Neutrophils are the more relevant cell type with specific recognition binding sites for LXA4 and 15-epi-LXA4 [11], and the signalling evoked by LXs in these cells has been suggested to be through phospholipase D (PLD) activation, arachidonic acid release, presqualene diphosphate (PSDP) increase and phosphorylation check details of lymphocyte-specific protein 1 (LSP-1) (reviewed

in [12]). LXA4 and 15-epi-LXA4, as well as their stable analogues, bind with high affinity to the GPCR formyl peptide receptor 2/LXA4 receptor (FPR2/ALX) (also known as formyl peptide receptor-like 1 (FPRL1) [13]. Several reports have shown the role of FPR2/ALX receptor in triggering the anti-inflammatory and pro-resolution properties associated with LXs. Deficiency in the FPR2/ALX receptor in mice decreases the ability of LXA4 to dampen inflammation in vivo [14, Sotrastaurin order 15], whereas over-expression of the human

LX receptor in mice enhances LX-mediated resolution of inflammation [16]. Of interest, in a heterodimer model using BLT1/FPR2/ALX chimera, the activation of each GPCR is mediated by the individual agonist binding to each subunit discarding transactivation mechanisms [17]. In humans, up-regulation of neutrophil FPR2/ALX expression has been observed after low-dose aspirin administration in acute inflammation [18]; most recently the promoter for FPR2/ALX has been identified, and LXA4 has shown to enhance both promoter activity and receptor expression in vitro [19]. Besides the anti-inflammatory properties described for FPR2/ALX, the receptor can also mediate proinflammatory actions, depending on the ligand characteristics (reviewed in [12]). Bioactive lipid mediators as well as specific small peptides/proteins, such as major histocompatibility complex (MHC) binding peptide and its surrogate MMK-1, and a photolytic product of the

acute phase response, serum amyloid protein A (SAA), interact in vitro with the same FPR2/ALX receptor. Opposite to lipid ligands not (e.g. LXs and 15-epi-LXs) that function as anti-inflammatory mediators, peptides are reported to stimulate calcium mobilization and neutrophil migration in vitro (reviewed in [12]). In addition to FPR2/ALX, 15-epi-LXA4 has also been described to bind to cysteinyl leukotriene receptor 1 (CysLT1) and competes for this receptor with equal affinity as the natural CysLT1 ligand leukotriene D4 (LTD)4 [20], suggesting a double role for 15-epi-LXA4 on CysLT1 signalling as well as on FPR2/ALX-regulated neutrophil migration and function. Of interest, the MK-571 leukotriene modifier drug with a related structure to montelukast (MK-476), a potent and selective CysLT1 antagonist used widely as an oral treatment of persistent asthma [21], has been described to bind to both FPR2/ALX and CysLT1 [20], suggesting the potential double function on both receptors.

96 These experiments have thus unveiled a causal role of FGF-23 in the pathogenesis of LVH. The association between FGF-23 and CV surrogate

markers described in Table 2 strongly suggests that the effect of FGF-23 on mortality in CKD is most likely mediated through a CV pathway. A recent clinical study of 200 CKD patients, which highlighted phosphate metabolism associated with vascular and cardiomyocyte dysfunction, also reported that FGF-23 levels were independently associated with BMS-777607 purchase the cardiac biomarker troponin-T.63 Despite the large body of observational evidence for an association between phosphate and adverse outcomes, very few randomized controlled trials (RCT) have assessed whether therapy with phosphate binders affects significant

clinical outcomes. One prospective cohort study of 10 044 incident haemodialysis patients, the Accelerated Mortality of Renal Replacement study, compared all-cause mortality at 1 year among patients either treated or not treated with phosphate binders during the first 90 days of dialysis.97 On multivariate analysis, as well as in propensity score-match comparison, this study showed that treatment with phosphate binders was independently associated with decreased mortality compared with no treatment. Another cohort study in non-dialysis patients also showed an association with phosphate binder administration and survival.98 This single-centre study of 1188 men with moderate to advanced CKD reported that selleckchem binders were associated with significantly lower all-cause mortality (HR 0.61 (95% CI 0.45–0.81)). Neither of these studies however were RCT and therefore may have significant potential confounders. Several RCT have assessed the effect of phosphate binders on vascular calcification (coronary

and aortic) in dialysis and pre-dialysis CKD patients.99–103 These studies however have all involved comparisons between calcium-based binders and non-calcium based binders, with most suggesting that non-calcium based binders contribute less to the development of heptaminol vascular calcification. A meta-analysis of eight RCT (collective sample size 2873 participants), however, showed no benefit of using non-calcium over calcium-based phosphate binders on mortality (RR 0.68, 95% CI 0.41–1.11) or in CV events (two RCT, n = 153, RR 0.85, 95% CI 0.35–2.03).104 The only RCT to directly address the impact of phosphate binders on survival as a primary end-point was also a comparison between calcium-based binders and sevelamer.105 The Dialysis Clinical Outcomes Revisited (DCOR) study was a multicentre, randomized, open-label trial comparing the different binders on all-cause and cause-specific mortality. Unfortunately despite 2103 patients initially randomized to treatment, only 1068 patients completed the study in which the primary end-point was negative.

This uncommon clinical aspect is mostly seen, although not

exclusively, in immunosuppressed patients. The principal isolated organism is Trichophyton spp. but the entity can also be caused by non-dermatophyte moulds. The mechanism of infection is unclear; it could be acquired through the proximal nail fold, or, as more recently proposed, may be secondary to lymphatic or vascular dissemination. To analyse the clinical, mycological and histopathological features of fungal leuconychia, we included 10 patients with the clinical diagnosis of fungal leuconychia. Direct examination of culture and nail plate biopsy were performed. Nine patients had confirmed fungal leuconychia. Four had a positive Fulvestrant manufacturer culture and all had positive haematoxylin–eosin (H&E) and Periodic Acid Schiff (PAS) stains for fungal elements with varying degrees

of nail plate invasion. Seven of our patients were immunosuppressed FK506 cell line and the isolated aetiological agents are the same as previously reported. The direct examination is reliable, fast and inexpensive to establish the diagnosis. The correlation of onychomycosis with histology, stained with H&E and PAS was 100%. We think that the site of nail plate invasion provides more information to support the theory that the infection reaches the ungual apparatus through systemic dissemination. “
“The red algae Asparagopsis taxiformis collected from the Straits of Messina (Italy) were screened for antifungal activity against Aspergillus species. EUCAST methodology was applied and extracts showed antifungal activity against A. fumigatus, A. terreus and A. flavus. The lowest minimum inhibitory concentrations observed were <0.15 mg ml−1 and the highest were >5 mg ml−1 for Aspergillus spp. tested. Agar diffusion assays confirmed antifungal activity of A. taxiformis extracts in Aspergillus species. “
“Patients with heart transplantation have a high incidence of infectious complications, especially fungal infections. The aim of the systematic review was to determine the best pharmacological strategy to prevent fungal infections among Methamphetamine patients with heart transplant. We searched the PubMed and Embase

databases for studies reporting the effectivenesss of pharmacologic strategies to prevent fungal infections in adult patient with a heart transplant. Our search yielded five studies (1176 patients), four of them with historical controls. Two studies used inhaled amphotericin B deoxycholate, three used itraconazole and one used targeted echinocandin. All studies showed significant reduction in the prophylaxis arm. Different products, doses and outcomes were noted. There is a highly probable benefit of prophylaxis use, however, better studies with standardised doses and comparators should be performed. “
“There is an increasing frequency of candidaemia caused by Candida glabrata which has decreased in vitro susceptibility to fluconazole.

Importantly, adoptive transfer of antigen-loaded DCs stimulated with GLA-SE in vivo was sufficient to induce specific Th1-cell responses in naïve mice. In contrast, DCs stimulated with emulsion alone were unable to prime T cells. Since the DCs also had to express MHCII, this indicates that their T-cell immunizing function required direct presentation of antigen in the mice primed by adoptively transferred DCs. To our surprise, Selleckchem Sirolimus antibody responses were unaltered after CD11c+

depletion. In this paper, we only analyzed total IgG responses. Maturation of DCs may still have a role in antibody affinity. The type of immune response that eliminates an infection depends on the type of pathogen. Induction of CD4+ T-cell responses by vaccination was learn more associated with diminished simian immunodeficiency virus (siv) replication after intrarectal challenge and decreased HIV acquisition

in the Thai HIV vaccine trial 44, 45. The results presented here demonstrate that GLA-SE is an efficient adjuvant for the generation of HIV-gag-specific Th1-cell immune response. IFN-γ was produced in large amounts by antigen-specific T cells in both spleen and lymph nodes. HIV-1 vaccines will most likely need to induce mucosal immunity. Mucosal tissues are the major site of natural HIV transmission and the reservoir for HIV replication quickly leading to a rapid loss of T cells in the intestine 46, 47. In addition, Th1 type CD4+ T cells are known to improve the mobilization of the cognate antigen-specific CD8+ T cells to a site of infectious challenge 48, 49. Thus GLA-SE has the capacity to adjuvant a protein vaccine to

induce mucosal immunity that potentially is valuable to limit viral replication and curtail systemic dissemination. Previous studies successfully showed that local immune responses were able to prevent virus spread from the gut mucosa into the systemic circulation 50–52. However, the general belief is that local but not systemic immunization is required to induce robust mucosal responses 53–55. Interestingly, we Interleukin-2 receptor found that s.c. injection of the GLA-SE and anti-DEC-HIV gag p24 vaccine was able to induce strong mucosal T-cell responses. Immunization with HIV-gag targeted or untargeted protein plus GLA-SE induced a broad range of different antibody isotypes and therefore a combination of Th1 and Th2-cell responses. This contrast, i.e. with polarized Th1 T-cell responses, may be explained by the different requirement for DC priming. This result is consistent with previous studies where addition of GLA-SE gives a mixed Th1/Th2-cell response but also increases the IgG2/IgG1 ratio to an existent M. Tuberculosis and Influenza vaccine 27, 56.

Studies on collagen type II (CII)-induced arthritis in susceptible DBA/1 mice revealed that administration of anti-OX40L antibodies reduced the associated pathological lesions significantly; it did not inhibit the development of CII-reactive T cells, but suppressed IFN-γ and anti-CII IgG2a production [70]. Similarly, the synovial fluid of patients with active RA contained increased numbers of OX40+ T cells [71]. An important role of OX40 signalling in the progression of CII-induced check details RA has been demonstrated in studies with IL-1α/β−/−, mice where a reduced incidence of CII-induced RA was

correlated with decreased expression of OX40 on T cells [72]. Perivascular infiltrates of the central nervous system (CNS) of mice treated with myelin oligodendrocyte glycoprotein (MOG)35–55 peptide, and of patients with multiple sclerosis, contain a large number of CD134+ cells [73]. That CD134 signalling is important in the resolution of EAE was confirmed by showing that induction of EAE in CD134−/− mice yielded in clinical evidence of reduced severity, and decreased inflammatory infiltrates markedly within the CNS [73]. Moreover, the resistance to EAE of CD134−/− mice was found to be associated with a marked reduction in the number of pathogenic

IFN-γ-producing T cells infiltrating the CNS [73]. Conversely, triggering OX40 signalling exacerbated EAE [74,75]. In accordance, blockade of CD134–CD134L interaction by soluble CD134 at the onset of disease reduced disease symptoms [76]. Increased OX40 expression on the CD4+ T cells of patients suffering from myasthenia Y-27632 gravis, a protoypic antibody-mediated organ-specific autoimmune disease, has also been reported [77]. Pakala et al. [78] have demonstrated that administration of blocking anti-CD134L mAb

to NOD mice had TCL reduced glucose levels and islet infiltrating leucocytes and reduced the incidence of diabetes significantly. The significance of CD134–CD134L in autoimmune diseases is highlighted in Table 1 and Fig. 1d. CD137 (4-1BB), an important T cell co-stimulatory molecule [9], exists as both a 30-kDa monomer and 55-kDa homodimer [79]. Its expression is activation-induced [79,80] and it is expressed primarily on activated CD4+ and CD8+ T cells [79] and on activated NK and NK T cells [81]. In contrast, 4-1BB is expressed constitutively on primary human monocytes, DCs, blood vessel endothelial cells and human follicular DCs, as well as CD4+CD25+ regulatory T cells (Tregs) [82–86]. In vitro and in vivo studies indicate that signalling via 4-1BB preferentially activates CD8+ T over CD4+ T cells [87]. Soluble forms of CD137 (sCD137) and sCD137L have been observed in sera of RA and MS patients, where levels of sCD137 and sCD137L correlated with disease severity [88–91]. The precise role of sCD137 and sCD137L in autoimmune diseases is, however, not understood completely.

The experiments were carried out in triplicate. In our study, the chequerboard method was used for the measurement of interactive inhibition of synergy between the antibiotics and fungal extract (White et al., 1996). Synergistic combinations were prepared using the fungal extract and the antibiotics to which the bacterial strains were resistant. The concentrations of the fungal extract and antibiotics were started at their MIC value and then serially diluted into twofold steps. The effects of combination were evaluated by calculating the fractional inhibitory concentration index (FICI) of each combination. The synergistic experiments

were carried out in triplicate. FIC of fungal extract=MIC of fungal extract in combination with antibiotics/MIC of fungal extract alone • FIC of antibiotics=MIC of antibiotics in combination with fungal extract/MIC of antibiotics alone • FICI=FIC of selleck chemical fungal extract+FIC of antibiotics Synergy was defined as an FICI≤0.5. An FICI between 0.5 Ganetespib and 4.0 indicates that there is no interaction between the agents. An FIC>4.0 indicates

that there is antagonism between the two agents (Odds, 2003). The morphological characteristics of the endophytic fungus were observed on PDA after 10 days of growth at 30 °C. Colonies on PDA were circular, raised, at first orange-white, sometimes grey and becoming pale orange with age, with white, dense, cottony aerial mycelia without visible conidial masses, reverse bright orange but sometimes yellowish-brown to olive-brown and very slow growing. Acervuli and setae were absent in culture. Conidia were hyaline, unicellular and cylindrical with obtuse apices and tapering bases. Average conidial size was 14.7 × 3.8 μm. Traditionally, identification of Colletotrichum sp. has been based on the size and shape of conidia and culture characteristics such as colony colour, growth rate and texture (Smith & Black, 1990). Morphological characteristics allowed the identification of the endophytic fungus as C. gloeosporioides, which was reinforced by the sequence of its 18S rRNA gene that gave

a 91% sequence similarity to those accessible at the blastn of C. gloeosporioides. Niclosamide The maximum growth of the fungus was observed on PDA medium. The optimum pH for the maximal growth of the fungus was found to be 5.0. The antimicrobial activity of the extract against bacterial and fungal strains was investigated by the disk diffusion method. The results showed that methanol extract had an effective antimicrobial activity against all the tested microorganisms (Table 1). The methanol extract produced a maximum inhibition zone of 21.6 mm against S. aureus, 19.6 mm against B. subtilis, 18.3 mm against E. coli, 18.6 mm against P. aeruginosa and 17.6 mm against C. albicans. In contrast, the hexane extract had no inhibitory effect against all the tested organisms. The ethyl acetate extract exhibited moderate antimicrobial activity against all the tested microorganisms. Similarly, Lu et al.

After washes, the number of tumor-infiltrated CD8+, CD4+Foxp3− and CD4+Foxp3+ cells were analyzed using flow cytometry assay and the following antibodies: FITC-labeled anti-mouse CD8, FITC-labeled anti-mouse CD4 (both from BD Biosciences) and PE-labeled anti-mouse Foxp3 mAb (eBiosciences), and appropriate

FITC- and PE-labeled isotype control Ab (BD Biosciences). see more The level of CD4+Foxp3+ cells (Treg cells) was also evaluated in spleens of tumor-bearing treated and control mice using the same flow cytometry assay. The expression of PDL-1 on the surface of TC-1 cells was detected by flow cytometry using anti-PDL-1 (CD274) mAb (eBiosciences). Briefly, confluent TC-1 cells were trypsinized, left for an hour on ice and stained with PE-labeled anti-mouse PDL-1 antibody for 30 min at 4oC. After washing, surface expression of PDL-1 on TC-1 cells was analyzed using FACScan flow cytometer and CellQuest software (BD Biosciences). The ability of CT-011 antibody to inhibit the TC-1 tumor-mediated suppression of CD4+CD25− T-cell proliferation was assessed by carboxyfluorescein

diacetate, succinimidyl ester (CFSE)-based suppression assay. The CD4+CD25− T (Tconv) cells were purified from the spleens of naïve mice using the Militenyi Biotec MACS T-cell purification kit as suggested by the manufacturer. Cells were labeled with 1 μM CFSE dye as suggested by the manufacturer (Invitrogen), as suggested by the manufacturer. After washes, CFSE-labeled Tconv cells were stimulated with α-CD3 α-CD28 polystrene dynal beads Wnt drug (Invitrogen) and co-incubated with TC-1 cells at a 1:1 ratio for 4 days, alone or

in the presence of 50 μg/mL concentrations of CT-011 antibody, PDL-1-IgG protein or isotype control antibody. After washes, samples were evaluated for CFSE dye dilution using FACScan flow cytometer and CellQuest software (BD Biosciences). All Erastin cost statistical parameters (average values, SD, significant differences between groups) were calculated using the GraphPad Prism Software. Statistical significance between groups was determined by one-way ANOVA with Tukey’s multiple comparison post-test (p<0.05 was considered statistically significant). The authors thank Daniel O'Mard, Ashley Reynolds and Gail McMullen from the NIH animal facility for their technical assistance with animal injections. This work was supported by the Intramural Research Program of the Center for Cancer Research, NCI, NIH. Conflict of interest: R. R. Y. is an employee of CureTech Ltd., which provided CT-011. The remaining authors declare no financial or commercial conflict of interest. "
“Th1 CD4+ T cells and their derived cytokines are crucial for protection against Mycobacterium tuberculosis.

9 A recent paper that measured the thymi of African children demonstrated a closer relation between mortality factor and thymus size, and children who had malaria had smaller thymi.10 Thymocyte migration seems to be controlled by the combined effects of a series of molecular interactions, including those mediated by extracellular matrix proteins, as well as by chemokines, all being produced/secreted by thymic microenvironmental cells.9,11 For example, the chemokines CXCL12 and CCL25 are relevant for inducing the migration of developing thymocytes, an effect that is mediated by the CXCR4 and CCR9 receptors, respectively.12 The extracellular matrix (ECM) ligands, Sirolimus fibronectin

and laminin, are also very important for the migration of developing thymocytes through their interaction with specific integrin-type receptors, including VLA-4 and VLA-5

(CD49d/CD29 and CD49e/CD29) with fibronectin, and VLA-6 (CD49f/CD29) with laminin.11,13,14 Again, any changes in these interactions might lead to a disturbance in thymocyte migration. In fact, this has been demonstrated in the thymus of the non-obese diabetic mouse, which has an expression/functional defect of VLA-5.15,16 Moreover, in Trypanosoma cruzi experimental infection, the thymic atrophy, here defined by loss of thymus weight and cellularity, was characterized by premature escape of immature cells, mainly the DP subpopulation, probably as a result of hyper-responsiveness to ECM and chemokine components, and resulting in the premature and abnormal escape of DP lymphocytes

and the consequent presence of immature T cells in selleckchem the periphery.17,18 Following from this, changes in the expression/function of one or more of the cell-migration-related molecules discussed above may result in abnormal intrathymic T-cell development with consequences in the shaping of the peripheral T-cell pool. Herein we investigated the intrathymic expression of ECM ligands and receptors, as well as chemokines and their respective receptors, during the experimental P. berghei infection. We also evaluated thymic atrophy in this infectious disease, and its possible mafosfamide consequences for the T-cell migratory response. Our data explain the significant intrathymic alterations in P. berghei-infected mice, comprising the expression of cell-migration-related ligands, including the ECM elements laminin and fibronectin, as well as the chemokines CCL25 and CXCL12. Moreover, the thymocyte migratory response to these ECM and chemokine ligands is enhanced in infected mice, suggesting that a defect in cell-migration-related thymic function may contribute to shaping the abnormal peripheral pool of T lymphocytes seen in murine malaria. Specific pathogen-free 8-week-old male BALB/c mice were purchased from CEMIB/UNICAMP (Campinas, São Paulo, Brazil) and housed in microisolator cages with free access to water and food.

In future, the ability of other groups to perform assays developed in other laboratories needs to be addressed; an assay is of little value if it cannot be performed by scientists worldwide. Combinations of the different approaches described here also deserve testing. For example, it may be that stimulating cells with nitrocellulose-bound islet antigens followed by tetramer analysis of the responding population, detected by CFSE dilution, will be more informative than any of these assays alone. The ability to measure mRNA transcripts readily from antigen-stimulated PBMCs adds another weapon to the arsenal. Molecular approaches are well suited to broad screening of many transcripts, potentially giving

a detailed picture of how cells are responding to islet and control antigens. Again, these approaches may be combined with current assays such as ELISPOT to confirm JQ1 datasheet that induction of a transcript correlates with protein secretion. Currently, none of the methods can measure directly the activation and function of islet-antigen specific regulatory T cells. ELISPOT

assays for IL-10 have been used successfully to detect IL-10 secretion following in vitro stimulation with islet antigen-derived BIBW2992 peptides [28,58]. While IL-10 is clearly secreted by some human regulatory T cells [59,60], it is not the only cytokine or cellular pathway used by regulatory T cells [61]. Hence, a more direct measure of regulatory T cell function would be a useful tool. T cell responses measured by an in vitro assay are the outcome of complex interactions between antigen-presenting

cells, effector and regulatory T cell subsets, antigen and components of the innate immune system. Many of these components are yet to be delineated clearly, but measuring the outcome of these interactions will help to dissect the contributing events. Despite the challenges inherent in the detection and analysis of human islet autoantigen-specific T cells, several methods have been developed. The assays on this ‘short-list’ Gefitinib clinical trial are currently being tested and optimized and will aid greatly in the development of immune therapies for T1D and other immune-based diseases. The T-cell Workshop Committee of the Immunology of Diabetes Society (IDS) is generously supported by the Juvenile Diabetes Research Foundation (JDRF grant no. 5-2009-413). We thank members of the IDS Council for critical reading of the manuscript. The authors have no conflicts of interest to declare. Members of the T-Cell Workshop Committee of the Immunology of Diabetes Society: Barbara M. Brooks-Worrell, Veterans Affairs Puget Sound Health Care System, University of Washington, Seattle, WA, USA; Corrado M. Cilio, Lund University, Department. of Clinical Sciences, Cellular Autoimmunity Unit, Malmö, Sweden; Ivana Durinovic-Bellò, Benaroya Research Institute, Seattle, WA, USA; Peter A.

Vertebrates cannot synthesize chitin; however, their genomes contain genes for chitinases and chitinase-like proteins which might play a role in recognition and immune defense of fungi and helminth parasites 1–3. Chitinase-like proteins are linked to genomic regions encoding MHC paralogous genes, suggesting that they might have been part of a “proto MHC” before the bilateral expansion 4, 5. Natural Ab to N-acetyl-glucosamine, the sugar monomer of chitin, have

been detected in various mouse strains with increased titers in aged mice 6. In addition, chitin-specific Ab have been generated in rabbits 7. This demonstrates that the adaptive immune system can recognize and respond to chitin. Infections with helminths generally induce expression of the acidic mammalian chitinase (AMCase) and Fostamatinib chemical structure the chitinase-like proteins Ym1/Ym2 in an IL-4 or IL-13-dependent manner 8, 9. AMCase was also found to be induced after allergic provocation of the lung and pathology could be ameliorated by administration of the allosteric inhibitor allosamidin 10. However, constitutive expression of AMCase in the lung of transgenic mice did not cause inflammation or airway hyper-reactivity and rather protected against chitin-induced recruitment of eosinophils and basophils 9. Macrophages and DC are

probably click here the main cell types that recognize chitin and subsequently modulate the adaptive immune response. Potential transmembrane receptors for chitin include the mannose receptor 11, TLR2 and dectin-112 and the recently described fibrinogen C domain-containing protein 1 13. The modulation of immune responses by chitin is still poorly understood and may depend on particle size and route of administration. Baricitinib It has been shown that

intravenous injection of chitin induces IFN-γ release from NK cells and activation of alveolar macrophages 14. We noticed a transient recruitment of eosinophils and basophils after intranasal application of chitin 9. Furthermore, chitin induced expression of arginase 1 (Arg1) in macrophages. This gene is known to be strongly upregulated by the Th2-associated cytokines IL-4 or IL-13 and serves as prototypic marker for alternatively activated macrophages (AAM) 9. Therefore, chitin may promote type 2 immune responses. However, reduced eosinophilia and lower levels of Th2 cytokines were observed after oral or intranasal chitin administration during allergic immunization with OVA or extracts from ragweed, Dermatophagoides pteronyssinus or Aspergillus fumigatus15–17. Chitin was further found to induce IL-17A and TNF-α expression by BM-derived or peritoneal macrophages in a TLR2- and dectin-1-dependent manner 12, 18. In addition, small chitin particles (<40 μm) also induced IL-10 expression by macrophages in vitro, suggesting that chitin-exposed macrophages may have immune suppressive functions 12. Macrophages serve as APC for CD4+ T cells, as they take up antigens and present them in the context of peptide/MHC-II complexes.