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1.
Ann Rheum Dis ; 78(8): 1025-1032, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31018962

RESUMO

BACKGROUND: Different diagnostic and classification criteria are available for hereditary recurrent fevers (HRF)-familial Mediterranean fever (FMF), tumour necrosis factor receptor-associated periodic fever syndrome (TRAPS), mevalonate kinase deficiency (MKD) and cryopyrin-associated periodic syndromes (CAPS)-and for the non-hereditary, periodic fever, aphthosis, pharyngitis and adenitis (PFAPA). We aimed to develop and validate new evidence-based classification criteria for HRF/PFAPA. METHODS: Step 1: selection of clinical, laboratory and genetic candidate variables; step 2: classification of 360 random patients from the Eurofever Registry by a panel of 25 clinicians and 8 geneticists blinded to patients' diagnosis (consensus ≥80%); step 3: statistical analysis for the selection of the best candidate classification criteria; step 4: nominal group technique consensus conference with 33 panellists for the discussion and selection of the final classification criteria; step 5: cross-sectional validation of the novel criteria. RESULTS: The panellists achieved consensus to classify 281 of 360 (78%) patients (32 CAPS, 36 FMF, 56 MKD, 37 PFAPA, 39 TRAPS, 81 undefined recurrent fever). Consensus was reached for two sets of criteria for each HRF, one including genetic and clinical variables, the other with clinical variables only, plus new criteria for PFAPA. The four HRF criteria demonstrated sensitivity of 0.94-1 and specificity of 0.95-1; for PFAPA, criteria sensitivity and specificity were 0.97 and 0.93, respectively. Validation of these criteria in an independent data set of 1018 patients shows a high accuracy (from 0.81 to 0.98). CONCLUSION: Eurofever proposes a novel set of validated classification criteria for HRF and PFAPA with high sensitivity and specificity.

2.
Front Immunol ; 9: 636, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29867916

RESUMO

Common variable immunodeficiency (CVID) is the most frequent symptomatic primary immunodeficiency characterized by recurrent infections, hypogammaglobulinemia and poor response to vaccines. Its diagnosis is made based on clinical and immunological criteria, after exclusion of other diseases that can cause similar phenotypes. Currently, less than 20% of cases of CVID have a known underlying genetic cause. We have analyzed whole-exome sequencing and copy number variants data of 36 children and adolescents diagnosed with CVID and healthy relatives to estimate the proportion of monogenic cases. We have replicated an association of CVID to p.C104R in TNFRSF13B and reported the second case of homozygous patient to date. Our results also identify five causative genetic variants in LRBA, CTLA4, NFKB1, and PIK3R1, as well as other very likely causative variants in PRKCD, MAPK8, or DOCK8 among others. We experimentally validate the effect of the LRBA stop-gain mutation which abolishes protein production and downregulates the expression of CTLA4, and of the frameshift indel in CTLA4 producing expression downregulation of the protein. Our results indicate a monogenic origin of at least 15-24% of the CVID cases included in the study. The proportion of monogenic patients seems to be lower in CVID than in other PID that have also been analyzed by whole exome or targeted gene panels sequencing. Regardless of the exact proportion of CVID monogenic cases, other genetic models have to be considered for CVID. We propose that because of its prevalence and other features as intermediate penetrancies and phenotypic variation within families, CVID could fit with other more complex genetic scenarios. In particular, in this work, we explore the possibility of CVID being originated by an oligogenic model with the presence of heterozygous mutations in interacting proteins or by the accumulation of detrimental variants in particular immunological pathways, as well as perform association tests to detect association with rare genetic functional variation in the CVID cohort compared to healthy controls.


Assuntos
Antígeno CTLA-4/genética , Imunodeficiência de Variável Comum/genética , Genótipo , Mutação/genética , Proteína Transmembrana Ativadora e Interagente do CAML/genética , Adolescente , Células Cultivadas , Criança , Pré-Escolar , Estudos de Coortes , Estudos de Associação Genética , Predisposição Genética para Doença , Humanos , Leucócitos Mononucleares/fisiologia , Ativação Linfocitária , Modelos Biológicos , Sequenciamento Completo do Exoma
5.
Australas J Dermatol ; 59(1): e70-e73, 2018 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-28776328

RESUMO

Acute generalised exanthematous pustulosis (AGEP) is a rare toxicoderma characterised by an acute onset rash, with many sterile pustules on the surface, high fever and increased acute phase reactants. We report the case of a patient who presented to the dermatology department with an AGEP and polyarthritis, in which a novel CARD14 mutation was identified. The pathophysiological mechanism of AGEP remains unclear, although mutations in the IL36RN gene have been identified in a small subset of AGEP patients. Similarly, mutations in the CARD14 gene have been linked to pustular types of psoriasis and familiar cases of pityriasis rubra pilaris; however, there are no reports associating mutations in the CARD14 gene with AGEP.


Assuntos
Pustulose Exantematosa Aguda Generalizada/genética , Artrite/genética , Proteínas Adaptadoras de Sinalização CARD/genética , Guanilato Ciclase/genética , Proteínas de Membrana/genética , Pustulose Exantematosa Aguda Generalizada/complicações , Artrite/complicações , Humanos , Masculino , Pessoa de Meia-Idade , Mutação
6.
Nat Commun ; 8(1): 1462, 2017 11 13.
Artigo em Inglês | MEDLINE | ID: mdl-29133782

RESUMO

Mechanistic target of rapamycin (mTOR) enhances immunity in addition to orchestrating metabolism. Here we show that mTOR coordinates immunometabolic reconfiguration of marginal zone (MZ) B cells, a pre-activated lymphocyte subset that mounts antibody responses to T-cell-independent antigens through a Toll-like receptor (TLR)-amplified pathway involving transmembrane activator and CAML interactor (TACI). This receptor interacts with mTOR via the TLR adapter MyD88. The resulting mTOR activation instigates MZ B-cell proliferation, immunoglobulin G (IgG) class switching, and plasmablast differentiation through a rapamycin-sensitive pathway that integrates metabolic and antibody-inducing transcription programs, including NF-κB. Disruption of TACI-mTOR interaction by rapamycin, truncation of the MyD88-binding domain of TACI, or B-cell-conditional mTOR deficiency interrupts TACI signaling via NF-κB and cooperation with TLRs, thereby hampering IgG production to T-cell-independent antigens but not B-cell survival. Thus, mTOR drives innate-like antibody responses by linking proximal TACI signaling events with distal immunometabolic transcription programs.


Assuntos
Linfócitos B/imunologia , Imunoglobulina G/imunologia , Alvo Mecanístico do Complexo 1 de Rapamicina/imunologia , Fator 88 de Diferenciação Mieloide/metabolismo , Serina-Treonina Quinases TOR/imunologia , Proteína Transmembrana Ativadora e Interagente do CAML/imunologia , Animais , Linhagem Celular , Proliferação de Células , Ativação Enzimática , Perfilação da Expressão Gênica , Células HEK293 , Humanos , Switching de Imunoglobulina/genética , Switching de Imunoglobulina/imunologia , Imunoglobulina G/biossíntese , Ativação Linfocitária/imunologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , NF-kappa B/metabolismo , Transdução de Sinais/imunologia , Sirolimo/farmacologia
7.
Clin Exp Rheumatol ; 35 Suppl 108(6): 27-31, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28079503

RESUMO

OBJECTIVES: Cryopyrin-associated periodic syndromes (CAPS) usually start during infancy as an urticarial-like rash and a marked acute phase response, with additional manifestations appearing during its evolution. The aim of this study was to expand the clinical diversity of CAPS by the description of novel atypical features. METHODS: Clinical data were collected from patients' medical charts. Sanger sequencing analyzed NLRP3. Response to anti-IL-1 blockade was evaluated by clinical assessments and by measurements of laboratory parameters. RESULTS: Seventeen patients from two families (A and B), carrying the p.Ala439Thr and p.Arg260Trp NLRP3 mutations respectively, were enrolled. The disease was unexpectedly atypical in all members of Family A, with a 16-year-old asymptomatic carrier, and onset in adulthood associated with absence of skin lesions in four affected members. Surprisingly, one patient from each family suffered from severe haemorrhagic cystitis due to AA amyloidosis in the urinary bladder. Members of Family B displayed a classical phenotype, with two patients suffering from olfactive disorders. CONCLUSIONS: Our evidence suggests that CAPS may occasionally be presented as a late-onset, recurrent inflammatory disease without urticarial-like rash. In some patients, AA amyloidosis in strange locations like urinary bladder may complicate the clinical course. The response to IL-1 blockade in these atypical CAPS was similar to that described in classical forms. Consequently, we suggest that CAPS should be included in the differential diagnosis of adult patients with unexplained, recurrent inflammatory diseases, and once confirmed, the early initiation of anti-IL-1 blockade will probably prevent the development of life-threatening complications.


Assuntos
Amiloidose/etiologia , Síndromes Periódicas Associadas à Criopirina/complicações , Cistite/etiologia , Nefropatias/etiologia , Adolescente , Idade de Início , Idoso , Amiloidose/tratamento farmacológico , Amiloidose/genética , Amiloidose/imunologia , Doenças Assintomáticas , Síndromes Periódicas Associadas à Criopirina/tratamento farmacológico , Síndromes Periódicas Associadas à Criopirina/genética , Síndromes Periódicas Associadas à Criopirina/imunologia , Cistite/tratamento farmacológico , Cistite/genética , Cistite/imunologia , Feminino , Predisposição Genética para Doença , Hematúria/etiologia , Humanos , Imunossupressores/uso terapêutico , Interleucina-1/antagonistas & inibidores , Interleucina-1/imunologia , Nefropatias/tratamento farmacológico , Nefropatias/genética , Nefropatias/imunologia , Masculino , Mutação , Proteína 3 que Contém Domínio de Pirina da Família NLR/genética , Linhagem , Fenótipo , Resultado do Tratamento
8.
Pediatr Dermatol ; 33(6): 602-614, 2016 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-27699831

RESUMO

Specific gene mutations leading to dysregulation of innate immune response produce the expanding spectrum of monogenic autoinflammatory diseases (AIDs). They are characterized by seemingly unprovoked, recurrent episodes of systemic inflammation in which a myriad of manifestations usually affect skin. Novel genetic technologies have led to the discovery of new AIDs and phenotypes that were not previously clinically described. Consequently the number of AIDs is continuously growing and their recognition and the disclosure of their pathophysiology will prompt early diagnosis and targeted treatment of affected patients. The objective of the present work is to review those newly described AIDs with prominent dermatologic manifestations that may constitute a major criterion for their diagnosis.


Assuntos
Doenças Hereditárias Autoinflamatórias , Doenças Autoimunes , Criança , Dermatologia , Doenças Hereditárias Autoinflamatórias/complicações , Doenças Hereditárias Autoinflamatórias/patologia , Humanos , Imunidade Inata , Inflamação , Fenótipo , Pele
9.
Nat Immunol ; 15(4): 354-364, 2014 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-24562309

RESUMO

Innate lymphoid cells (ILCs) regulate stromal cells, epithelial cells and cells of the immune system, but their effect on B cells remains unclear. Here we identified RORγt(+) ILCs near the marginal zone (MZ), a splenic compartment that contains innate-like B cells highly responsive to circulating T cell-independent (TI) antigens. Splenic ILCs established bidirectional crosstalk with MAdCAM-1(+) marginal reticular cells by providing tumor-necrosis factor (TNF) and lymphotoxin, and they stimulated MZ B cells via B cell-activation factor (BAFF), the ligand of the costimulatory receptor CD40 (CD40L) and the Notch ligand Delta-like 1 (DLL1). Splenic ILCs further helped MZ B cells and their plasma-cell progeny by coopting neutrophils through release of the cytokine GM-CSF. Consequently, depletion of ILCs impaired both pre- and post-immune TI antibody responses. Thus, ILCs integrate stromal and myeloid signals to orchestrate innate-like antibody production at the interface between the immune system and circulatory system.


Assuntos
Formação de Anticorpos , Linfócitos B/imunologia , Linfócitos/imunologia , Plasmócitos/imunologia , Baço/imunologia , Animais , Anticorpos/sangue , Antígenos T-Independentes/imunologia , Proteínas Sanguíneas/imunologia , Comunicação Celular/imunologia , Diferenciação Celular , Células Cultivadas , Fator Estimulador de Colônias de Granulócitos e Macrófagos/metabolismo , Humanos , Imunidade Inata , Imunoglobulinas/metabolismo , Ativação Linfocitária , Camundongos , Camundongos Endogâmicos C57BL , Mucoproteínas/metabolismo , Neutrófilos/imunologia , Membro 3 do Grupo F da Subfamília 1 de Receptores Nucleares/metabolismo , Picratos/imunologia , Transdução de Sinais/imunologia , Células Estromais/imunologia
14.
Nat Immunol ; 13(2): 170-80, 2011 Dec 25.
Artigo em Inglês | MEDLINE | ID: mdl-22197976

RESUMO

Neutrophils use immunoglobulins to clear antigen, but their role in immunoglobulin production is unknown. Here we identified neutrophils around the marginal zone (MZ) of the spleen, a B cell area specialized in T cell-independent immunoglobulin responses to circulating antigen. Neutrophils colonized peri-MZ areas after postnatal mucosal colonization by microbes and enhanced their B cell-helper function after receiving reprogramming signals, including interleukin 10 (IL-10), from splenic sinusoidal endothelial cells. Splenic neutrophils induced immunoglobulin class switching, somatic hypermutation and antibody production by activating MZ B cells through a mechanism that involved the cytokines BAFF, APRIL and IL-21. Neutropenic patients had fewer and hypomutated MZ B cells and a lower abundance of preimmune immunoglobulins to T cell-independent antigens, which indicates that neutrophils generate an innate layer of antimicrobial immunoglobulin defense by interacting with MZ B cells.


Assuntos
Linfócitos B/imunologia , Imunoglobulinas/biossíntese , Imunoglobulinas/imunologia , Neutrófilos/imunologia , Baço/imunologia , Adolescente , Adulto , Animais , Anticorpos/imunologia , Anticorpos/metabolismo , Células Cultivadas , Criança , Doenças Transmissíveis/imunologia , Citocinas/imunologia , Feminino , Infecções por HIV/imunologia , Humanos , Switching de Imunoglobulina/imunologia , Interleucina-10/imunologia , Lúpus Eritematoso Sistêmico/imunologia , Macaca mulatta/imunologia , Masculino , Camundongos , Pessoa de Meia-Idade , Hipermutação Somática de Imunoglobulina/imunologia , Adulto Jovem
15.
Biol Blood Marrow Transplant ; 17(7): 1084-7, 2011 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-21215814

RESUMO

The current definition of complete remission (CR) in multiple myeloma (MM) requires a negative serum and urine immunofixation (IFE) and <5% bone marrow plasma cells (BMPCs). The aim of this study was to determine the value of BMPCs count by standard microscopic evaluation in patients with MM in serologic CR after autologous stem cell transplantation (ASCT). Thirty-five patients with a median follow-up after ASCT of 7.3 years were studied. The percentage of BMPCs was an independent predictor of progression in multivariate model (hazard ratio 2.02, P = .009). Patients with >1.5% BMPCs (median: 0.8%) after ASCT had an increased risk of progression (P = .016) and a trend toward a shorter survival (P = .195). In conclusion, conventional morphology of bone marrow is a useful and rapid tool as a first step to assess the residual tumor mass in patients with MM in CR after ASCT, and it constitutes a strong predictor for disease progression.


Assuntos
Exame de Medula Óssea/métodos , Medula Óssea/patologia , Mieloma Múltiplo/cirurgia , Transplante de Células-Tronco de Sangue Periférico , Plasmócitos/patologia , Adulto , Idoso , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Bussulfano/administração & dosagem , Contagem de Células , Terapia Combinada , Progressão da Doença , Feminino , Humanos , Estimativa de Kaplan-Meier , Masculino , Melfalan/administração & dosagem , Pessoa de Meia-Idade , Mieloma Múltiplo/tratamento farmacológico , Mieloma Múltiplo/patologia , Neoplasia Residual , Prognóstico , Modelos de Riscos Proporcionais , Indução de Remissão , Fatores de Risco , Sensibilidade e Especificidade , Condicionamento Pré-Transplante/métodos , Transplante Autólogo , Irradiação Corporal Total
16.
Medicine (Baltimore) ; 89(6): 403-25, 2010 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-21057262

RESUMO

Autosomal recessive interleukin-1 receptor-associated kinase (IRAK)-4 and myeloid differentiation factor (MyD)88 deficiencies impair Toll-like receptor (TLR)- and interleukin-1 receptor-mediated immunity. We documented the clinical features and outcome of 48 patients with IRAK-4 deficiency and 12 patients with MyD88 deficiency, from 37 kindreds in 15 countries.The clinical features of IRAK-4 and MyD88 deficiency were indistinguishable. There were no severe viral, parasitic, and fungal diseases, and the range of bacterial infections was narrow. Noninvasive bacterial infections occurred in 52 patients, with a high incidence of infections of the upper respiratory tract and the skin, mostly caused by Pseudomonas aeruginosa and Staphylococcus aureus, respectively. The leading threat was invasive pneumococcal disease, documented in 41 patients (68%) and causing 72 documented invasive infections (52.2%). P. aeruginosa and Staph. aureus documented invasive infections also occurred (16.7% and 16%, respectively, in 13 and 13 patients, respectively). Systemic signs of inflammation were usually weak or delayed. The first invasive infection occurred before the age of 2 years in 53 (88.3%) and in the neonatal period in 19 (32.7%) patients. Multiple or recurrent invasive infections were observed in most survivors (n = 36/50, 72%).Clinical outcome was poor, with 24 deaths, in 10 cases during the first invasive episode and in 16 cases of invasive pneumococcal disease. However, no death and invasive infectious disease were reported in patients after the age of 8 years and 14 years, respectively. Antibiotic prophylaxis (n = 34), antipneumococcal vaccination (n = 31), and/or IgG infusion (n = 19), when instituted, had a beneficial impact on patients until the teenage years, with no seemingly detectable impact thereafter.IRAK-4 and MyD88 deficiencies predispose patients to recurrent life-threatening bacterial diseases, such as invasive pneumococcal disease in particular, in infancy and early childhood, with weak signs of inflammation. Patients and families should be informed of the risk of developing life-threatening infections; empiric antibacterial treatment and immediate medical consultation are strongly recommended in cases of suspected infection or moderate fever. Prophylactic measures in childhood are beneficial, until spontaneous improvement occurs in adolescence.


Assuntos
Quinases Associadas a Receptores de Interleucina-1/deficiência , Fator 88 de Diferenciação Mieloide/deficiência , Adolescente , Antibacterianos/uso terapêutico , Infecções Bacterianas/epidemiologia , Infecções Bacterianas/prevenção & controle , Criança , Pré-Escolar , Suscetibilidade a Doenças , Feminino , Humanos , Imunidade , Lactente , Quinases Associadas a Receptores de Interleucina-1/genética , Masculino , Mutação , Fator 88 de Diferenciação Mieloide/genética , Receptores de Interleucina-1/metabolismo , Receptores Toll-Like/metabolismo
17.
Blood ; 114(24): 4954-6, 2009 Dec 03.
Artigo em Inglês | MEDLINE | ID: mdl-19797521

RESUMO

The prevalence of an abnormal serum free light chain (FLC) ratio in 34 patients with multiple myeloma in complete response (CR) after hematopoietic stem cell transplantation was studied. Fourteen of 34 patients (41.2%) showed an abnormal FLC ratio. The frequency of abnormal FLC ratio in patients with or without oligoclonal bands was 72.7% versus 26%, respectively (P = .023). The median value of FLC ratio was 2.55 (95% confidence interval, 1.89-3.20) in patients with oligoclonal bands versus 0.87 (95% confidence interval, 0.70-1.04) for those with no oligoclonal bands (P = .011). This is the first report showing that the presence of oligoclonal bands in patients with multiple myeloma in CR frequently results in an abnormal FLC ratio. Because an oligoclonal immune response is associated with a good outcome, our results question the current definition of stringent CR and support that the prognostic impact of oligoclonal bands should be also assessed on multivariate analysis.


Assuntos
Cadeias Leves de Imunoglobulina/sangue , Mieloma Múltiplo/sangue , Bandas Oligoclonais/sangue , Adulto , Idoso , Feminino , Transplante de Células-Tronco Hematopoéticas , Humanos , Masculino , Pessoa de Meia-Idade , Mieloma Múltiplo/terapia , Mieloma Múltiplo/urina , Bandas Oligoclonais/urina , Indução de Remissão
18.
Blood ; 112(10): 4337-42, 2008 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-18772453

RESUMO

The inflammasomes are macromolecular cytosolic complexes involved in the production of interleukin-1beta (IL-1beta) and IL-18 in response to several pathogen-derived stimuli. Such interleukins have been implicated in the origin of severe allogeneic stem cell transplant (allo-SCT) complications. We analyzed the relationship between the interindividual variability in inflammasome protein-encoding genes in donors and patients and clinical outcome after allo-SCT. Fourteen common genetic variants in 5 genes of the inflammasome, namely, NLRP1, NLRP2, NLRP3, CARD8, and CASP5, were genotyped in 133 human leukocyte antigen-identical sibling pairs undergoing allo-SCT. In the multivariate analysis, donor variants in NLRP2 and NLRP3 were the most important prognostic factors for the clinical outcome after allo-SCT. Thus, donor TT genotype at rs10925027 in NLRP3 was associated with disease relapse (odds ratio (OR) = 6.3, P = 1 x 10(-7)), and donor GG genotype at rs1043684 in NLRP2 was associated with nonrelapse mortality (OR = 4.4, P = 6 x 10(-4)) and overall survival (OR = 3.1, P = .001). In addition, patient AA genotype at rs5862 in NLRP1 was associated with nonrelapse mortality (OR = 2.8, P = .005) and overall survival (OR = 2.0, P = .009). These results suggest that inflammasome genetic variants are important prognostic factors for the outcome of allo-SCT. If validated in larger studies, including unrelated allo-SCT, NLRPs genotype would become an important factor in donor selection.


Assuntos
Proteínas Adaptadoras de Transdução de Sinal/genética , Proteínas de Transporte/genética , Variação Genética , Antígenos HLA , Irmãos , Transplante de Células-Tronco , Proteínas Adaptadoras de Transdução de Sinal/metabolismo , Adolescente , Adulto , Proteínas Reguladoras de Apoptose/genética , Proteínas Reguladoras de Apoptose/metabolismo , Proteínas Adaptadoras de Sinalização CARD/genética , Proteínas Adaptadoras de Sinalização CARD/metabolismo , Proteínas de Transporte/metabolismo , Caspases/genética , Caspases/metabolismo , Intervalo Livre de Doença , Feminino , Genótipo , Neoplasias Hematológicas/genética , Neoplasias Hematológicas/metabolismo , Neoplasias Hematológicas/mortalidade , Humanos , Interleucina-18 , Interleucina-1beta/metabolismo , Masculino , Pessoa de Meia-Idade , Proteína 3 que Contém Domínio de Pirina da Família NLR , Proteínas de Neoplasias/genética , Proteínas de Neoplasias/metabolismo , Valor Preditivo dos Testes , Recidiva , Estudos Retrospectivos , Taxa de Sobrevida , Transplante Homólogo
19.
Science ; 321(5889): 691-6, 2008 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-18669862

RESUMO

MyD88 is a key downstream adapter for most Toll-like receptors (TLRs) and interleukin-1 receptors (IL-1Rs). MyD88 deficiency in mice leads to susceptibility to a broad range of pathogens in experimental settings of infection. We describe a distinct situation in a natural setting of human infection. Nine children with autosomal recessive MyD88 deficiency suffered from life-threatening, often recurrent pyogenic bacterial infections, including invasive pneumococcal disease. However, these patients were otherwise healthy, with normal resistance to other microbes. Their clinical status improved with age, but not due to any cellular leakiness in MyD88 deficiency. The MyD88-dependent TLRs and IL-1Rs are therefore essential for protective immunity to a small number of pyogenic bacteria, but redundant for host defense to most natural infections.


Assuntos
Infecções Bacterianas/genética , Infecções Bacterianas/imunologia , Fator 88 de Diferenciação Mieloide/deficiência , Adolescente , Animais , Linhagem Celular Transformada , Criança , Pré-Escolar , Citocinas/metabolismo , Suscetibilidade a Doenças , Feminino , Deleção de Genes , Humanos , Imunidade Inata , Masculino , Camundongos , Mutação de Sentido Incorreto , Fator 88 de Diferenciação Mieloide/genética , Fator 88 de Diferenciação Mieloide/metabolismo , Infecções Pneumocócicas/genética , Infecções Pneumocócicas/imunologia , Infecções por Pseudomonas/genética , Infecções por Pseudomonas/imunologia , Receptores de Interleucina-1/imunologia , Receptores de Interleucina-1/metabolismo , Transdução de Sinais , Infecções Estafilocócicas/genética , Infecções Estafilocócicas/imunologia , Receptores Toll-Like/imunologia , Receptores Toll-Like/metabolismo , Transfecção
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