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The application of foliar sprays of suspensions of relatively insoluble essential element salts is gradually becoming common, chiefly with the introduction of nano-technology approaches in agriculture. However, there is controversy about the effectiveness of such sparingly soluble nutrient sources as foliar fertilizers. In this work, we focussed on analysing the effect of adding Ca-carbonate (calcite, CaCO3) micro- and nano-particles as model sparingly soluble mineral compounds to foliar fertilizer formulations in terms of increasing the rate of foliar absorption. For these purposes, we carried out short-term foliar application experiments by treating leaves of species with variable surface features and wettability rates. The leaf absorption efficacy of foliar formulations containing a surfactant and model soluble nutrient sources, namely Ca-chloride (CaCl2), magnesium sulphate (MgSO4), potassium nitrate (KNO3), or zinc sulphate (ZnSO4), was evaluated alone or after addition of calcite particles. In general, the combination of the Ca-carbonate particles with an essential element salt had a synergistic effect and improved the absorption of Ca and the nutrient element provided. In light of the positive effects of using calcite particles as foliar formulation adjuvants, dolomite nano- and micro-particles were also tested as foliar formulation additives, and the results were also positive in terms of increasing foliar uptake. The observed nutrient element foliar absorption efficacy can be partially explained by geochemical modelling, which enabled us to predict how these formulations will perform at least in chemical terms. Our results show the major potential of adding mineral particles as foliar formulation additives, but the associated mechanisms of action and possible additional benefits to plants should be characterised in future investigations. [ABSTRACT FROM AUTHOR]

Copyright of Boletín de la Asociación de Geógrafos Españoles is the property of Asociacion de Geografos Espanoles and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Writing presents considerable challenges to students’ motivation. Yet there is a dearth of studies assessing the role of affect and motivation in writing performance for students with migration backgrounds (MB), who often underachieve in writing. Our study addressed this research gap by investigating the interplay between writing self-efficacy, writing anxiety, and text quality in 208 secondary students with and without MB using Response Surface Analyses. The data showed comparable levels of self-efficacy and, notably, lower writing anxiety levels among students with MB despite lower writing achievements. In the full sample, we observed positive correlations between self-efficacy and text quality and negative correlations between writing anxiety and text quality. When modeling efficacy and anxiety measures and their interplay to predict text quality, self-efficacy measures continued to account for statistically detectable unique variance in text quality, whereas writing anxiety did not. However, students with MB demonstrated differing interplay patterns, with less efficacious students with MB showing positive relations between writing anxiety and text quality. [ABSTRACT FROM AUTHOR]

Private engagement has always been central to biodiversity conservation. Recently, the role of private enterprises in (eco)tourism have increased, and private lands play a pivotal role in expanding protected areas within societies throughout the world. This paper contributes to discussions of private engagement in conservation and its relation to tourism (recreation generally), with novel insight on how the conservation-tourism nexus on private land is approached in different geographical contexts. We present a systematic literature review that results in five thematic clusters characterized by different conservation approaches to tourism in Global North and South. Research concerning Global South tends to emphasize (eco)tourism as a main inducement for conservation, while research concerning Global North emphasizes expansion of private protected areas where access for tourist-recreational use has to be compensated. We propose a future research agenda to exploring environmentally and socially just approaches to conservation and recreation in both Global North and South. [ABSTRACT FROM AUTHOR]

This thematic issue examines the insurance function as a mechanism to underlie wealth effects on various outcomes. The articles in this issue shed an innovative light on the insurance function of wealth concerning a range of topics relevant to social stratification and social policy researchers. This editorial provides an overview of the contributions of this thematic issue and highlights some gaps and remaining open questions. Altogether, the contributions suggest that wealth can provide insurance against adverse life events in various contexts. However, this insurance effect depends on welfare state characteristics, wealth portfolios, and the way families handle their wealth. [ABSTRACT FROM AUTHOR]

Kinesins are motor proteins found in all eukaryotic lineages that move along microtubules to mediate cellular processes such as mitosis and intracellular transport. In trypanosomatids, the kinesin superfamily has undergone a prominent expansion, resulting in one of the most diverse kinesin repertoires that includes the two kinetoplastid‐restricted families X1 and X2. Here, we characterize in Trypanosoma brucei TbKifX2A, an orphaned X2 kinesin. TbKifX2A tightly interacts with TbPH1, a kinesin‐like protein with a likely inactive motor domain, a rarely reported occurrence. Both TbKifX2A and TbPH1 localize to the microtubule quartet (MtQ), a characteristic but poorly understood cytoskeletal structure that wraps around the flagellar pocket as it extends to the cell body anterior. The proximal proteome of TbPH1 revealed two other interacting proteins, the flagellar pocket protein FP45 and intriguingly another X2 kinesin, TbKifX2C. Simultaneous ablation of TbKifX2A/TbPH1 results in the depletion of FP45 and TbKifX2C and also an expansion of the flagellar pocket, among other morphological defects. TbKifX2A is the first motor protein to be localized to the MtQ. The observation that TbKifX2C also associates with the MtQ suggests that the X2 kinesin family may have co‐evolved with the MtQ, both kinetoplastid‐specific traits. [ABSTRACT FROM AUTHOR]

Underlying the idea of the middle classes there is a contradictory positionality, the relations of which ultimately enhance capital accumulation. By opening Marxist critique to Weberian approaches to class, we explain how the self‐ascription of short‐term rental (STR) suppliers to the middle‐class idea boosts exploitation and accumulation. Housing income, and recently that originating in STRs, has been used to maintain the symbolic and material status of the so‐called middle classes in Spain, and specifically in Palma. Based on statistical data analysis and interviews with STR suppliers, managers and workers, we analyse the contradictory class positionality of STR suppliers in Palma (Majorca, Spain). First, we argue, that STR suppliers are part of the middle classes since they bear attributes of rent, labour and also capital, as they employ workers to produce a tourism commodity. Second, we contend that STR overnight stays should not only be considered as land rent payments, but also as the sale of a tourism commodity. Third, we claim that the contradictory positionality of the middle classes fuels self‐exploitation, for STR suppliers misalign their interests with those of capital. [ABSTRACT FROM AUTHOR]

While debt is not problematic per se, it can become an additional burden when people experience negative life events–like unemployment, a severe disease, divorce, or their partner's death–which can be detrimental for individuals' subjective wellbeing. We investigate first, a potential moderating effect of economic resources or, better yet, lack thereof in the relations between negative life events and general life satisfaction, and second, whether this moderating effect is a function of state-level policies. We expect that, on average, debt has a reinforcing effect on the negative relationship between negative life events and general life satisfaction. Moreover, we expect that country-level policies protecting individuals from the negative consequences of experiencing a negative life event or indebtedness can explain the country differences in the moderating effect of debt. We test our assumptions among the population aged 50+ applying data from the Survey of Health, Ageing and Retirement (SHARE). We apply a two-stage fixed-effects regression approach to estimate the moderation effect of debt on the relationship between negative life events and general life satisfaction within and across countries. Although we find an almost zero average moderating effect of debt across countries, we find large variance in the moderating effects between countries. This variance can be explained by debt regime, but not by the generosity of the public unemployment and the public health systems, or the level of gender equality. [ABSTRACT FROM AUTHOR]

Since the beginning of the 2008 economic crisis, Majorca has experienced an increase in tourism, which has been made possible partly by the expansion of short-term renting. Research on short-term rentals is a growing field in critical urban and tourism geographies. This paper contributes to these fields by examining the structure of actors involved in the development of short-term rentals and their power relations. Our case study focuses on the municipality of Pollença (Majorca, Spain). Pollença was chosen due to its status as one of the most noteworthy airbnbificated places in Europe and because of the number of holiday rentals in the municipality's rural areas. While a great deal of research has focused on rent gaps and gentrification caused by short-term rentals in cities, the rentier coalition associated with short-term rentals has been comparatively overlooked. We address who the rentiers of short-term rentals are, the power relations that lie behind short-term rentals, and how these rentiers form part of a locally based coalition that has the ability to adapt planning regulations to suit their own interests. We used mixed methods, including quantitative spatial analysis and qualitative analysis in the form of interviews with those who benefit locally from short-term rentals. Our qualitative approach further included in-depth fieldwork and activist research. We conclude that a powerful rentier growth coalition has corrupted democracy because the regulatory framework has been adjusted to satisfy their interests and the conversion of properties into holiday rentals has been done either illegally or on the verge of legality without strong legal consequences. [ABSTRACT FROM AUTHOR]

In this paper we apply the method of stochastic characteristics to a Lighthill–Whitham–Richards model. The stochastic perturbation can be seen as errors in measurement of the traffic density. For concrete examples we solve the equation perturbed by a standard Brownian motion and the geometric Brownian motion without drift. [ABSTRACT FROM AUTHOR]

Copyright of Monografies de la Societat ďHistòria Natural de les Balears is the property of Societat d'Historia Natural de les Balears and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Over recent decades, we have seen a delay of marriage and simultaneously an expansion of the educational system and massive changes in the labour market in most Western countries. In this paper, we link these phenomena within the unique historical context of the Federal Republic of Germany (FRG) and the former German Democratic Republic (GDR). Making use of data from the German National Educational Panel Study (NEPS), we analyse the associations between individuals' current economic roles --full- and part-time employed, unemployed, enrolment in education or training-- and the timing of their first marriage for men and women born between 1944 and 1986 in the former FRG and GDR. We find that full-time employees are most likely to enter first marriage, while being unemployed or enrolled in education are associated with a delay of first marriage. However, there are crucial differences by gender, region and birth cohort. Women are more likely to marry when they finish education, while for men it seems to be more important to find gainful employment. These associations rarely change over birth cohorts in West Germany. In East Germany, the situation differs significantly. For the older (pre-reunification) cohorts, we find almost no associations between economic roles and marriage timing. For the younger (post-reunification) cohorts, we find convergence to the West German patterns. [ABSTRACT FROM AUTHOR]

The immune suppressants cyclosporin A (CsA) and tacrolimus (FK506) are used worldwide in transplantation medicine to suppress graft rejection. Both CsA and FK506 inhibit the phosphatase calcineurin (CN) whose activity controls the immune receptor-mediated activation of lymphocytes. Downstream targets of CN in lymphocytes are the nuclear factors of activated T cells (NFATs). We show here that the activity of NFATc1, the most prominent NFAT factor in activated lymphocytes supports the acute rejection of heterotopic heart allografts. While ablation of NFATc1 in T cells prevented graft rejection, ectopic expression of inducible NFATc1/αA isoform led to rejection of heart allografts in recipient mice. Acceptance of transplanted hearts in mice bearing NFATc1-deficient T cells was accompanied by a reduction in number and cytotoxicity of graft infiltrating cells. In CD8+ T cells, NFATc1 controls numerous intracellular signaling pathways that lead to the metabolic switch to aerobic glycolysis and the expression of numerous lymphokines, chemokines, and their receptors, including Cxcr3 that supports the rejection of allogeneic heart transplants. These findings favors NFATc1 as a molecular target for the development of new strategies to control the cytotoxicity of T cells upon organ transplantation. [ABSTRACT FROM AUTHOR]

Cytotoxic T lymphocytes are effector CD8+ T cells that eradicate infected and malignant cells. Here we show that the transcription factor NFATc1 controls the cytotoxicity of mouse cytotoxic T lymphocytes. Activation of Nfatc1-/- cytotoxic T lymphocytes showed a defective cytoskeleton organization and recruitment of cytosolic organelles to immunological synapses. These cells have reduced cytotoxicity against tumor cells, and mice with NFATc1-deficient T cells are defective in controlling Listeria infection. Transcriptome analysis shows diminished RNA levels of numerous genes in Nfatc1-/- CD8+ T cells, including Tbx21, Gzmb and genes encoding cytokines and chemokines, and genes controlling glycolysis. Nfatc1-/-, but not Nfatc2-/- CD8+ T cells have an impaired metabolic switch to glycolysis, which can be restored by IL-2. Genome-wide ChIP-seq shows that NFATc1 binds many genes that control cytotoxic T lymphocyte activity. Together these data indicate that NFATc1 is an important regulator of cytotoxic T lymphocyte effector functions. [ABSTRACT FROM AUTHOR]

Introduction. Medical preparedness at mass gatherings is challenging, as little is known about the optimal planning. Most studies and case reports are based on mass casualty incidents, so the results cannot be extrapolated to mass gatherings. Aim of this study was to evaluate the preclinical medical structure and the frequency of specific injuries and medical emergencies during the event. Methods. Retrospective analysis of a prospectively collected database. Three on-site medical assistance points were set up, completed by mobile teams, and coordinated by an on-site operational management team. Medical staff requirements were calculated using Maurer’s formula. Results. A total of 1,533 patients were treated during the three-day event. Overall, the medical usage rate (MUR; patients per 10,000 visitors) was 51.1. A total of 58 patients (3.8%) required a hospital transfer. In 1,063 cases (69.3%) a diagnosis was documented. Of these, 503 patients (47.3%) suffered from hymenoptera stings; the two most common non-trauma-related diagnoses were alcohol/drug intoxication (4.1%) and gastrointestinal diseases (4.0%). Conclusion. Overall, the on-site medical care worked well. However, a high frequency of hymenoptera stings occurred, resulting in a shortage of antihistamine medication. Moreover, more than half of the patients were managed at the second largest medical assistance point. Prospective and critical evaluation of medical care at mass gatherings is crucial in order to optimize on-site medical preparedness at future events. [ABSTRACT FROM AUTHOR]

Though mostly defective, human endogenous retroviruses (HERV) can retain open reading frames, which are especially expressed in the placenta. There, the envelope (env) proteins of HERV-W (Syncytin-1), HERV-FRD (Syncytin-2), and HERV-K (HML-2) were implicated in tolerance against the semi-allogenic fetus. Here, we show that the known HERV env-binding receptors ASCT-1 and -2 and MFSD2 are expressed by DCs and T-cells. When used as effectors in coculture systems, CHO cells transfected to express Syncytin-1, -2, or HML-2 did not affect T-cell expansion or overall LPS-driven phenotypic DC maturation, however, promoted release of IL-12 and TNF-α rather than IL-10. In contrast, HERV env expressing choriocarcinoma cell lines suppressed T-cell proliferation and LPS-induced TNF-α and IL-12 release, however, promoted IL-10 accumulation, indicating that these effects might not rely on HERV env interactions. However, DCs conditioned by choriocarcinoma, but also transgenic CHO cells failed to promote allogenic T-cell expansion. This was associated with a loss of DC/T-cell conjugate frequencies, impaired Ca2+ mobilization, and aberrant patterning of f-actin and tyrosine phosphorylated proteins in T-cells. Altogether, these findings suggest that HERV env proteins target T-cell activation indirectly by modulating the stimulatory activity of DCs. [ABSTRACT FROM AUTHOR]

Host T cell activation, a key step in obtaining adaptive immunity against pathogens, is initiated by the binding of the T cell receptor to a foreign antigenic peptide presented by the major histocompatibility complex on the surface of an antigen-presenting cell and, consequently, formation of an immunological synapse. Within the immunological synapse, the engagement of the T cell receptor in cooperation with simultaneous ligation of co-stimulatory molecules induces a precisely organized cascade of signaling events and pathways that regulate clonal expansion and differentiation of naïve T cells into effector T cells contributing to pathogen clearance. The biochemical changes that underlie T cell activation and differentiation, however, not only involve proteins but also lipids. In particular, catabolic cleavage of sphingomyelin generating ceramide can substantially influence functional responses in cells of the immune system. Changes in sphingomyelin and ceramide content have been reported to directly impact on membrane physiology, thus modifying signal transmission and interfering with diverse aspects of T cell activity. In this review we will focus on sphingomyelin breakdown/ceramide generation in T cells with regard to their function and development of T cell-mediated immunity. [ABSTRACT FROM AUTHOR]

Human brain microvascular endothelial cells forming the blood-brain barrier (BBB) release soluble vascular cell adhesion molecule-1 (sVCAM-1) under inflammatory conditions. Furthermore, sVCAM-1 serum levels in untreated patients with multiple sclerosis (MS) correlate with a breakdown of the BBB as measured by gadolinium-enhanced MRI. To date, it is unknown whether sVCAM-1 itself modulates BBB permeability. Here, we provide evidence that human brain endothelium expresses integrin α-4/β-1, the molecular binding partner of sVCAM-1, and that sVCAM-1 directly impairs BBB function by inducing intracellular signalling events through integrin α-4. Primary human brain microvascular endothelial cells showed low to moderate integrin α-4 and strong β-1 but no definite β-7 expression in vitro and in situ. Increased brain endothelial integrin α-4 expression was observed in active MS lesions in situ and after angiogenic stimulation in vitro. Exposure of cultured primary brain endothelial cells to recombinant sVCAM-1 significantly increased their permeability to the soluble tracer dextran, which was paralleled by formation of actin stress fibres and reduced staining of tight junction-associated molecules. Soluble VCAM-1 was also found to activate Rho GTPase and p38 MAP kinase. Chemical inhibition of these signalling pathways partially prevented sVCAM-1-induced changes of tight junction arrangement. Importantly, natalizumab, a neutralising recombinant monoclonal antibody against integrin α-4 approved for the treatment of patients with relapsing-remitting MS, partially antagonised the barrier-disturbing effect of sVCAM-1. In summary, we newly characterised sVCAM-1 as a compromising factor of brain endothelial barrier function that may be partially blocked by the MS therapeutic natalizumab. [ABSTRACT FROM AUTHOR]

Copyright of German Journal for Young Researchers / Zeitschrift für Nachwuchswissenschafter is the property of Zeitschrift fur Nachwuchswissenschaftler / German Journal for Young Researchers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Problem During pregnancy, the immune and the endocrine system cooperate to ensure that the fetal allograft develops without eliciting a maternal immune response. This is presumably in part achieved by dendritic cells (DCs) that play a dominant role in maintaining peripheral tolerance. In this study, we investigated whether female sex hormones, such as human chorionic gonadotropin (hCG), progesterone (Prog), and estradiol (E2), which are highly elevated during pregnancy, induce the differentiation of DCs into a tolerance-inducing phenotype. Methods/Results Immature DCs were generated from blood-derived monocytes and differentiated in the presence of hCG, Prog, E2, or Dexamethasone (Dex) as a control. Unlike Dex, female sex hormones did not prevent the upregulation of surface markers characteristic for mature DCs, such as CD40, CD83, and CD86, except for hCG, which inhibited HLA-DR expression. Similarly, hCG, Prog, and E2 had any impact on neither the rearrangement of the F-actin cytoskeleton nor the enhanced chemokine secretion following DC maturation, both of which were strongly altered by Dex. Nevertheless, the T-cell stimulatory capacity of DCs was significantly reduced after hCG and E2 exposure. Conclusion Our findings suggest that the female sex hormones hCG and E2 inhibit the T-cell stimulatory capacity of DCs, which may help in preventing an allogenic T-cell response against the embryo. [ABSTRACT FROM AUTHOR]

Members of the tetraspanin family including CD9 contribute to the structural organization and plasticity of the plasma membrane. K41, a CD9-specific monoclonal antibody, inhibits the release of HIV-1 and canine distemper virus (CDV)- but not measles virus (MV)-induced cell–cell fusion. We now report that K41, which recognizes a conformational epitope on the large extracellular loop of CD9, induces rapid relocation and clustering of CD9 in net-like structures at cell–cell contact areas. High-resolution analyses revealed that CD9 clustering is accompanied by the formation of microvilli that protrude from either side of adjacent cell surfaces, thus forming structures like microvilli zippers. While the cellular CD9-associated proteins β1-integrin and EWI-F were co-clustered with CD9 at cell–cell interfaces, viral proteins in infected cells were differentially affected. MV envelope proteins were detected within CD9 clusters, whereas CDV proteins were excluded from CD9 clusters. Thus, the tetraspanin CD9 can regulate cell–cell fusion by controlling the access of the fusion machinery to cell contact areas. [ABSTRACT FROM AUTHOR]

Background: Pregnancy represents an exclusive situation in which the immune and the endocrine system cooperate to prevent rejection of the embryo by the maternal immune system. While immature dendritic cells (iDC) in the early pregnancy decidua presumably contribute to the establishment of peripheral tolerance, glycoprotein-hormones of the transforming growth factor beta (TGF-beta) family including activin A (ActA) and inhibin A (InA) are candidates that could direct the differentiation of DCs into a tolerance-inducing phenotype. Methods: To test this hypothesis we generated iDCs from peripheral-blood-monocytes and exposed them to TGF-beta1, ActA, as well as InA and Dexamethasone (Dex) as controls. Results: Both glycoprotein-hormones prevented up-regulation of HLA-DR during cytokine-induced DC maturation similar to Dex but did not influence the expression of CD 40, CD 83 and CD 86. Visualization of the F-actin cytoskeleton confirmed that the DCs retained a partially immature phenotype under these conditions. The T-cell stimulatory capacity of DCs was reduced after ActA and InA exposure while the secretion of cytokines and chemokines was unaffected. Conclusion: These findings suggest that ActA and InA interfere with selected aspects of DC maturation and may thereby help preventing activation of allogenic T-cells by the embryo. Thus, we have identified two novel members of the TGF-beta superfamily that could promote the generation of tolerance-inducing DCs. [ABSTRACT FROM AUTHOR]

Glucocorticoids (GCs) are involved in the modulation of macrophage function and thereby control the host's immune responses to pathogens. However, neither the role of hormone concentration nor the differential contribution of the glucocorticoid (GR) and the mineralocorticoid receptors (MR) to these activities are known. Here we show that low levels of corticosterone enhance NO production as well as mRNA expression of pro-inflammatory cytokines, chemokines and enzymes required for mediator synthesis. In contrast, at high corticosterone concentrations macrophage function was strongly repressed. Importantly, inactivation of the GR by lentiviral delivery of siRNAs abrogated both the immunostimulatory and the immunosuppressive GC actions whereas inactivation of the MR had no effect. Furthermore, removal of endogenous GCs by adrenalectomy in vivo induced a preactivated state in macrophages that could be modulated by corticosterone. We conclude that GCs exert distinct effects on macrophage function dependent on their concentration, and that they primarily act through the GR despite concomitant expression of the MR. [ABSTRACT FROM AUTHOR]

CD3/CD28-induced activation of the PI3/Akt kinase pathway and proliferation is impaired in T cells after contact with the measles virus (MV) glycoprotein (gp) complex. We now show that this signal also impairs actin cytoskeletal remodeling in T cells, which loose their ability to adhere and to promote microvilli formation. MV exposure results in an almost complete collapse of membrane protrusions associated with reduced phosphorylation levels of cofilin and ezrin/radixin/moesin (ERM) proteins. Consistent with their inability to activate Cdc42 and Rac1 in response to the ligation of CD3/CD28, T cells exposed to MV fail to acquire a morphology consistent with spreading and lamellopodia formation. In spite of these impairments of cytoskeleton-driven morphological alterations, these cells are recruited into conjugates with dendritic cells as efficiently as control T cells. The signal elicited by MV, however, prevents T cells to polarize as documented by a failure to redistribute the microtubule organizing center toward the synapse. Moreover, CD3 cannot be efficiently clustered and redistributed to the central region of the immunological synapse. Thus, by inducing microvillar collapse and interfering with cytoskeletal remodeling, MV signaling disturbs the ability of T cells to adhere, spread, and cluster receptors essential for sustained T-cell activation. [ABSTRACT FROM AUTHOR]

Background: Parkinson's disease (PD) is characterized at the cellular level by a destruction of neuromelanin (NM)-containing dopaminergic cells and a profound reduction in striatal dopamine. It has been shown recently that anti-melanin antibodies are increased in sera of Parkinson patients, suggesting that NM may act as an autoantigen. In this study we tested whether NM is being recognized by dendritic cells (DCs), the major cell type for inducing T- and B-cell responses in vivo. This recognition of NM by DCs is a prerequisite to trigger an adaptive autoimmune response directed against NM-associated structures.Results: Murine DCs were treated with NM of substantia nigra (SN) from human subjects or with synthetic dopamine melanin (DAM). DCs effectively phagocytized NM and subsequently developed a mature phenotype (CD86(high)/MHCII(high)). NM-activated DCs secreted the proinflammatory cytokines IL-6 and TNF-α. In addition, they potently triggered T cell proliferation in a mixed lymphocyte reaction, showing that DC activation was functional to induce a primary T cell response. In contrast, DAM, which lacks the protein and lipid components of NM but mimics the dopamine-melanin backbone of NM, had only very little effect on DC phenotype and function.Conclusions: NM is recognized by DCs in vitro and triggers their maturation. If operative in vivo, this would allow the DC-mediated transport and presentation of SN antigens to the adaptive immune system, leading to autoimmmunity in susceptible individuals. Our data provide a rationale for an autoimmune-based pathomechanism of PD with NM as the initial trigger. [ABSTRACT FROM AUTHOR]