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1.
Sci Adv ; 8(40): eabn6552, 2022 10 07.
Artigo em Inglês | MEDLINE | ID: mdl-36206339

RESUMO

T cell activation and function depend on Ca2+ signals mediated by store-operated Ca2+ entry (SOCE) through Ca2+ release-activated Ca2+ (CRAC) channels formed by ORAI1 proteins. We here investigated how SOCE controls T cell function in pulmonary inflammation during a T helper 1 (TH1) cell-mediated response to influenza A virus (IAV) infection and TH2 cell-mediated allergic airway inflammation. T cell-specific deletion of Orai1 did not exacerbate pulmonary inflammation and viral burdens following IAV infection but protected mice from house dust mite-induced allergic airway inflammation. ORAI1 controlled the expression of genes including p53 and E2F transcription factors that regulate the cell cycle in TH2 cells in response to allergen stimulation and the expression of transcription factors and cytokines that regulate TH2 cell function. Systemic application of a CRAC channel blocker suppressed allergic airway inflammation without compromising immunity to IAV infection, suggesting that inhibition of SOCE is a potential treatment for allergic airway disease.


Assuntos
Canais de Cálcio , Vírus da Influenza A , Alérgenos , Animais , Cálcio/metabolismo , Canais de Cálcio/genética , Canais de Cálcio/metabolismo , Sinalização do Cálcio , Citocinas/metabolismo , Fatores de Transcrição E2F , Inflamação , Camundongos , Proteína ORAI1/genética , Proteína ORAI1/metabolismo , Molécula 1 de Interação Estromal/metabolismo , Fatores de Transcrição/metabolismo , Proteína Supressora de Tumor p53/metabolismo
2.
Allergy ; 74(10): 1920-1933, 2019 10.
Artigo em Inglês | MEDLINE | ID: mdl-30937919

RESUMO

BACKGROUND: Atopic dermatitis (AD) is one of the most common skin diseases with a multifactorial etiology. Mutations leading to loss of skin barrier function are associated with the development of AD with group 2 innate lymphoid cells (ILC2) promoting acute skin inflammation. Filaggrin-mutant (Flgft/ft ) mice develop spontaneous skin inflammation accompanied by an increase in skin ILC2 numbers, IL-1ß production, and other cytokines recapitulating human AD. Here, we investigated the role of ILC2, effector cytokines, inflammasome activation, and mast cell function on the development of chronic AD-like inflammation in mice. METHODS: Mice with a frameshift mutation in the filaggrin gene develop spontaneous dermatitis. Flgft/ft mice were crossed to cell- or cytokine-deficient mouse strains, or bred under germ-free conditions. Skin inflammation was scored, and microbiome composition was analyzed. Skin protein expression was measured by multiplex immunoassay. Infiltrating cells were analyzed by flow cytometry. RESULTS: Wild-type and Flgft/ft mice significantly differ in their microbiome composition. Furthermore, mutant mice do not develop skin inflammation under germ-free conditions. ILC2 deficiency did not ameliorate chronic dermatitis in Flgft/ft mice, which was also independent of IL-4, IL-5, IL-9, IL-13, IL-17A, and IL-22. Inflammation was independent of NLRP3 inflammasome activation but required IL-1ß and IL-1R1-signaling. Mechanistically, IL-1ß promoted hyperactivation of IL-1R1-expressing mast cells. Treatment with anti-IL-1ß-antibody alleviated dermatitis exacerbation, while antibiotic intervention ameliorated dermatitis in neonatal mice but not in adults with established inflammation. CONCLUSIONS: In summary, we identified a critical role for the microbiome and IL-1ß mediating chronic inflammation in mice with an impaired skin barrier.


Assuntos
Dermatite Atópica/imunologia , Dermatite Atópica/metabolismo , Imunidade Inata , Interleucina-1beta/metabolismo , Linfócitos/imunologia , Linfócitos/metabolismo , Animais , Biópsia , Citocinas/metabolismo , Dermatite Atópica/patologia , Modelos Animais de Doenças , Proteínas Filagrinas , Inflamassomos/metabolismo , Linfócitos/patologia , Mastócitos/imunologia , Mastócitos/metabolismo , Camundongos , Camundongos Transgênicos , Microbiota , Fenótipo , Transdução de Sinais , Pele/imunologia , Pele/metabolismo , Pele/patologia
3.
J Immunol ; 199(2): 707-717, 2017 07 15.
Artigo em Inglês | MEDLINE | ID: mdl-28615416

RESUMO

Atopic dermatitis (AD) is a common inflammatory skin disease affecting up to 20% of children and 3% of adults worldwide and is associated with dysregulation of the skin barrier. Although type 2 responses are implicated in AD, emerging evidence indicates a potential role for the IL-17A signaling axis in AD pathogenesis. In this study we show that in the filaggrin mutant mouse model of spontaneous AD, IL-17RA deficiency (Il17ra-/- ) resulted in severe exacerbation of skin inflammation. Interestingly, Il17ra-/- mice without the filaggrin mutation also developed spontaneous progressive skin inflammation with eosinophilia, as well as increased levels of thymic stromal lymphopoietin (TSLP) and IL-5 in the skin. Il17ra-/- mice have a defective skin barrier with altered filaggrin expression. The barrier dysregulation and spontaneous skin inflammation in Il17ra-/- mice was dependent on TSLP, but not the other alarmins IL-25 and IL-33. The associated skin inflammation was mediated by IL-5-expressing pathogenic effector Th2 cells and was independent of TCRγδ T cells and IL-22. An absence of IL-17RA in nonhematopoietic cells, but not in the hematopoietic cells, was required for the development of spontaneous skin inflammation. Skin microbiome dysbiosis developed in the absence of IL-17RA, with antibiotic intervention resulting in significant amelioration of skin inflammation and reductions in skin-infiltrating pathogenic effector Th2 cells and TSLP. This study describes a previously unappreciated protective role for IL-17RA signaling in regulation of the skin barrier and maintenance of skin immune homeostasis.


Assuntos
Dermatite Atópica/imunologia , Receptores de Interleucina-17/imunologia , Receptores de Interleucina-17/metabolismo , Pele/crescimento & desenvolvimento , Pele/patologia , Animais , Citocinas/imunologia , Dermatite Atópica/patologia , Modelos Animais de Doenças , Disbiose , Eosinofilia/imunologia , Proteínas Filagrinas , Regulação da Expressão Gênica , Homeostase , Interleucina-33/imunologia , Interleucina-5/genética , Interleucina-5/imunologia , Interleucinas/genética , Interleucinas/imunologia , Proteínas de Filamentos Intermediários/deficiência , Proteínas de Filamentos Intermediários/genética , Camundongos , Microbiota , Mutação , Receptores de Antígenos de Linfócitos T gama-delta/imunologia , Receptores de Interleucina-17/deficiência , Receptores de Interleucina-17/genética , Transdução de Sinais , Pele/imunologia , Pele/microbiologia , Células Th2/imunologia , Linfopoietina do Estroma do Timo , Interleucina 22
4.
Sci Transl Med ; 7(303): 303ra140, 2015 Sep 02.
Artigo em Inglês | MEDLINE | ID: mdl-26333936

RESUMO

Sepsis is the most frequent cause of death in hospitalized patients, and severe sepsis is a leading contributory factor to acute respiratory distress syndrome (ARDS). At present, there is no effective treatment for these conditions, and care is primarily supportive. Murine sialic acid-binding immunoglobulin-like lectin-E (Siglec-E) and its human orthologs Siglec-7 and Siglec-9 are immunomodulatory receptors found predominantly on hematopoietic cells. These receptors are important negative regulators of acute inflammatory responses and are potential targets for the treatment of sepsis and ARDS. We describe a Siglec-targeting platform consisting of poly(lactic-co-glycolic acid) nanoparticles decorated with a natural Siglec ligand, di(α2→8) N-acetylneuraminic acid (α2,8 NANA-NP). This nanoparticle induced enhanced oligomerization of the murine Siglec-E receptor on the surface of macrophages, unlike the free α2,8 NANA ligand. Furthermore, treatment of murine macrophages with these nanoparticles blocked the production of lipopolysaccharide-induced inflammatory cytokines in a Siglec-E-dependent manner. The nanoparticles were also therapeutically beneficial in vivo in both systemic and pulmonary murine models replicating inflammatory features of sepsis and ARDS. Moreover, we confirmed the anti-inflammatory effect of these nanoparticles on human monocytes and macrophages in vitro and in a human ex vivo lung perfusion (EVLP) model of lung injury. We also established that interleukin-10 (IL-10) induced Siglec-E expression and α2,8 NANA-NP further augmented the expression of IL-10. Indeed, the effectiveness of the nanoparticle depended on IL-10. Collectively, these results demonstrated a therapeutic effect of targeting Siglec receptors with a nanoparticle-based platform under inflammatory conditions.


Assuntos
Inflamação/prevenção & controle , Ácido N-Acetilneuramínico/química , Nanopartículas , Lectinas Semelhantes a Imunoglobulina de Ligação ao Ácido Siálico/efeitos dos fármacos , Animais , Humanos , Interleucina-10/fisiologia , Camundongos , Camundongos Endogâmicos C57BL , Lectinas Semelhantes a Imunoglobulina de Ligação ao Ácido Siálico/metabolismo , Regulação para Cima
5.
Sci Transl Med ; 6(230): 230ra44, 2014 Apr 02.
Artigo em Inglês | MEDLINE | ID: mdl-24695684

RESUMO

Age-related macular degeneration (AMD) is the most common form of central retinal blindness globally. Distinct processes of the innate immune system, specifically activation of the NLRP3 inflammasome, have been shown to play a central role in the development of both "dry" and neovascular ("wet") forms of the disease. We show that the inflammatory cytokine interleukin-18 (IL-18) can regulate choroidal neovascularization formation in mice. We observed that exogenous administration of mature recombinant IL-18 has no effect on retinal pigment epithelial (RPE) cell viability, but that overexpression of pro-IL-18 or pro-IL-1ß alone can cause RPE cell swelling and subsequent atrophy, a process that can be inhibited by the promotion of autophagy. A direct comparison of local and systemic administration of mature recombinant IL-18 with current anti-VEGF (vascular endothelial growth factor)-based therapeutic strategies shows that IL-18 treatment works effectively alone and more effectively in combination with anti-VEGF therapy and represents a novel therapeutic strategy for the treatment of wet AMD.


Assuntos
Neovascularização de Coroide/tratamento farmacológico , Neovascularização de Coroide/prevenção & controle , Interleucina-18/uso terapêutico , Degeneração Macular/tratamento farmacológico , Animais , Autofagia/efeitos dos fármacos , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Neovascularização de Coroide/complicações , Neovascularização de Coroide/patologia , Hematopoese/efeitos dos fármacos , Humanos , Interleucina-18/farmacologia , Interleucina-1beta/farmacologia , Interleucina-1beta/uso terapêutico , Injeções Intravítreas , Lasers , Degeneração Macular/complicações , Degeneração Macular/patologia , Camundongos , Modelos Biológicos , Permeabilidade/efeitos dos fármacos , Epitélio Pigmentado da Retina/efeitos dos fármacos , Epitélio Pigmentado da Retina/patologia , Fator A de Crescimento do Endotélio Vascular/antagonistas & inibidores , Fator A de Crescimento do Endotélio Vascular/metabolismo
6.
Proc Natl Acad Sci U S A ; 111(1): 367-72, 2014 Jan 07.
Artigo em Inglês | MEDLINE | ID: mdl-24344271

RESUMO

Disease conditions associated with pulmonary fibrosis are progressive and have a poor long-term prognosis with irreversible changes in airway architecture leading to marked morbidity and mortalities. Using murine models we demonstrate a role for interleukin (IL)-25 in the generation of pulmonary fibrosis. Mechanistically, we identify IL-13 release from type 2 innate lymphoid cells (ILC2) as sufficient to drive collagen deposition in the lungs of challenged mice and suggest this as a potential mechanism through which IL-25 is acting. Additionally, we demonstrate that in human idiopathic pulmonary fibrosis there is increased pulmonary expression of IL-25 and also observe a population ILC2 in the lungs of idiopathic pulmonary fibrosis patients. Collectively, we present an innate mechanism for the generation of pulmonary fibrosis, via IL-25 and ILC2, that occurs independently of T-cell-mediated antigen-specific immune responses. These results suggest the potential of therapeutically targeting IL-25 and ILC2 for the treatment of human fibrotic diseases.


Assuntos
Regulação da Expressão Gênica , Interleucina-17/metabolismo , Interleucinas/metabolismo , Linfócitos/citologia , Fibrose Pulmonar/metabolismo , Idoso , Animais , Moléculas de Adesão Celular/metabolismo , Colágeno/química , Colágeno/metabolismo , Feminino , Humanos , Fibrose Pulmonar Idiopática/patologia , Imunidade Inata , Inflamação , Interleucina-13/metabolismo , Fígado/parasitologia , Pulmão/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Pessoa de Meia-Idade , Fibrose Pulmonar/patologia , Schistosoma mansoni
7.
Immunity ; 38(1): 66-78, 2013 Jan 24.
Artigo em Inglês | MEDLINE | ID: mdl-23177319

RESUMO

Suppressors of cytokine signaling (SOCS) are important regulators of lipopolysaccharide (LPS) and cytokine responses but their role in macrophage polarization is unknown. We have shown here that myeloid-restricted Socs3 deletion (Socs3(Lyz2cre)) resulted in resistance to LPS-induced endotoxic shock, whereas Socs2(-/-) mice were highly susceptible. We observed striking bias toward M2-like macrophages in Socs3(Lyz2cre) mice, whereas the M1-like population was enriched in Socs2(-/-) mice. Adoptive transfer experiments showed that responses to endotoxic shock and polymicrobial sepsis were transferable and macrophage dependent. Critically, this dichotomous response was associated with enhanced regulatory T (Treg) cell recruitment by Socs3(Lyz2cre) cells, whereas Treg cell recruitment was absent in the presence of Socs2(-/-) macrophages. In addition, altered polarization coincided with enhanced interferon-gamma (IFN-γ)-induced signal transducer and activator of transcription-1 (STAT1) activation in Socs2(-/-) macrophages and enhanced interleukin-4 (IL-4) plus IL-13-induced STAT6 phosphorylation in Socs3(Lyz2cre) macrophages. SOCS, therefore, are essential controllers of macrophage polarization, regulating inflammatory responses.


Assuntos
Polaridade Celular/genética , Macrófagos/imunologia , Macrófagos/metabolismo , Proteínas Supressoras da Sinalização de Citocina/genética , Transferência Adotiva , Animais , Regulação da Expressão Gênica , Interleucina-10/imunologia , Interleucina-10/metabolismo , Macrófagos/transplante , Camundongos , Fatores de Transcrição STAT/metabolismo , Sepse/genética , Sepse/imunologia , Sepse/prevenção & controle , Transdução de Sinais , Proteína 3 Supressora da Sinalização de Citocinas , Proteínas Supressoras da Sinalização de Citocina/imunologia , Linfócitos T Reguladores/imunologia , Linfócitos T Reguladores/metabolismo , Transplante Isogênico
8.
Shock ; 36(3): 295-302, 2011 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-21844787

RESUMO

Localized tissue hypoxia is a feature of infection and inflammation, resulting in the upregulation of the transcription factors hypoxia-inducible factor 1α and nuclear factor κB (NF-κB) via inhibition of oxygen sensing hydroxylase enzymes. Previous studies have demonstrated a beneficial role for the hydroxylase inhibitor dimethyloxallyl glycine (DMOG) in inflammatory conditions, including experimental colitis, by regulating the activity of hypoxia-inducible factor 1 and NF-κB. We have demonstrated in vivo that pretreatment with DMOG attenuates systemic LPS-induced activation of the NF-κB pathway. Furthermore, mice treated with DMOG had significantly increased survival in LPS-induced shock. Conversely, in models of polymicrobial sepsis, DMOG exacerbates disease severity. Dimethyloxallyl glycine treatment of mice promotes M2 polarization in macrophages within the peritoneal cavity, resulting in the downregulation of proinflammatory cytokines such as TNF-α. In addition, in vivo DMOG treatment upregulates IL-10 expression, specifically in the peritoneal B1 cell population. This study demonstrates cell type-specific roles for hydroxylase inhibition in vivo and provides insight into the mechanism underlying the protection conveyed by DMOG in models of endotoxic shock.


Assuntos
Aminoácidos Dicarboxílicos/uso terapêutico , Macrófagos/efeitos dos fármacos , Macrófagos/metabolismo , Choque Séptico/tratamento farmacológico , Animais , Citometria de Fluxo , Immunoblotting , Interleucina-10/metabolismo , Lipopolissacarídeos/toxicidade , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Oxigenases de Função Mista/antagonistas & inibidores , NF-kappa B/metabolismo , Reação em Cadeia da Polimerase , Receptores de Interleucina-10/sangue , Sepse/tratamento farmacológico , Choque Séptico/induzido quimicamente
9.
Gastroenterology ; 139(6): 2093-101, 2010 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-20600011

RESUMO

BACKGROUND & AIMS: Hypoxia inducible factor (HIF) prolyl hydroxylase inhibitors are protective in mouse models of inflammatory bowel disease (IBD). Here, we investigated the therapeutic target(s) and mechanism(s) involved. METHODS: The effect of genetic deletion of individual HIF-prolyl hydroxylase (PHD) enzymes on the development of dextran sulphate sodium (DSS)-induced colitis was examined in mice. RESULTS: PHD1(-/-), but not PHD2(+/-) or PHD3(-/-), mice were less susceptible to the development of colitis than wild-type controls as determined by weight loss, disease activity, colon histology, neutrophil infiltration, and cytokine expression. Reduced susceptibility of PHD1(-/-) mice to colitis was associated with increased density of colonic epithelial cells relative to wild-type controls, which was because of decreased levels of apoptosis that resulted in enhanced epithelial barrier function. Furthermore, with the use of cultured epithelial cells it was confirmed that hydroxylase inhibition reversed DSS-induced apoptosis and barrier dysfunction. Finally, PHD1 levels were increased with disease severity in intestinal tissue from patients with IBD and in colonic tissues from DSS-treated mice. CONCLUSIONS: These results imply a role for PHD1 as a positive regulator of intestinal epithelial cell apoptosis in the inflamed colon. Genetic loss of PHD1 is protective against colitis through decreased epithelial cell apoptosis and consequent enhancement of intestinal epithelial barrier function. Thus, targeted PHD1 inhibition may represent a new therapeutic approach in IBD.


Assuntos
Apoptose/fisiologia , Colite/metabolismo , Dioxigenases/metabolismo , Células Epiteliais/metabolismo , Mucosa Intestinal/metabolismo , Proteínas Nucleares/metabolismo , Pró-Colágeno-Prolina Dioxigenase/metabolismo , Animais , Colite/induzido quimicamente , Colite/patologia , Sulfato de Dextrana/toxicidade , Dioxigenases/genética , Modelos Animais de Doenças , Enterócitos/metabolismo , Enterócitos/patologia , Células Epiteliais/patologia , Humanos , Hipóxia/metabolismo , Hipóxia/patologia , Prolina Dioxigenases do Fator Induzível por Hipóxia , Absorção Intestinal/fisiologia , Mucosa Intestinal/patologia , Camundongos , Camundongos da Linhagem 129 , Camundongos Knockout , Proteínas Nucleares/genética , Pró-Colágeno-Prolina Dioxigenase/genética , Índice de Gravidade de Doença
10.
J Immunol ; 184(5): 2627-37, 2010 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-20130211

RESUMO

Pathogen recognition receptors (PRRs) function to maintain the balance between controlled responses to pathogens and uncontrolled innate immune activation leading to inflammation. In the context of commensal bacteria and the etiology of inflammatory bowel disease, although a role for the TLRs is known, there is a less defined function for C-type lectin receptors (CLRs). We demonstrate that mice deficient ((-/-)) in the CLR specific intracellular adhesion molecule-3 grabbing nonintegrin homolog-related 1 (SIGN-R1) (CD209b) have reduced susceptibility to experimental colitis, with a reduction in the disease severity, colon damage, and levels of the proinflammatory cytokines IL-1beta, TNF-alpha, and IL-6. To determine whether SIGN-R1(-/-) mice had a systemic defect in innate activation, we examined the responsiveness of macrophages from SIGN-R1(-/-) mice to TLR ligands. SIGN-R1(-/-) peritoneal macrophages, but not bone marrow-derived macrophages, have a specific defect in IL-1beta and IL-18 production, but not other cytokines, in response to the TLR4 ligand LPS. In vivo SIGN-R1(-/-) mice had significantly reduced susceptibility to LPS-induced shock. To address the synergistic relationship between SIGN-R1 and TLR4 in the context of experimental colitis, SIGN-R1/TLR4(-/-) mice were generated. SIGN-R1/TLR4(-/-) mice displayed reduced susceptibility to experimental colitis relative to severity of disease observed in wild-type or TLR4(-/-) mice. The in vivo use of a blocking mAb confirmed a functional role for SIGN-R1 in LPS-induced shock and experimental colitis. These data indicate a role for SIGN-R1 in the regulation of inflammation in a model of experimental colitis and illustrate that SIGN-R1 is a critical innate factor in response to LPS.


Assuntos
Moléculas de Adesão Celular/fisiologia , Colite/fisiopatologia , Lectinas Tipo C/fisiologia , Lipopolissacarídeos/toxicidade , Receptores de Superfície Celular/fisiologia , Animais , Moléculas de Adesão Celular/genética , Moléculas de Adesão Celular/metabolismo , Colite/induzido quimicamente , Colite/genética , Colo/efeitos dos fármacos , Colo/metabolismo , Colo/patologia , Sulfato de Dextrana , Feminino , Citometria de Fluxo , Imunofluorescência , Predisposição Genética para Doença , Interleucina-18/metabolismo , Interleucina-1beta/metabolismo , Interleucina-6/metabolismo , Lectinas Tipo C/genética , Lectinas Tipo C/metabolismo , Macrófagos Peritoneais/efeitos dos fármacos , Macrófagos Peritoneais/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Fator 88 de Diferenciação Mieloide/deficiência , Fator 88 de Diferenciação Mieloide/genética , Receptores de Superfície Celular/genética , Receptores de Superfície Celular/metabolismo , Choque/induzido quimicamente , Choque/genética , Choque/fisiopatologia , Receptor 2 Toll-Like/deficiência , Receptor 2 Toll-Like/genética , Receptor 4 Toll-Like/deficiência , Receptor 4 Toll-Like/genética , Fator de Necrose Tumoral alfa/metabolismo
11.
Infect Immun ; 77(1): 399-404, 2009 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-18981244

RESUMO

The de novo immune response to infectious organisms arises from the innate recognition of pathogen-associated molecular patterns (PAMPs) by the host's pattern recognition receptors (PRRs). As the generation of type 2 cytokine responses by the human trematode parasite Schistosoma mansoni is glycan mediated, there is a particular potential role for a C-type lectin receptor (CLR) to mediate the innate recognition of schistosome PAMPs. One such CLR, dendritic cell-specific intracellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN; CD209), has been shown to recognize glycans expressed by S. mansoni eggs. We show that SIGNR1 (SIGN-related 1; CD209b), a murine homologue of DC-SIGN that is expressed on macrophages, also binds both schistosome-soluble egg antigens and worm antigens in vitro. The generation of schistosome egg-induced pulmonary egg granulomas was not altered in SIGNR1-deficient mice. Following S. mansoni infection, the SIGNR1-deficient mice had an unaltered phenotype with an intact immunological response and no difference in pathology. In this study we demonstrate that although SIGNR1 recognizes S. mansoni antigens in vitro, this CLR is redundant during infection. This study highlights the finding that although there was binding of SIGNR1 to immunogenic factors produced in the S. mansoni life cycle, this recognition does not translate to a functional in vivo role for the PRR during infection.


Assuntos
Antígenos de Helmintos/imunologia , Antígenos de Helmintos/metabolismo , Moléculas de Adesão Celular/imunologia , Moléculas de Adesão Celular/metabolismo , Lectinas Tipo C/imunologia , Lectinas Tipo C/metabolismo , Receptores de Superfície Celular/imunologia , Receptores de Superfície Celular/metabolismo , Schistosoma mansoni/imunologia , Animais , Moléculas de Adesão Celular/deficiência , Células Cultivadas , Citocinas/metabolismo , Granuloma/parasitologia , Granuloma/patologia , Lectinas Tipo C/deficiência , Leucócitos Mononucleares/imunologia , Pulmão/parasitologia , Pulmão/patologia , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Knockout , Ligação Proteica , Receptores de Superfície Celular/deficiência , Esquistossomose mansoni/imunologia , Esquistossomose mansoni/patologia , Baço/imunologia
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