula free flap does not produce significant function morbidity to the donor leg.[6] In a recent report of 18 fibula flaps used for pediatric mandibular reconstruction,[7] the authors state that the flap would not grow concomitantly with the child. These authors

preserved at least 6 cm of the distal fibula at the donor Celecoxib site in an effort to maintain ankle stability. They were successful in preventing ankle deformities in all of their patients, but other procedures were necessary to correct the length of the transplanted bone. In this case, a long segment of the fibula diaphysis had to be harvested due to the extent of the defect. The proximal and distal ends of the diaphysis of long bones are the regions where most of the bone longitudinal growth occurs through endochondral ossification. We believe that incorporating a more distal segment of the bone into the flap is probably the reason for the continuous growth of the flap and the ankle deformity at the donor site in our case. Other authors have reported similar donor site complications, requiring corrective orthopedic procedures.[8, 9] Interestingly, the flap presented with the expected growth of the mandible segment it replaced. We believe that the same stimulus of the surrounding bone structures and soft tissue that would modulate mandibular growth affected the flap.

However, a few studies have reported that artificially programmed DCs exhibited remarkable changes in phenotype. Immature DCs pre-treated with dexamethasone and subsequently stimulated with tumor necrosis factor-α (TNF-α) exhibited an endocytic

capacity four times higher (at maximum dexamethasone concentration) than iDCs treated with only TNF-α.[34] Clingan et al.,[35] reported that pre-treatment of iDCs with either interleukin-4 (IL-4) or interferon-γ (IFN-γ) inhibited the migration of iDCs in response to CCL3. Coincidentally, they observed that when IL-4 or IFN-γ pre-treated DCs were incubated with FITC-dextran in the presence of CCL3 for 2 min, dextran uptake capacity of the DCs was significantly enhanced by approximately fourfold (IFN-γ) or fivefold (IL-4) versus MLN0128 purchase without CCL3. Yanagawa and Onoe,[36] found that CCL3 and CCL19 rapidly (in less than an hour) selleck inhibitor and selectively enhanced the internalization ability of iDCs and mDCs, respectively, when dextran and chemokines were added simultaneously to

the cell culture. They also noted that CCL19 induced an actin-reorganization related to the endocytic behaviour of mDCs.[37] Moreover, the synergistic effects of combinations of cytokines have been shown on the expansion of blood progenitors,[38] on the endocytic pathway in insulin-producing cells,[39] and on the migration and development of other phenotypes in endothelial cells.[40] Hence it may be possible, using selected chemokines or their combinations, to artificially program iDCs, thereby controlling their phenotypes and maturation status in order to enhance antigen uptake and presentation. We report here the first study to engineer DC phenotypes with select chemokine application to enhance antigen uptake and processing capacity of DCs, which can directly affect antigen presentation and DC-based vaccine efficiency in future. Dendritic cells were pre-treated with Lepirudin the individual chemokines CCL3, CCL19, or their combination in various ratios. Then, 24 hr later, DCs were exposed to lipopolysaccharide (LPS), [a Toll-like receptor 4 (TLR4) ligand], to induce maturation. We demonstrate that when DCs are pre-treated with a chemokine combination of CCL3 : CCL19

in a specific ratio then subsequently stimulated with LPS, certain phenotypic changes arise that are significantly different from those of iDCs or DCs stimulated only with LPS. Dendritic cells programmed with a specific chemokine combination (CCL3 : CCL19 = 7 : 3) retained antigen uptake capacity and exhibited antigen-processing capacity, even after subsequent LPS maturation stimulus, at levels higher than iDCs (36%), and iDCs treated only with LPS (27%), respectively. Along with antigen uptake, this chemokine programming of DCs also modulated expression of MHC molecules and various cytokine responses of DCs even after maturation of DCs. Results here suggest chemokine programming may be a new tool for enhancing ex vivo and in vivo immunotherapy vaccine strategies.

Data are shown as mean ± SEM. Two-tailed Student’s t-test was used to calculate p-values for all experiments. A value of p < 0.05 was considered statistically significant. *p < 0.05, **p < 0.01, ***p < 0.001. We are grateful to Dr. A. Singer and Dr. R. Etzensperger

for critical review of the manuscript. This study was supported by the Intramural Research Program of the US National Institutes of Health, National Cancer Institute, and Center for Cancer Research. The authors declare no financial or commercial conflict of interest. As a service to our authors and readers, this journal provides supporting information supplied by the authors. Such materials are peer reviewed and may be re-organized for online delivery, but are not copy-edited or typeset. selleck inhibitor Technical support issues arising from supporting information (other than missing files) should be addressed to the authors. Figure S1. Characterization of Pim1 transgenic mice. Figure S2. T cell development in LY294002 research buy Pim1TgγcKO mice. Figure S3. LN T cell analysis of Pim1TgγcKO mice “
“Immunoglobulin A is an important mucosal antibody that can neutralize mucosal pathogens by either preventing attachment to epithelia (immune exclusion) or alternatively inhibit intra-epithelial replication following transcytosis by the polymeric immunoglobulin

receptor (pIgR). Chlamydia trachomatis is a major human pathogen that initially targets the endocervical or urethral epithelium in women and men, respectively. As both tissues contain abundant secretory IgA (SIgA) we assessed the protection afforded by IgA targeting different chlamydial antigens expressed during the extra- and intra-epithelial stages of

infection. We developed an in vitro model using polarizing cells expressing the murine pIgR together with antigen-specific mouse IgA, and an in vivo model using pIgR−/− mice. Secretory IgA targeting the extra-epithelial chlamydial antigen, the major outer membrane protein, significantly reduced infection in vitro Tolmetin by 24% and in vivo by 44%. Conversely, pIgR-mediated delivery of IgA targeting the intra-epithelial inclusion membrane protein A bound to the inclusion but did not reduce infection in vitro or in vivo. Similarly, intra-epithelial IgA targeting the secreted protease Chlamydia protease-like activity factor also failed to reduce infection. Together, these data suggest the importance of pIgR-mediated delivery of IgA targeting extra-epithelial, but not intra-epithelial, chlamydial antigens for protection against a genital tract infection. “
“Migration of dendritic cells (DCs) plays an important role in T-cell-mediated adaptive immune responses. Lipopolysaccharide (LPS) sensed by Toll-like receptor 4 (TLR4) serves as a signal for DC migration. We analyzed LPS-induced DC volume changes preceding the directed movement towards chemoattractants.

“
“The development of T-cell responses in pigs vaccinated against Aujeszky’s disease in the presence of maternal-derived antibodies (MDA) was examined. The aim of study was to evaluate the influence of MDA on the postvaccinal T-cell responses and optimization vaccination protocols in MDA-positive pigs. Pigs born to immune sows were vaccinated at different ages against Aujeszky’s disease virus (ADV). For estimation of T-cell responses the lymphocyte proliferation and interferon (IFN)-γ and interleukin-4 production were evaluated. High values of stimulation index were noted in groups vaccinated at 8 or 12 weeks of age (in 60% and 100% animals, respectively). In weaners

vaccinated at 10 and 14 weeks of age, as well as in those vaccinated at 7 days and revaccinated at 8 or 12 weeks of age, CP-690550 mw click here 100% of animals positively responded in the lymphocyte proliferation

assay after booster. At 20 weeks of life, only animals vaccinated at 12 weeks of age, 7 days and 12 weeks of age, and 10 and 14 weeks of age showed antigen-specific proliferation. Similar results were observed with IFN-γ secretion after exposure to live ADV. We demonstrate that early vaccination with a live glycoprotein E-deleted ADV vaccine, in the face of high levels of MDA, could be effective, but the intensity and duration of the anamnestic response depends on the time of booster injection. Vaccination of neonates faces many challenges due to the immaturity of the neonatal immune system and interference by maternal-derived antibodies (MDA) present at vaccination (Fischer et al., 2003). Interference of MDA with vaccine antigen may reduce or even eliminate Depsipeptide datasheet the immune response against live as well as inactivated vaccines. Various degrees of interference of vaccine-induced immune responses

by MDA have been reported for live vaccines as well as for nonreplicating vaccines (i.e. inactivated or subunit vaccines) (Andries et al., 1978; Bouma et al., 1998; Siegrist et al., 1998a, b; Dagan et al., 2000; Klinkenberg et al., 2002; Endsley et al., 2003; Fiore et al., 2003; Loeffen et al., 2003; Premenko-Lanier et al., 2006). It seems that attenuated vaccines are more efficient in protecting animals with passive immunity than inactivated ones (Casal et al., 2004). Optimally, vaccination of animals should begin just after the time of disappearance of maternal antibodies, but this approach may be impracticable due to a high degree of variability between individuals (Monteil et al., 1997). The titer of specific antibodies is often not correlated with protection against the challenge, which is why the targets of successful immunization against most pathogens should include the induction of strong and persistent memory T-cell responses.

The second strategy, developed mainly over the past decade, consisted of more ambitious forms of immune therapy

not aiming at immunosuppression but at inducing/restoring self-tolerance CDK inhibitor to well-defined β cell antigens. The rationale was based on the well-established notion that antigen delivery depends upon the molecular form of the antigen and its route of inoculation, and may lead either to effective immunization or to immune tolerance. This concept stemmed from pioneering experiments performed by D. W. Dresser in the early 1960s, showing that heterologous immunoglobulins that are immunogenic if administered in aggregated form induce specific unresponsiveness/immune tolerance, or ‘immune paralysis’, if injected intravenously (i.v.) in non-aggregated form [19]. Thus it made sense to use well-defined autoantigens as therapeutic tools to attempt inducing/restoring self-tolerance in T1D. As in many other autoimmune diseases, in T1D various candidate autoantigens have been incriminated as potential triggers and targets of the disease. These include the main β cell hormone proinsulin/insulin itself, glutamic acid decarboxylase (GAD), a β cell-specific protein

phosphatase IA-2, a peptide (p277) of heat shock protein 60 (hsp60), the islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP), a preferential

target of pathogenic CD8+ T cells, and the most recently characterized zinc transporter Ivacaftor order ZnT8. Targeting some of these antigens has proved successful in NOD mice, as disease was effectively prevented by administration of protein or specific peptide antigens such as pro-insulin, insulin, GAD, the p277 peptide of hsp60 using various routes [i.v., subcutaneous (s.c.), oral, intrathymic, intranasal][20]. Although highly effective in the experimental setting, the transfer to the clinic of β cell autoantigen-induced strategies was beset by a number of difficulties. Antigens used in patients included insulin or altered insulin peptides, GAD65 and the hsp60 Unoprostone p277 peptide (DiaPep277). Most applications have been via administration of the antigen or peptide alone, and one approach has included the administration of antigen plus adjuvant. Insulin has been the main antigen used clinically. It was readily available for clinical use; experiments in animal models consistently showed effects in preventing diabetes; and several evidences suggested that insulin could be a primary autoantigen in T1D. Insulin has been used as an immunotherapy via s.c., i.v., oral and intranasal routes. Two trials performed after diabetes onset in approximately 100 patients have tested the use of oral insulin at a limited dose range without observing efficacy [21,22].

Epidemiological [46,87,121,122] and experimental [6,14,97] data also suggest that obesity-related microvascular dysfunction may contribute to the development of cardiometabolic risk factors such as hypertension and insulin resistance. In most forms of experimental and clinical hypertension, peripheral vascular resistance is increased in proportion to the increase in blood pressure [69]. This increase in peripheral vascular resistance is likely to reflect GSK126 clinical trial changes in the microcirculation. In several tissues, both microvascular endothelium-dependent vasodilatation and capillary density has been found to correlate inversely with blood pressure in hypertensive and normotensive

subjects

[22,98–100]. Although it has been known for many years that increased wall-to-lumen ratio and microvascular rarefaction can be secondary to sustained elevation BGJ398 clinical trial of blood pressure [69], there is also evidence that abnormalities in the microcirculation precede and thus may be a causal component of high blood pressure. Microvascular rarefaction, similar in magnitude to the rarefaction observed in patients with established hypertension, can already be demonstrated in subjects with mild intermittent hypertension and in normotensive subjects with a genetic predisposition to high blood pressure [3,88]. Moreover, in hypertensive subjects, capillary rarefaction in muscle has been shown to predict the increase in mean arterial pressure over two decades [39]. More recently, a smaller retinal arteriolar diameter has been shown to predict the occurrence and development of hypertension in a prospective, population-based study of normotensive middle-aged persons [46,121]. Other, indirect, Adenosine evidence comes from studies demonstrating that inhibitors of angiogenesis and especially inhibitors of VEGF/VEGFR-2 signaling cause arterial hypertension, which, in severity,

is paralleled by microvascular rarefaction, and reversible upon discontinuation of the angiogenesis inhibitor [18,70]. In addition, calculations by mathematical modeling of in vivo microvascular networks predict an exponential relationship between capillary and arteriolar number and vascular resistance [18,34]. Total vessel rarefaction up to 42% (within the range observed in hypertensive humans) can increase tissue vascular resistance by 21% [43]. In a microvascular network maturation model, rarefaction of vessels below a critical diameter was shown to be important in determining the mature network structure and its response to hypertension [47]. It was shown that there was a network density threshold below which resistance to flow dramatically increased. In addition, simulating hypertension in a mature and already compromised network leads to further rarefaction [48].

The procedure was performed

according to the instructions of the manufacturer and the acquisition and analysis was performed as described previously (Vissers et al., 2010). Proliferation was studied by intracellular expression of the nuclear Ki-67 antigen (BD Pharmingen, San Diego, CA) by flow cytometric analysis. Cultured cells were collected on both 4 and 8 days of culture. In each assay, 5 × 105 hPBMC were incubated with 100 μL cytofix/cytoperm (BD Pharmingen) for 15–20 min on ice to fix and permeabilize the cells. Cells were washed twice with perm/wash buffer (BD Pharmingen) and incubated with Selleckchem BGB324 an anti-Ki-67 PE antibody (or the matched isotype control) diluted in perm/wash buffer for 30 min on ice in the dark. Hereafter, the cells were washed once again with the perm/wash buffer, resuspended in PBS and measured selleck chemicals llc on the flow cytometer. Values are expressed as the percentage of stimulated cells positive for the Ki-67 mAb corrected for the percentage of stimulated cells that were positively stained by the isotype control. Cytokine production by hPBMC was analyzed in supernatants of cells cultured for 1, 4 and 8 days. The production of the innate and

adaptive cytokines IL-1β, IL-10, IL-12p70, IL-13, IFN-γ and TNF-α was detected using cytometric bead array (cba; BD Biosciences). All buffers used in this protocol were obtained from the BD CBA Soluble Protein Master Buffer Kit (BD Pharmingen) and the procedure was performed according to the manufacturer’s protocol. The detection limits according to the manufacturer were as follows: 1.1 pg mL−1 IL-1β, 2.3 pg mL−1 IL-10, 2.2 pg mL−1 IL-12p70, 1.6 pg mL−1 IL-13, 0.3 pg mL−1 IFN-γ and 0.7 pg mL−1 TNF-α. The samples were measured on the FACSCanto II, using fcap software (BD Biosciences). Because of a nonnormal distribution PLEKHB2 of most of the data the nonparametric Wilcoxon signed-rank test was used. This test allowed to compare data from cultures in the absence of a bacterial strain with cultures in the presence of the different

strains and to compare data from cultures of different strains. The Wilcoxon signed-rank test was also used to compare cytokine data on different days and to compare cytokine data on day 8 of not-restimulated and restimulated cells. When P<0.05, the difference was considered to be statistically significant. The statistical analysis was performed using spss software (version 15.0; SPSS Inc., Chicago). Experimental data are presented as mean ± SEM. Although differences in hPBMC subset composition were observed between the different donors, all values were within the normal range of leukocytes present in the peripheral blood as assessed by Erkeller-Yuksel et al. (1992) and Jentsch-Ullrich et al. (2005) (data not shown). Viability of hPBMC directly after isolation was above 80% for all donors and the percentage late apoptotic/necrotic cells was below 5% (data not shown).

Data are presented as mean±SD of independently analysed mice.

Statistical significance was calculated using the paired Student’s t-test. A value of p<0.05 was considered significant (*p<0.01; **p<0.001; ***p<0.0001). This work was supported by the FWF project P-19017, P-22419, W-1213 the OeNB grant 11710 and the DocForte fellowship 22174 of the OeAW. Work at SIAF was supported by the Swiss National Science Foundation grants no. 320030_127618/1 and 316030_128813/1 and by the Christine Kühne-Center for Allergy Research and Education, Davos (CK-CARE). Conflict of interest: The authors declare no financial or PF-02341066 datasheet commercial conflict of interest. Detailed facts of importance to specialist readers are published as ”Supporting Information”. Such documents are peer-reviewed, but not copy-edited or typeset. They are made available as submitted by the authors. “
“This chapter contains sections titled: Introduction to the innate immune system Innate immune receptors and cells TLRs and pattern recognition TLR signalling in response to LPS Peptidoglycan and Nods

Nod-like receptors recognize PAMPs and DAMPs Damage associated molecular patterns (DAMPs) Complement proteins perform several innate immune functions The classical complement pathway The lectin and alternative complement pathways Biological properties of complement cleavage products Opsonization by complement proteins Phagocytosis Fc receptors induce phagocytosis RO4929097 Neutrophil function and the respiratory burst ADCC NK cells recognize missing self Activating adaptive immunity Dendritic cells link innate and adaptive immunity Summary “
“Inflammatory bowel disease (IBD) is associated with neutrophil

infiltration into the mucosa and crypt abscesses. The chemokine interleukin (IL)-8 [murine homologues (KC) and macrophage inflammatory protein (MIP)-2] and its receptor CXCR2 are required for neutrophil recruitment; thus, blocking this engagement is a potential therapeutic strategy. In the present study, we developed Selleck ZD1839 a preclinical model of neutrophil migration suitable for investigating the biology of and testing new drugs that target neutrophil trafficking. Peritoneal exudate neutrophils from transgenic β-actin-luciferase mice were isolated 12 h after intraperitoneal injection with thioglycollate, and were assessed phenotypically and functionally. Exudate cells were injected intravenously into recipients with dextran sodium sulphate (DSS)-induced colitis followed by bioluminescence imaging of whole-body and ex vivo organs at 2, 4 and 16–22 h post-transfer. Anti-KC antibody or an isotype control were administered at 20 µg/mouse 1 h before transfer, followed by whole-body and organ imaging 4 h post-transfer. The peritoneal exudate consisted of 80% neutrophils, 39% of which were CXCR2+. In vitro migration towards KC was inhibited by anti-KC.