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‣ IL-17 Receptor Signaling Is Required to Control Polymicrobial Sepsis

FREITAS, Andressa; ALVES-FILHO, Jose C.; VICTONI, Tatiana; SECHER, Thomas; LEMOS, Henrique P.; SONEGO, Fabiane; CUNHA, Fernando Q.; RYFFEL, Bernhard
Fonte: AMER ASSOC IMMUNOLOGISTS Publicador: AMER ASSOC IMMUNOLOGISTS
Tipo: Artigo de Revista Científica
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Sepsis is a systemic inflammatory response resulting from the inability of the host to contain the infection locally. Previously, we demonstrated that during severe sepsis there is a marked failure of neutrophil migration to the infection site, which contributes to dissemination of infection, resulting in high mortality. IL-17 plays an important role in neutrophil recruitment. Herein, we investigated the role of IL-17R signaling in polymicrobial sepsis induced by cecal ligation and puncture (CLP). It was observed that IL-17R-deficient mice, subjected to CLP-induced non-severe sepsis, show reduced neutrophil recruitment into the peritoneal cavity, spread of infection, and increased systemic inflammatory response as compared with C57BL/6 littermates. As a consequence, the mice showed an increased mortality rate. The ability of IL-17 to induce neutrophil migration was demonstrated in vivo and in vitro. Beside its role in neutrophil recruitment to the infection focus, IL-17 enhanced the microbicidal activity of the migrating neutrophils by a mechanism dependent on NO. Therefore, IL-17 plays a critical role in host protection during polymicrobial sepsis. The Journal of Immunology, 2009, 182: 7846-7854.; FAPESP Fundacao de Amparo a Pesquisa do Estado de Sao Paulo; CNPq Conselho Nacional de Pesquisa a Desenvolvimento Tecnologico

‣ Crucial Role of TNF Receptors 1 and 2 in the Control of Polymicrobial Sepsis

SECHER, Thomas; VASSEUR, Virginie; POISSON, Didier Marc; MITCHELL, Jane A.; CUNHA, Fernando Q.; ALVES-FILHO, Jose Carlos; RYFFEL, Bernhard
Fonte: AMER ASSOC IMMUNOLOGISTS Publicador: AMER ASSOC IMMUNOLOGISTS
Tipo: Artigo de Revista Científica
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Sepsis is still a major cause of mortality in the intensive critical care unit and results from an overwhelming immune response to the infection. TNF signaling pathway plays a central role in the activation of innate immunity in response to pathogens. Using a model of polymicrobial sepsis by i.p. injection of cecal microflora, we demonstrate a critical role of TNFR1 and R2 activation in the deregulated immune responses and death associated with sepsis. A large and persistent production of TNF was found in wild-type (B6) mice. TNFR1/R2-deficient mice, compared with B6 mice, survive lethal polymicrobial infection with enhanced neutrophil recruitment and bacterial clearance in the peritoneal cavity. Absence of TNFR signaling leads to a decreased local and systemic inflammatory response with diminished organ injury. Furthermore, using TNFR1/R2-deficient mice, TNF was found to be responsible for a decrease in CXCR2 expression, explaining reduced neutrophil extravasation and migration to the infectious site, and in neutrophil apoptosis. In line with the clinical experience, administration of Enbrel, a TNF-neutralizing protein, induced however only a partial protection in B6 mice, with no improvement of clinical settings, suggesting that future TNF immunomodulatory strategies should target TNFR1 and R2. In conclusion...

‣ Cutting Edge: Nucleotide-Binding Oligomerization Domain 1-Dependent Responses Account for Murine Resistance against Trypanosoma cruzi Infection

SILVA, Grace K.; GUTIERREZ, Fredy R. S.; GUEDES, Paulo M. M.; HORTA, Catarina V.; CUNHA, Larissa D.; MINEO, Tiago W. P.; SANTIAGO-SILVA, Juliana; KOBAYASHI, Koichi S.; FLAVELL, Richard A.; SILVA, Joao S.; ZAMBONI, Dario S.
Fonte: AMER ASSOC IMMUNOLOGISTS Publicador: AMER ASSOC IMMUNOLOGISTS
Tipo: Artigo de Revista Científica
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An effective innate immune recognition of the intracellular protozoan parasite Trypanosoma cruzi is critical for host resistance against Chagas disease, a severe and chronic illness that affects millions of people in Latin America. In this study, we evaluated the participation of nucleotide-binding oligomerization domain (Nod)like receptor proteins in host response to T cruzi infection and found that Nod1-dependent, but not Nod2-dependent, responses are required for host resistance against infection. Bone marrow-derived macrophages from Nod1(-/-) mice showed an impaired induction of NF-kappa B-dependent products in response to infection and failed to restrict T cruzi infection in presence of IFN-gamma. Despite normal cytokine production in the sera, Nod1(-/-) mice were highly susceptible to T cruzi infection, in a similar manner to MyD88(-/-) and NO synthase 2(-/-) mice. These studies indicate that Nod1-dependent responses account for host resistance against T cruzi infection by mechanisms independent of cytokine production. The Journal of Immunology, 2010, 184: 1148-1152.; FAPESP Fundacao de Amparo a Pesquisa do Estado de Sao Paulo[06/52867-4]; WHO World Health Organization/TDR; Instituto Nacional de Ciencia e Tecnologia de Vacinas INCT/ Conselho Nacional de Desenvolvimento Cientifico e Tecnológico CNPq

‣ Recognition by toll-like receptor 2 induces antigen-presenting cell activation and Th1 programming during infection by Neospora caninum

MINEO, Tiago W. P.; OLIVEIRA, Carlo J. F.; GUTIERREZ, Fredy R. S.; SILVA, Joao S.
Fonte: NATURE PUBLISHING GROUP Publicador: NATURE PUBLISHING GROUP
Tipo: Artigo de Revista Científica
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Neospora caninum is an apicomplexan parasite responsible for major economic losses due to abortions in cattle. Toll-like receptors (TLRs) sense specific microbial products and direct downstream signaling pathways in immune cells, linking innate, and adaptive immunity. Here, we analyze the role of TLR2 on innate and adaptive immune responses during N. caninum infection. Inflammatory peritoneal macrophages and bone marrow-derived dendritic cells exposed to N. caninum-soluble antigens presented an upregulated expression of TLR2. Increased receptor expression was correlated to TLR2/MyD88-dependent antigen-presenting cell maturation and pro-inflammatory cytokine production after stimulation by antigens. Impaired innate responses observed after infection of mice genetically deficient for TLR2((-/-)) was followed by downregulation of adaptive T helper 1 (Th1) immunity, represented by diminished parasite-specific CD4(+) and CD8(+) T-cell proliferation, IFN-gamma:interleukin (IL)-10 ratio, and IgG subclass synthesis. In parallel, TLR2(-/-) mice presented higher parasite burden than wild-type (WT) mice at acute and chronic stages of infection. These results show that initial recognition of N. caninum by TLR2 participates in the generation of effector immune responses against N. caninum and imply that the receptor may be a target for future prophylactic strategies against neosporosis. Immunology and Cell Biology (2010) 88...

‣ Primary immunodeficiency diseases in Latin America: Proceedings of the Second Latin American Society for Immunodeficiencies (LASID) Advisory Board

LEIVA, L. E.; BEZRODNIK, L.; OLEASTRO, M.; CONDINO-NETO, A.; COSTA-CARVALHO, B. T.; GRUMACH, A. Sevciovic; ESPINOSA-ROSALES, F. J.; FRANCO, J. Luis; KING, A.; INOSTROZA, J.; QUEZADA, A.; PORRAS, O.; SORENSEN, R. U.
Fonte: ELSEVIER DOYMA SL Publicador: ELSEVIER DOYMA SL
Tipo: Artigo de Revista Científica
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Early diagnosis and appropriate therapy are essential for the best prognosis and quality of life in patients with primary immunodeficiency diseases (PIDDs). Experts from several Latin American countries have been meeting on a regular basis as part of an ongoing effort to improve the diagnosis and treatment of PIDD in this region. Three programmes are in development that will expand education and training and improve access to testing facilities throughout Latin America. These programmes are: an educational outreach programme (The L-Project); an immunology fellowship programme; and the establishment of a laboratory network to expand access to testing facilities. This report provides the status of these programmes based on the most recent discussions and describes the next steps toward full implementation of these programmes. (C) 2010 SEICAP. Published by Elsevier Espana, S.L. All rights reserved.; Baxter Biosciences; Baxter

‣ Critical, issues and needs in management of primary immunodeficiency diseases in Latin America

CONDINO-NETO, A.; FRANCO, J. L.; TRUJILLO-VARGAS, C.; ESPINOSA-ROSALES, F. J.; LEIVA, L. E.; RODRIGUEZ-QUIROZ, F.; KING, A.; LAGOS, M.; OLEASTRO, M.; BEZRODNIK, L.; GRUMACH, A. S.; COSTA-CARVALHO, B. T.; SORENSEN, R. U.
Fonte: ELSEVIER DOYMA SL Publicador: ELSEVIER DOYMA SL
Tipo: Artigo de Revista Científica
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Experts from six Latin American countries met to discuss critical issues and needs in the diagnosis and management of primary immunodeficiency diseases (PIDD). The diagnosis of PIDD is generally made following referral to an immunology centre located in a major city, but many paediatricians and general practitioners are not sufficiently trained to suspect PIDD in the first place. Access to laboratory testing is generally limited, and only some screening tests are typically covered by government health programmes. Specialised diagnostic tests are generally not reimbursed. Access to treatment varies by country reflecting differences in healthcare systems and reimbursement policies. An online PIDD Registry Programme for Latin America has been available since 2009, which will provide information about PIDD epidemiology in the region. Additional collaboration across countries appears feasible in at least two areas: a laboratory network to facilitate the diagnosis of PIDD, and educational programmes to improve PIDD awareness. In total, these collaborations should make it possible to advance the diagnosis and management of PIDD in Latin America. (C) 2010 SEICAP. Published by Elsevier Espana, S.L. All rights reserved.; Baxter; Baxter; Baxter; Baxter Biosciences

‣ Melatonin Protects CD4(+) T Cells from Activation-Induced Cell Death by Blocking NFAT-Mediated CD95 Ligand Upregulation

PEDROSA, Alziana Moreno da Cunha; WEINLICH, Ricardo; MOGNOL, Giuliana Patricia; ROBBS, Bruno Kaufmann; VIOLA, Joao Paulo de Biaso; CAMPA, Ana; AMARANTE-MENDES, Gustavo Pessini
Fonte: AMER ASSOC IMMUNOLOGISTS Publicador: AMER ASSOC IMMUNOLOGISTS
Tipo: Artigo de Revista Científica
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Over the past 20 y, the hormone melatonin was found to be produced in extrapineal sites, including cells of the immune system. Despite the increasing data regarding the biological effects of melatonin on the regulation of the immune system, the effect of this molecule on T cell survival remains largely unknown. Activation-induced cell death plays a critical role in the maintenance of the homeostasis of the immune system by eliminating self-reactive or chronically stimulated T cells. Because activated T cells not only synthesize melatonin but also respond to it, we investigated whether melatonin could modulate activation-induced cell death. We found that melatonin protects human and murine CD4(+) T cells from apoptosis by inhibiting CD95 ligand mRNA and protein upregulation in response to TCR/CD3 stimulation. This inhibition is a result of the interference with calmodulin/calcineurin activation of NFAT that prevents the translocation of NFAT to the nucleus. Accordingly, melatonin has no effect on T cells transfected with a constitutively active form of NFAT capable of migrating to the nucleus and transactivating target genes in the absence of calcineurin activity. Our results revealed a novel biochemical pathway that regulates the expression of CD95 ligand and potentially other downstream targets of NFAT activation. The Journal of Immunology...

‣ TLR2 Is a Negative Regulator of Th17 Cells and Tissue Pathology in a Pulmonary Model of Fungal Infection

LOURES, Flavio V.; PINA, Adriana; FELONATO, Maira; CALICH, Vera L. G.
Fonte: AMER ASSOC IMMUNOLOGISTS Publicador: AMER ASSOC IMMUNOLOGISTS
Tipo: Artigo de Revista Científica
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To study the role of TLR2 in a experimental model of chronic pulmonary infection, TLR2-deficient and wild-type mice were intratracheally infected with Paracoccidioides brasiliensis, a primary fungal pathogen. Compared with control, TLR2(-/-) mice developed a less severe pulmonary infection and decreased NO synthesis. Equivalent results were detected with in vitro-infected macrophages. Unexpectedly, despite the differences in fungal loads both mouse strains showed equivalent survival times and severe pulmonary inflammatory reactions. Studies on lung-infiltrating leukocytes of TLR2(-/-) mice demonstrated an increased presence of polymorphonuclear neutrophils that control fungal loads but were associated with diminished numbers of activated CD4(+) and CD8(+) T lymphocytes. TLR2 deficiency leads to minor differences in the levels of pulmonary type 1 and type 2 cytokines, but results in increased production of KC, a CXC chemokine involved in neutrophils chemotaxis, as well as TGF-beta, IL-6, IL-23, and IL-17 skewing T cell immunity to a Th17 pattern. In addition, the preferential Th17 immunity of TLR2(-/-) mice was associated with impaired expansion of regulatory CD4(+)CD25(+)FoxP3(+) T cells. This is the first study to show that TLR2 activation controls innate and adaptive immunity to P. brasiliensis infection. TLR2 deficiency results in increased Th17 immunity associated with diminished expansion of regulatory T cells and increased lung pathology due to unrestrained inflammatory reactions. The Journal of Immunology...

‣ The Immunomodulatory Action of Sialostatin L on Dendritic Cells Reveals Its Potential to Interfere with Autoimmunity

SA-NUNES, Anderson; BAFICA, Andre; ANTONELLI, Lis R.; CHOI, Eun Young; FRANCISCHETTI, Ivo M. B.; ANDERSEN, John F.; SHI, Guo-Ping; CHAVAKIS, Triantafyllos; RIBEIRO, Jose M.; KOTSYFAKIS, Michalis
Fonte: AMER ASSOC IMMUNOLOGISTS Publicador: AMER ASSOC IMMUNOLOGISTS
Tipo: Artigo de Revista Científica
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Sialostatin L (SialoL) is a secreted cysteine protease inhibitor identified in the salivary glands of the Lyme disease vector Ixodes scapularis. In this study, we reveal the mechanisms of SialoL immunomodulatory actions on the vertebrate host. LPS-induced maturation of dendritic cells from C57BL/6 mice was significantly reduced in the presence of SialoL. Although OVA degradation was not affected by the presence of SialoL in dendritic cell cultures, cathepsin S activity was partially inhibited, leading to an accumulation of a 10-kDa invariant chain intermediate in these cells. As a consequence, in vitro Ag-specific CD4(+) T cell proliferation was inhibited in a time-dependent manner by SialoL, and further studies engaging cathepsin S(-/-) or cathepsin L(-/-) dendritic cells confirmed that the immunomodulatory actions of SialoL are mediated by inhibition of cathepsin S. Moreover, mice treated with SialoL displayed decreased early T cell expansion and recall response upon antigenic stimulation. Finally, SialoL administration during the immunization phase of experimental autoimmune encephalomyelitis in mice significantly prevented disease symptoms, which was associated with impaired IFN-gamma and IL-17 production and specific T cell proliferation. These results illuminate the dual mechanism by which a human disease vector protein modulates vertebrate host immunity and reveals its potential in prevention of an autoimmune disease. The Journal of Immunology...

‣ Gradual Decline in Malaria-Specific Memory T Cell Responses Leads to Failure to Maintain Long-Term Protective Immunity to Plasmodium chabaudi AS Despite Persistence of B Cell Memory and Circulating Antibody

ROSARIO, Ana Paula Freitas do; MUXEL, Sandra Marcia; RODRIGUEZ-MALAGA, Sergio Marcelo; SARDINHA, Luiz Roberto; ZAGO, Claudia Augusta; CASTILLO-MENDEZ, Sheyla Ines; ALVAREZ, Jose Maria; LIMA, Maria Regina D`Imperio
Fonte: AMER ASSOC IMMUNOLOGISTS Publicador: AMER ASSOC IMMUNOLOGISTS
Tipo: Artigo de Revista Científica
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The mechanisms responsible for the generation and maintenance of immunological memory to Plasmodium are poorly understood and the reasons why protective immunity in humans is so difficult to achieve and rapidly lost remain a matter for debate. A possible explanation for the difficulty in building up an efficient immune response against this parasite is the massive T cell apoptosis resulting from exposure to high-dose parasite Ag. To determine the immunological mechanisms required for long-term protection against P. chabaudi malaria and the consequences of high and low acute phase parasite loads for acquisition of protective immunity, we performed a detailed analysis of T and B cell compartments over a period of 200 days following untreated and drug-treated infections in female C57BL/6 mice. By comparing several immunological parameters with the capacity to control a secondary parasite challenge, we concluded that loss of full protective immunity is not determined by acute phase parasite load nor by serum levels of specific IgG2a and IgG1. Abs, but appears to be a consequence of the progressive decline in memory T cell response to parasites, which occurs similarly in untreated and drug-treated mice with time after infection. Furthermore...

‣ Heme Impairs Prostaglandin E(2) and TGF-beta Production by Human Mononuclear Cells via Cu/Zn Superoxide Dismutase: Insight into the Pathogenesis of Severe Malaria

ANDRADE, Bruno B.; ARAUJO-SANTOS, Theo; LUZ, Nivea F.; KHOURI, Ricardo; BOZZA, Marcelo T.; CAMARGO, Luis M. A.; BARRAL, Aldina; BORGES, Valeria M.; BARRAL-NETTO, Manoel
Fonte: AMER ASSOC IMMUNOLOGISTS Publicador: AMER ASSOC IMMUNOLOGISTS
Tipo: Artigo de Revista Científica
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In many hemolytic disorders, such as malaria, the release of free heme has been involved in the triggering of oxidative stress and tissue damage. Patients presenting with severe forms of malaria commonly have impaired regulatory responses. Although intriguing, there is scarce data about the involvement of heme on the regulation of immune responses. In this study, we investigated the relation of free heme and the suppression of anti-inflammatory mediators such as PGE(2) and TGF-beta in human vivax malaria. Patients with severe disease presented higher hemolysis and higher plasma concentrations of Cu/Zn superoxide dismutase (SOD-1) and lower concentrations of PGE(2) and TGF-beta than those with mild disease. In addition, there was a positive correlation between SOD-1 concentrations and plasma levels of TNF-alpha. During antimalaria treatment, the concentrations of plasma SOD-1 reduced whereas PGE(2) and TGF-beta increased in the individuals severely ill. Using an in vitro model with human mononuclear cells, we demonstrated that the heme effect on the impairment of the production of PGE(2) and TGF-beta partially involves heme binding to CD14 and depends on the production of SOD-1. Aside from furthering the current knowledge about the pathogenesis of vivax malaria...

‣ Sialic Acid Residues Are Essential for the Anaphylactic Activity of Murine IgG1 Antibodies

SILVA, Sandriana R.; CASABUONO, Adriana; JACYSYN, Jacqueline F.; FAVORETTO, Bruna C.; FERNANDES, Irene; MACEDO, Mahasti S.; COUTO, Alicia S.; FAQUIM-MAURO, Eliana L.
Fonte: AMER ASSOC IMMUNOLOGISTS Publicador: AMER ASSOC IMMUNOLOGISTS
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Glycosylation of the Ab molecule is essential for maintaining the functional structure of Fc region and consequently for Ab-mediated effector functions, such as binding to cells or complement system activation. Alterations in the composition of the sugar moiety can dramatically influence Ab activity; however, it is not completely clear how differences in the N-linked oligosaccharide structure impact the biological function of Abs. We have described that murine IgG1 Abs can be separated according to their ability to elicit in vivo anaphylaxis in a fraction of anaphylactic and other of non-anaphylactic molecules. Furthermore, we showed that the N-linked oligosaccharide chain is essential for the structural conformation of the anaphylactic IgG1, the binding to Fc gamma RIII on mast cells, and, consequently, for the ability to mediate anaphylactic reactions. In this study, we evaluated the contribution of individual sugar residues to this biological function. Differences in the glycan composition were observed when we analyzed oligosaccharide chains from anaphylactic or non-anaphylactic IgG1, mainly the presence of more sialic acid and fucose residues in anaphylactic molecules. Interestingly, the enzymatic removal of terminal sialic acid residues in anaphylactic IgG1 resulted in loss of the ability to trigger mast cell degranulation and in vivo anaphylactic reaction...

‣ B Lymphocyte-Induced Maturation Protein-1 Contributes to Intestinal Mucosa Homeostasis by Limiting the Number of IL-17-Producing CD4(+) T Cells

Salehi, Soofia; Bankoti, Rashmi; Benevides, Luciana; Witten, Jessica; Couse, Michael; Silva, Joao S.; Dhall, Deepti; Meffre, Eric; Targan, Stephan; Martins, Gistaine A.
Fonte: AMER ASSOC IMMUNOLOGISTS; BETHESDA Publicador: AMER ASSOC IMMUNOLOGISTS; BETHESDA
Tipo: Artigo de Revista Científica
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The transcription factor B lymphocyte induced maturation protein-1 (Blimp-1) plays important roles in embryonic development and immunity. Blimp-1 is required for the differentiation of plasma cells, and mice with T cell specific deletion of Blimp-1 (Blimp-1CKO mice) develop a fatal inflammatory response in the colon. Previous work demonstrated that lack of Blimp-1 in CD4(+) and CD8(+) T cells leads to intrinsic functional defects, but little is known about the functional role of Blimp-1 in regulating differentiation of Th cells in vivo and their contribution to the chronic intestinal inflammation observed in the Blimp1CKO mice. In this study, we show that Blimp-1 is required to restrain the production of the inflammatory cytokine IL-17 by Th cells in vivo. Blimp-1CKO mice have greater numbers of IL-17 producing TCR beta(+)CD4(+)cells in lymphoid organs and in the intestinal mucosa. The increase in IL-17 producing cells was not restored to normal levels in wild-type and Blimp-1CKO mixed bone marrow chimeric mice, suggesting an intrinsic role for Blimp-1 in constraining the production of IL-17 in vivo. The observation that Blimp-1 deficient CD4(+) T cells are more prone to differentiate into IL-17(+)/IFN-gamma(+) cells and cause severe colitis when transferred to Rag1-deficient mice provides further evidence that Blimp-1 represses IL-17 production. Analysis of Blimp-1 expression at the single cell level during Th differentiation reveals that Blimp-1 expression is induced in Th1 and Th2 but repressed by TGF-beta in Th17 cells. Collectively...

‣ Cutting Edge: Brazilian Pemphigus Foliaceus Anti-Desmoglein 1 Autoantibodies Cross-React with Sand Fly Salivary LJM11 Antigen

Qian, Ye; Jeong, Joseph S.; Maldonado, Mike; Valenzuela, Jesus G.; Gomes, Regis; Teixeira, Clarissa; Evangelista, Flor; Qaqish, Bahjat; Aoki, Valeria; Hans, Gunter, Jr.; Rivitti, Evandro A.; Eaton, Donald; Diaz, Luis A.
Fonte: AMER ASSOC IMMUNOLOGISTS; BETHESDA Publicador: AMER ASSOC IMMUNOLOGISTS; BETHESDA
Tipo: Artigo de Revista Científica
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The environmental factors that contribute to the development of autoimmune diseases are largely unknown. Endemic pemphigus foliaceus in humans, known as Fogo Selvagem (FS) in Brazil, is mediated by pathogenic IgG4 autoantibodies against desmoglein 1 (Dsg1). Clusters of FS overlap with those of leishmaniasis, a disease transmitted by sand fly (Lutzomyia longipalpis) bites. In this study, we show that salivary Ags from the sand fly, and specifically the LJM11 salivary protein, are recognized by FS Abs. Anti-Dsg1 monoclonal autoantibodies derived from FS patients also cross-react with LJM11. Mice immunized with LJM11 generate anti-Dsg1 Abs. Thus, insect bites may deliver salivary Ags that initiate a cross-reactive IgG4 Ab response in genetically susceptible individuals and lead to subsequent FS. Our findings establish a clear relationship between an environmental, noninfectious Ag and the development of potentially pathogenic autoantibodies in an autoimmune disease. The Journal of Immunology, 2012, 189: 1535-1539.; National Institutes of Health; National Institutes of Health [R01 AR30281, R01 AR32599, K01 AR056378]; Dermatology Foundation research award; Dermatology Foundation research award; American Skin Association Alice P. Melly research grant; American Skin Association Alice P. Melly research grant

‣ Macrophage Dectin-1 Expression Is Controlled by Leukotriene B-4 via a GM-CSF/PU.1 Axis

Serezani, C. Henrique; Kane, Steve; Collins, Latima; Marques, Mariana Morato; Osterholzer, John J.; Peters-Golden, Marc
Fonte: AMER ASSOC IMMUNOLOGISTS; BETHESDA Publicador: AMER ASSOC IMMUNOLOGISTS; BETHESDA
Tipo: Artigo de Revista Científica
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Pattern recognition receptors for fungi include dectin-1 and mannose receptor, and these mediate phagocytosis, as well as production of cytokines, reactive oxygen species, and the lipid mediator leukotriene B-4 (LTB4). The influence of G protein-coupled receptor ligands such as LTB4 on fungal pattern recognition receptor expression is unknown. In this study, we investigated the role of LTB4 signaling in dectin-1 expression and responsiveness in macrophages. Genetic and pharmacologic approaches showed that LTB4 production and signaling through its high-affinity G protein-coupled receptor leukotriene B4 receptor 1 (BLT1) direct dectin-1-dependent binding, ingestion, and cytokine production both in vitro and in vivo. Impaired responses to fungal glucans correlated with lower dectin-1 expression in macrophages from leukotriene (LT)- and BLT1-deficent mice than their wildtype counterparts. LTB4 increased the expression of the transcription factor responsible for dectin-1 expression, PU.1, and PU.1 small interfering RNA abolished LTB4-enhanced dectin-1 expression. GM-CSF controls PU.1 expression, and this cytokine was decreased in LT-deficient macrophages. Addition of GM-CSF to LT-deficient cells restored expression of dectin-1 and PU.1...

‣ Exogenous Administration of 15d-PGJ(2)-Loaded Nanocapsules Inhibits Bone Resorption in a Mouse Periodontitis Model

Napimoga, Marcelo H.; da Silva, Carlos A. T.; Carregaro, Vanessa; Farnesi-de-Assuncao, Thais S.; Duarte, Poliana M.; de Melo, Nathalie F. S.; Fraceto, Leonardo F.
Fonte: AMER ASSOC IMMUNOLOGISTS; BETHESDA Publicador: AMER ASSOC IMMUNOLOGISTS; BETHESDA
Tipo: Artigo de Revista Científica
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The 15-deoxy-(Delta 12,14)-PG J(2) (15d-PGJ(2)) has demonstrated excellent anti-inflammatory results in different experimental models. It can be used with a polymeric nanostructure system for modified drug release, which can change the therapeutic properties of the active principle, leading to increased stability and slower/prolonged release. The aim of the current study was to test a nano-technological formulation as a carrier for 15d-PGJ(2), and to investigate the immunomodulatory effects of this formulation in a mouse periodontitis model. Poly (D, L-lactide-coglycolide) nanocapsules (NC) were used to encapsulate 15d-PGJ(2). BALB/c mice were infected on days 0, 2, and 4 with Aggregatibacter actinomycetemcomitans and divided into groups (n = 5) that were treated daily during 15 d with 1, 3, or 10 mu g/kg 15d-PGJ(2)-NC. The animals were sacrificed, the submandibular lymph nodes were removed for FACS analysis, and the jaws were analyzed for bone resorption by morphometry. Immunoinflammatory markers in the gingival tissue were analyzed by reverse transcriptase-quantitative PCR, Western blotting, or ELISA. Infected animals treated with the 15d-PGJ(2)-NC presented lower bone resorption than infected animals without treatment (p < 0.05). Furthermore...

‣ Joint NOD2/RIPK2 Signaling Regulates IL-17 Axis and Contributes to the Development of Experimental Arthritis

Vieira, Silvio M.; Cunha, Thiago M.; Franca, Rafael F. O.; Pinto, Larissa G.; Talbot, Jhimmy; Turato, Walter M.; Lemos, Henrique P.; Lima, Jonilson B.; Verri, Waldiceu A., Jr.; Almeida, Sergio C. L.; Ferreira, Sergio H.; Louzada-Junior, Paulo; Zamboni, Da
Fonte: AMER ASSOC IMMUNOLOGISTS; BETHESDA Publicador: AMER ASSOC IMMUNOLOGISTS; BETHESDA
Tipo: Artigo de Revista Científica
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Intracellular pattern recognition receptors such as the nucleotide-binding oligomerization domain (NOD)-like receptors family members are key for innate immune recognition of microbial infection and may play important roles in the development of inflammatory diseases, including rheumatic diseases. In this study, we evaluated the role of NOD1 and NOD2 on development of experimental arthritis. Ag-induced arthritis was generated in wild-type, NOD1(-/-)!, NOD2(-/-), or receptor-interacting serine-threonine kinase 2(-/-) (RIPK2(-/-)) immunized mice challenged intra-articularly with methylated BSA. Nociception was determined by electronic Von Frey test. Neutrophil recruitment and histopathological analysis of proteoglycan lost was evaluated in inflamed joints. Joint levels of inflammatory cytokine/chemokine were measured by ELISA. Cytokine (IL-6 and IL-23) and NOD2 expressions were determined in mice synovial tissue by RT-PCR. The NOD2(-/-) and RIPK2(-/-), but not NOD1(-/-), mice are protected from Ag-induced arthritis, which was characterized by a reduction in neutrophil recruitment, nociception, and cartilage degradation. NOD2/RIPK2 signaling impairment was associated with a reduction in proinflammatory cytokines and chemokines (TNF, IL-1 beta...

‣ The Role of Nanometer-Scaled Ligand Patterns in Polyvalent Binding by Large Mannan-Binding Lectin Oligomers

Gjelstrup, Louise C.; Kaspersen, Jorn D.; Behrens, Manja A.; Pedersen, Jan S.; Thiel, Steffen; Kingshott, Peter; Oliveira, Cristiano Luis Pinto de; Thielens, Nicole M.; Vorup-Jensen, Thomas
Fonte: AMER ASSOC IMMUNOLOGISTS; BETHESDA Publicador: AMER ASSOC IMMUNOLOGISTS; BETHESDA
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Mannan-binding lectin (MBL) is an important protein of the innate immune system and protects the body against infection through opsonization and activation of the complement system on surfaces with an appropriate presentation of carbohydrate ligands. The quaternary structure of human MBL is built from oligomerization of structural units into polydisperse complexes typically with three to eight structural units, each containing three lectin domains. Insight into the connection between the structure and ligand-binding properties of these oligomers has been lacking. In this article, we present an analysis of the binding to neoglycoprotein-coated surfaces by size-fractionated human MBL oligomers studied with small-angle x-ray scattering and surface plasmon resonance spectroscopy. The MBL oligomers bound to these surfaces mainly in two modes, with dissociation constants in the micro to nanomolar order. The binding kinetics were markedly influenced by both the density of ligands and the number of ligand-binding domains in the oligomers. These findings demonstrated that the MBL-binding kinetics are critically dependent on structural characteristics on the nanometer scale, both with regard to the dimensions of the oligomer, as well as the ligand presentation on surfaces. Therefore...

‣ IFPA Meeting 2010 Workshop Report I: Immunology; Ion transport; Epigenetics; Vascular reactivity; Epitheliochorial placentation; Proteomics

Abad, C.; Antczak, D. F.; Carvalho, J.; Chamley, L. W.; Chen, Q.; Daher, S.; Damiano, A. E.; Dantzer, V.; Diaz, P.; Dunk, C. E.; Daly, E.; Escudero, C.; Falcon, B.; Guillomot, M.; Han, Y. W.; Harris, L. K.; Huidobro-Toro, J. P.; Illsley, N.; Jammes, H.; J
Fonte: W B Saunders Co Ltd Publicador: W B Saunders Co Ltd
Tipo: Outros Formato: S81-S89
Português
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Workshops are an important part of the IFPA annual meeting. At IFPA Meeting 2010 there were twelve themed workshops, six of which are summarized in this report 1. The immunology workshop focused on normal and pathological functions of the maternal immune system in pregnancy. 2. The transport workshop dealt with regulation of ion and water transport across the syncytiotrophoblast of human placenta. 3. The epigenetics workshop covered DNA methylation and its potential role in regulating gene expression in placental development and disease. 4. The vascular reactivity workshop concentrated on methodological approaches used to study placental vascular function. 5. The workshop on epitheliochorial placentation covered current advances from in vivo and in vitro studies of different domestic species. 6. The proteomics workshop focused on a variety of techniques and procedures necessary for proteomic analysis and how they may be implemented for placental research. (C) 2011 Published by IFPA and Elsevier Ltd.

‣ Sanidade Uterina Pós Parto: Aspectos Imunológicos e Terapêuticos

Scagion, Luiz Fernando Salgado
Fonte: Universidade Estadual Paulista (UNESP) Publicador: Universidade Estadual Paulista (UNESP)
Tipo: Trabalho de Conclusão de Curso
Português
Relevância na Pesquisa
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Function of the uterus is often compromised in cattle by bacterial contamination of the uterine lumen after parturition. Pathogenic bacteria often persist, causing uterine disease, a major cause of infertility in cattle. Knowledge of the immunological aspects of the uterus involved in maintaining reproductive healthiness is fundamental to the study of uterine infections that affect the uterus postpartum. Polymorphonuclear leukocytes have an important role because they are the first line of defense against colonization of bacteria in utero (Hammon and Goff, 2006). The establishment of uterine infection depends in parts of endocrine environment, particularly progesterone, which suppresses the immune system (Lewis, 2003). In the puerperium may occur uterine disorders, such as retained placenta, puerperal metritis, clinical and subclinical endometritis and pyometra, this review was proposed a study of the immunology involved in uterine health and a better understanding of uterine disorders, using the model of Sheldon et al. al, (2006) for classification of diseases, and a study of best treatment options and discussion about its functionality, because a lot of controversy among authors about choosing a treatment and another and between treated and untreated; A função do útero é muitas vezes comprometida em bovinos por contaminação bacteriana do lúmen uterino após o parto. As bactérias patogênicas freqüentemente persistem...