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1.
Infect Control Hosp Epidemiol ; 44(1): 40-46, 2023 01.
Artigo em Inglês | MEDLINE | ID: mdl-35311638

RESUMO

BACKGROUND: Methicillin-resistant Staphylococcus aureus (MRSA) is an important pathogen in neonatal intensive care units (NICU) that confers significant morbidity and mortality. OBJECTIVE: Improving our understanding of MRSA transmission dynamics, especially among high-risk patients, is an infection prevention priority. METHODS: We investigated a cluster of clinical MRSA cases in the NICU using a combination of epidemiologic review and whole-genome sequencing (WGS) of isolates from clinical and surveillance cultures obtained from patients and healthcare personnel (HCP). RESULTS: Phylogenetic analysis identified 2 genetically distinct phylogenetic clades and revealed multiple silent-transmission events between HCP and infants. The predominant outbreak strain harbored multiple virulence factors. Epidemiologic investigation and genomic analysis identified a HCP colonized with the dominant MRSA outbreak strain who cared for most NICU patients who were infected or colonized with the same strain, including 1 NICU patient with severe infection 7 months before the described outbreak. These results guided implementation of infection prevention interventions that prevented further transmission events. CONCLUSIONS: Silent transmission of MRSA between HCP and NICU patients likely contributed to a NICU outbreak involving a virulent MRSA strain. WGS enabled data-driven decision making to inform implementation of infection control policies that mitigated the outbreak. Prospective WGS coupled with epidemiologic analysis can be used to detect transmission events and prompt early implementation of control strategies.


Assuntos
Infecção Hospitalar , Staphylococcus aureus Resistente à Meticilina , Infecções Estafilocócicas , Recém-Nascido , Lactente , Humanos , Staphylococcus aureus Resistente à Meticilina/genética , Unidades de Terapia Intensiva Neonatal , Infecção Hospitalar/epidemiologia , Infecções Estafilocócicas/prevenção & controle , Virulência/genética , Estudos Prospectivos , Filogenia , Surtos de Doenças/prevenção & controle , Controle de Infecções/métodos , Genômica
2.
J Virol ; 96(18): e0092122, 2022 09 28.
Artigo em Inglês | MEDLINE | ID: mdl-36040175

RESUMO

The genus Henipavirus (family Paramyxoviridae) currently comprises seven viruses, four of which have demonstrated prior evidence of zoonotic capacity. These include the biosafety level 4 agents Hendra (HeV) and Nipah (NiV) viruses, which circulate naturally in pteropodid fruit bats. Here, we describe and characterize Angavokely virus (AngV), a divergent henipavirus identified in urine samples from wild, Madagascar fruit bats. We report the nearly complete 16,740-nucleotide genome of AngV, which encodes the six major henipavirus structural proteins (nucleocapsid, phosphoprotein, matrix, fusion, glycoprotein, and L polymerase). Within the phosphoprotein (P) gene, we identify an alternative start codon encoding the AngV C protein and a putative mRNA editing site where the insertion of one or two guanine residues encodes, respectively, additional V and W proteins. In other paramyxovirus systems, C, V, and W are accessory proteins involved in antagonism of host immune responses during infection. Phylogenetic analysis suggests that AngV is ancestral to all four previously described bat henipaviruses-HeV, NiV, Cedar virus (CedV), and Ghanaian bat virus (GhV)-but evolved more recently than rodent- and shrew-derived henipaviruses, Mojiang (MojV), Gamak (GAKV), and Daeryong (DARV) viruses. Predictive structure-based alignments suggest that AngV is unlikely to bind ephrin receptors, which mediate cell entry for all other known bat henipaviruses. Identification of the AngV receptor is needed to clarify the virus's potential host range. The presence of V and W proteins in the AngV genome suggest that the virus could be pathogenic following zoonotic spillover. IMPORTANCE Henipaviruses include highly pathogenic emerging zoonotic viruses, derived from bat, rodent, and shrew reservoirs. Bat-borne Hendra (HeV) and Nipah (NiV) are the most well-known henipaviruses, for which no effective antivirals or vaccines for humans have been described. Here, we report the discovery and characterization of a novel henipavirus, Angavokely virus (AngV), isolated from wild fruit bats in Madagascar. Genomic characterization of AngV reveals all major features associated with pathogenicity in other henipaviruses, suggesting that AngV could be pathogenic following spillover to human hosts. Our work suggests that AngV is an ancestral bat henipavirus that likely uses viral entry pathways distinct from those previously described for HeV and NiV. In Madagascar, bats are consumed as a source of human food, presenting opportunities for cross-species transmission. Characterization of novel henipaviruses and documentation of their pathogenic and zoonotic potential are essential to predicting and preventing the emergence of future zoonoses that cause pandemics.


Assuntos
Quirópteros , Genoma Viral , Infecções por Henipavirus , Henipavirus , Vírus Nipah , Animais , Quirópteros/genética , Genoma Viral/genética , Glicoproteínas/genética , Henipavirus/classificação , Henipavirus/genética , Infecções por Henipavirus/virologia , Humanos , Madagáscar , Vírus Nipah/genética , Filogenia , Urina/virologia , Zoonoses/genética
3.
Infect Control Hosp Epidemiol ; 43(10): 1416-1423, 2022 10.
Artigo em Inglês | MEDLINE | ID: mdl-34486503

RESUMO

OBJECTIVE: We compared the rates of hospital-onset secondary bacterial infections in patients with coronavirus disease 2019 (COVID-19) with rates in patients with influenza and controls, and we investigated reports of increased incidence of Enterococcus infections in patients with COVID-19. DESIGN: Retrospective cohort study. SETTING: An academic quaternary-care hospital in San Francisco, California. PATIENTS: Patients admitted between October 1, 2019, and October 1, 2020, with a positive SARS-CoV-2 PCR (N = 314) or influenza PCR (N = 82) within 2 weeks of admission were compared with inpatients without positive SARS-CoV-2 or influenza tests during the study period (N = 14,332). METHODS: National Healthcare Safety Network definitions were used to identify infection-related ventilator-associated complications (IVACs), probable ventilator-associated pneumonia (PVAP), bloodstream infections (BSIs), and catheter-associated urinary tract infections (CAUTIs). A multiple logistic regression model was used to control for likely confounders. RESULTS: COVID-19 patients had significantly higher rates of IVAC and PVAP compared to controls, with adjusted odds ratios of 4.7 (95% confidence interval [CI], 1.7-13.9) and 10.4 (95 % CI, 2.1-52.1), respectively. COVID-19 patients had higher incidence of BSI due to Enterococcus but not BSI generally, and whole-genome sequencing of Enterococcus isolates demonstrated that nosocomial transmission did not explain the increased rate. Subanalyses of patients admitted to the intensive care unit and patients who required mechanical ventilation revealed similar findings. CONCLUSIONS: COVID-19 is associated with an increased risk of IVAC, PVAP, and Enterococcus BSI compared with hospitalized controls, which is not fully explained by factors such as immunosuppressive treatments and duration of mechanical ventilation. The mechanism underlying increased rates of Enterococcus BSI in COVID-19 patients requires further investigation.


Assuntos
Bacteriemia , Infecções Bacterianas , COVID-19 , Coinfecção , Infecção Hospitalar , Influenza Humana , Humanos , COVID-19/epidemiologia , SARS-CoV-2 , Bacteriemia/microbiologia , Influenza Humana/complicações , Estudos Retrospectivos , Infecção Hospitalar/microbiologia , Enterococcus
4.
Sci Rep ; 11(1): 3044, 2021 02 04.
Artigo em Inglês | MEDLINE | ID: mdl-33542262

RESUMO

The role of children in the spread of the SARS-CoV-2 coronavirus has become a matter of urgent debate as societies in the US and abroad consider how to safely reopen schools. Small studies have suggested higher viral loads in young children. Here we present a multicenter investigation on over five thousand SARS-CoV-2 cases confirmed by real-time reverse transcription (RT) PCR assay. Notably, we found no discernable difference in amount of viral nucleic acid among young children and adults.


Assuntos
COVID-19 , Nasofaringe/virologia , RNA Viral/análise , SARS-CoV-2 , Carga Viral , Adolescente , Adulto , Idoso , Idoso de 80 Anos ou mais , COVID-19/diagnóstico , COVID-19/virologia , Teste para COVID-19 , California/epidemiologia , Criança , Pré-Escolar , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , SARS-CoV-2/genética , SARS-CoV-2/fisiologia , Adulto Jovem
5.
Microbiol Resour Announc ; 9(31)2020 Jul 30.
Artigo em Inglês | MEDLINE | ID: mdl-32732230

RESUMO

We report a draft genome sequence of extensively drug-resistant (XDR) Salmonella enterica serotype Typhi isolated from a returned traveler from Pakistan who developed sepsis. Whole-genome sequencing revealed relatedness to a previously reported outbreak in Pakistan and identified the bla CTX-M-15 and qnrS resistance genes.

6.
J Immunol ; 200(6): 1977-1981, 2018 03 15.
Artigo em Inglês | MEDLINE | ID: mdl-29440505

RESUMO

The T-box transcription factors T-bet and Eomesodermin (Eomes) instruct discrete stages in NK cell development. However, their role in the immune response of mature NK cells against pathogens remains unexplored. We used an inducible deletion system to elucidate the cell-intrinsic role of T-bet and Eomes in mature NK cells during the course of mouse CMV infection. We show both T-bet and Eomes to be necessary for the expansion of virus-specific NK cells, with T-bet upregulation induced by IL-12 signaling and STAT4 binding to a conserved enhancer region upstream of the Tbx21 loci. Interestingly, our data suggest maintenance of virus-specific memory NK cell numbers and phenotype was dependent on T-bet, but not Eomes. These findings uncover a nonredundant and stage-specific influence of T-box transcription factors in the antiviral NK cell response.


Assuntos
Memória Imunológica/imunologia , Células Matadoras Naturais/imunologia , Proteínas com Domínio T/imunologia , Animais , Infecções por Citomegalovirus/imunologia , Interleucina-12/imunologia , Camundongos , Fator de Transcrição STAT4/imunologia , Regulação para Cima/imunologia
7.
BMC Med Educ ; 17(1): 115, 2017 Jul 11.
Artigo em Inglês | MEDLINE | ID: mdl-28697782

RESUMO

BACKGROUND: Prior studies have described the career paths of physician-scientist candidates after graduation, but the factors that influence career choices at the candidate stage remain unclear. Additionally, previous work has focused on MD/PhDs, despite many physician-scientists being MDs. This study sought to identify career sector intentions, important factors in career selection, and experienced and predicted obstacles to career success that influence the career choices of MD candidates, MD candidates with research-intense career intentions (MD-RI), and MD/PhD candidates. METHODS: A 70-question survey was administered to students at 5 academic medical centers with Medical Scientist Training Programs (MSTPs) and Clinical and Translational Science Awards (CTSA) from the NIH. Data were analyzed using bivariate or multivariate analyses. RESULTS: More MD/PhD and MD-RI candidates anticipated or had experienced obstacles related to balancing academic and family responsibilities and to balancing clinical, research, and education responsibilities, whereas more MD candidates indicated experienced and predicted obstacles related to loan repayment. MD/PhD candidates expressed higher interest in basic and translational research compared to MD-RI candidates, who indicated more interest in clinical research. Overall, MD-RI candidates displayed a profile distinct from both MD/PhD and MD candidates. CONCLUSIONS: MD/PhD and MD-RI candidates experience obstacles that influence their intentions to pursue academic medical careers from the earliest training stage, obstacles which differ from those of their MD peers. The differences between the aspirations of and challenges facing MD, MD-RI and MD/PhD candidates present opportunities for training programs to target curricula and support services to ensure the career development of successful physician-scientists.


Assuntos
Pesquisa Biomédica/educação , Escolha da Profissão , Educação de Pós-Graduação , Educação de Pós-Graduação em Medicina , Médicos/psicologia , Pesquisadores/educação , Educação de Pós-Graduação em Medicina/estatística & dados numéricos , Humanos , Médicos/estatística & dados numéricos , Especialização , Apoio ao Desenvolvimento de Recursos Humanos
8.
J Exp Med ; 213(2): 225-33, 2016 Feb 08.
Artigo em Inglês | MEDLINE | ID: mdl-26755706

RESUMO

Type I interferon (IFN) is crucial in host antiviral defense. Previous studies have described the pleiotropic role of type I IFNs on innate and adaptive immune cells during viral infection. Here, we demonstrate that natural killer (NK) cells from mice lacking the type I IFN-α receptor (Ifnar(-/-)) or STAT1 (which signals downstream of IFNAR) are defective in expansion and memory cell formation after mouse cytomegalovirus (MCMV) infection. Despite comparable proliferation, Ifnar(-/-) NK cells showed diminished protection against MCMV infection and exhibited more apoptosis compared with wild-type NK cells. Furthermore, we show that Ifnar(-/-) NK cells express increased levels of NK group 2 member D (NKG2D) ligands during viral infection and are susceptible to NK cell-mediated fratricide in a perforin- and NKG2D-dependent manner. Adoptive transfer of Ifnar(-/-) NK cells into NK cell-deficient mice reverses the defect in survival and expansion. Our study reveals a novel type I IFN-dependent mechanism by which NK cells evade mechanisms of cell death after viral infection.


Assuntos
Infecções por Herpesviridae/imunologia , Interferon Tipo I/metabolismo , Células Matadoras Naturais/imunologia , Muromegalovirus , Animais , Apoptose , Proliferação de Células , Infecções por Herpesviridae/metabolismo , Infecções por Herpesviridae/patologia , Células Matadoras Naturais/metabolismo , Células Matadoras Naturais/patologia , Ativação Linfocitária , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Subfamília K de Receptores Semelhantes a Lectina de Células NK/metabolismo , Perforina/deficiência , Perforina/genética , Perforina/metabolismo , Receptor de Interferon alfa e beta/deficiência , Receptor de Interferon alfa e beta/genética , Receptor de Interferon alfa e beta/metabolismo , Fator de Transcrição STAT1/deficiência , Fator de Transcrição STAT1/genética , Fator de Transcrição STAT1/metabolismo
9.
Adv Exp Med Biol ; 850: 81-91, 2015.
Artigo em Inglês | MEDLINE | ID: mdl-26324348

RESUMO

Immunological memory is a hallmark of the adaptive immune system. Although natural killer (NK) cells have traditionally been classified as a component of the innate immune system, they have recently been shown in mice and humans to exhibit certain features of immunological memory, including an ability to undergo a clonal-like expansion during virus infection, generate long-lived progeny (i.e. memory cells), and mediate recall responses against previously encountered pathogens--all characteristics previously ascribed only to adaptive immune responses by B and T cells in mammals. To date, the molecular events that govern the generation of NK cell memory are not completely understood. Using a mouse model of cytomegalovirus infection, we demonstrate that individual pro-inflammatory IL-12, IL-18, and type I-IFN signaling pathways are indispensible and play non-redundant roles in the generation of virus-specific NK cell memory. Furthermore, we discovered that antigen-specific proliferation and protection by NK cells is mediated by the transcription factor Zbtb32, which is induced by pro-inflammatory cytokines and promotes a cell cycle program in activated NK cells. A greater understanding of the molecular mechanisms controlling NK cell responses will provide novel strategies for tailoring vaccines to target infectious disease.


Assuntos
Imunidade Adaptativa , Infecções por Herpesviridae/imunologia , Memória Imunológica/genética , Células Matadoras Naturais/imunologia , Transdução de Sinais/imunologia , Animais , Proliferação de Células , Regulação da Expressão Gênica , Infecções por Herpesviridae/genética , Infecções por Herpesviridae/patologia , Infecções por Herpesviridae/virologia , Interferon Tipo I/genética , Interferon Tipo I/imunologia , Interleucina-12/genética , Interleucina-12/imunologia , Interleucina-18/genética , Interleucina-18/imunologia , Células Matadoras Naturais/patologia , Células Matadoras Naturais/virologia , Camundongos , Muromegalovirus/imunologia , Proteínas Repressoras/genética , Proteínas Repressoras/imunologia
10.
J Immunol ; 194(4): 1408-12, 2015 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-25589075

RESUMO

Although NK cells are considered part of the innate immune system, recent studies have demonstrated the ability of Ag-experienced NK cells to become long-lived and contribute to potent recall responses similar to T and B cells. The precise signals that promote the generation of a long-lived NK cell response are largely undefined. In this article, we demonstrate that NK cells require IL-18 signaling to generate a robust primary response during mouse CMV (MCMV) infection but do not require this signal for memory cell maintenance or recall responses. IL-12 signaling and STAT4 in activated NK cells increased the expression of the adaptor protein MyD88, which mediates signaling downstream of the IL-18 and IL-1 receptors. During MCMV infection, NK cells required MyD88, but not IL-1R, for optimal expansion. Thus, an IL-18-MyD88 signaling axis facilitates the prolific expansion of NK cells in response to primary viral infection, but not recall responses.


Assuntos
Interleucina-18/imunologia , Células Matadoras Naturais/imunologia , Ativação Linfocitária/imunologia , Transdução de Sinais/imunologia , Imunidade Adaptativa/imunologia , Animais , Imunoprecipitação da Cromatina , Citometria de Fluxo , Infecções por Herpesviridae/imunologia , Imunidade Inata/imunologia , Memória Imunológica/imunologia , Camundongos , Muromegalovirus/imunologia , Fator 88 de Diferenciação Mieloide/imunologia , Reação em Cadeia da Polimerase em Tempo Real , Reação em Cadeia da Polimerase Via Transcriptase Reversa
11.
J Exp Med ; 211(7): 1289-96, 2014 Jun 30.
Artigo em Inglês | MEDLINE | ID: mdl-24958849

RESUMO

Apoptosis is critical for the elimination of activated lymphocytes after viral infection. Proapoptotic factor Bim (Bcl2l11) controls T lymphocyte contraction and the formation of memory T cells after infection. Natural killer (NK) cells also undergo antigen-driven expansion to become long-lived memory cells after mouse cytomegalovirus (MCMV) infection; therefore, we examined the role of Bim in regulating the MCMV-driven memory NK cell pool. Despite responding similarly early after infection, Bcl2l11(-/-) Ly49H(+) NK cells show impaired contraction and significantly outnumber wild-type (WT) cells after the expansion phase. The inability to reduce the effector pool leads to a larger Bcl2l11(-/-) NK memory subset, which displays a less mature phenotype (CD11b(lo), CD27(+)) and lower levels of NK cell memory-associated markers KLRG1 and Ly6C. Bcl2l11(-/-) memory NK cells demonstrate a reduced response to m157-mediated stimulation and do not protect as effectively as WT memory NK cells in an MCMV challenge model. Thus, Bim-mediated apoptosis drives selective contraction of effector NK cells to generate a pool of mature, MCMV-specific memory cells.


Assuntos
Antígenos Virais/imunologia , Proteínas Reguladoras de Apoptose/imunologia , Infecções por Herpesviridae/imunologia , Memória Imunológica , Células Matadoras Naturais/imunologia , Proteínas de Membrana/imunologia , Muromegalovirus/imunologia , Proteínas Proto-Oncogênicas/imunologia , Animais , Antígenos de Diferenciação/genética , Antígenos de Diferenciação/imunologia , Antígenos Virais/genética , Apoptose/genética , Apoptose/imunologia , Proteínas Reguladoras de Apoptose/genética , Proteína 11 Semelhante a Bcl-2 , Infecções por Herpesviridae/genética , Infecções por Herpesviridae/patologia , Células Matadoras Naturais/patologia , Proteínas de Membrana/genética , Camundongos , Camundongos Knockout , Proteínas Proto-Oncogênicas/genética
12.
J Exp Med ; 210(13): 2981-90, 2013 Dec 16.
Artigo em Inglês | MEDLINE | ID: mdl-24277151

RESUMO

Development of the natural killer (NK) cell lineage is dependent on the transcription factor Nfil3 (or E4BP4), which is thought to act downstream of IL-15 signaling. Nfil3-deficient mice lack NK cells, whereas other lymphocyte lineages (B, T, and NKT cells) remain largely intact. We report the appearance of Ly49H-expressing NK cells in Nfil3(-/-) mice infected with mouse cytomegalovirus (MCMV) or recombinant viruses expressing the viral m157 glycoprotein. Nfil3(-/-) NK cells at the peak of antigen-driven expansion were functionally similar to NK cells from infected wild-type mice with respect to IFN-γ production and cytotoxicity, and could comparably produce long-lived memory NK cells that persisted in lymphoid and nonlymphoid tissues for >60 d. We demonstrate that generation and maintenance of NK cell memory is an Nfil3-independent but IL-15-dependent process. Furthermore, specific ablation of Nfil3 in either immature NK cells in the bone marrow or mature peripheral NK cells had no observable effect on NK cell lineage maintenance or homeostasis. Thus, expression of Nfil3 is crucial only early in the development of NK cells, and signals through activating receptors and proinflammatory cytokines during viral infection can bypass the requirement for Nfil3, promoting the proliferation and long-term survival of virus-specific NK cells.


Assuntos
Fatores de Transcrição de Zíper de Leucina Básica/genética , Células Matadoras Naturais/citologia , Animais , Fatores de Transcrição de Zíper de Leucina Básica/metabolismo , Linhagem da Célula , Separação Celular , Sobrevivência Celular , Citocinas/metabolismo , Citometria de Fluxo , Regulação da Expressão Gênica , Homeostase , Inflamação , Interferon gama/metabolismo , Interleucina-15/metabolismo , Células Matadoras Naturais/virologia , Ligantes , Ativação Linfocitária , Camundongos , Camundongos Endogâmicos C57BL , Muromegalovirus/imunologia , Subfamília A de Receptores Semelhantes a Lectina de Células NK/metabolismo , Baço/citologia , Tamoxifeno/química
13.
J Exp Med ; 209(5): 947-54, 2012 May 07.
Artigo em Inglês | MEDLINE | ID: mdl-22493516

RESUMO

Although natural killer (NK) cells are classified as innate immune cells, recent studies demonstrate that NK cells can become long-lived memory cells and contribute to secondary immune responses. The precise signals that promote generation of long-lived memory NK cells are unknown. Using cytokine receptor-deficient mice, we show that interleukin-12 (IL-12) is indispensible for mouse cytomegalovirus (MCMV)-specific NK cell expansion and generation of memory NK cells. In contrast to wild-type NK cells that proliferated robustly and resided in lymphoid and nonlymphoid tissues for months after MCMV infection, IL-12 receptor-deficient NK cells failed to expand and were unable to mediate protection after MCMV challenge. We further demonstrate that a STAT4-dependent IFN-γ-independent mechanism contributes toward the generation of memory NK cells during MCMV infection. Understanding the full contribution of inflammatory cytokine signaling to the NK cell response against viral infection will be of interest for the development of vaccines and therapeutics.


Assuntos
Citocinas/imunologia , Infecções por Herpesviridae/imunologia , Memória Imunológica/imunologia , Interleucina-12/imunologia , Células Matadoras Naturais/imunologia , Muromegalovirus/imunologia , Transdução de Sinais/imunologia , Transferência Adotiva , Animais , Citometria de Fluxo , Células Matadoras Naturais/fisiologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , Receptores de Interleucina-12/genética , Fator de Transcrição STAT4/imunologia , Estatísticas não Paramétricas
14.
Immunity ; 36(1): 55-67, 2012 Jan 27.
Artigo em Inglês | MEDLINE | ID: mdl-22261438

RESUMO

Natural killer (NK) cells play critical roles defending against tumors and pathogens. We show that mice lacking both transcription factors Eomesodermin (Eomes) and T-bet failed to develop NK cells. Developmental stability of immature NK cells constitutively expressing the death ligand TRAIL depended on T-bet. Conversely, maturation characterized by loss of constitutive TRAIL expression and induction of Ly49 receptor diversity and integrin CD49b (DX5(+)) required Eomes. Mature NK cells from which Eomes was deleted reverted to phenotypic immaturity if T-bet was present or downregulated NK lineage antigens if T-bet was absent, despite retaining expression of Ly49 receptors. Fetal and adult hepatic hematopoiesis restricted Eomes expression and limited NK development to the T-bet-dependent, immature stage, whereas medullary hematopoiesis permitted Eomes-dependent NK maturation in adult mice. These findings reveal two sequential, genetically separable checkpoints of NK cell maturation, the progression of which is metered largely by the anatomic localization of hematopoiesis.


Assuntos
Ciclo Celular/genética , Diferenciação Celular , Células Matadoras Naturais/citologia , Células Matadoras Naturais/imunologia , Proteínas com Domínio T/metabolismo , Animais , Linhagem da Célula , Citometria de Fluxo , Deleção de Genes , Camundongos , Camundongos Knockout , Modelos Imunológicos , Reação em Cadeia da Polimerase em Tempo Real , Proteínas com Domínio T/genética
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