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2.
Sci Immunol ; 6(55)2021 01 21.
Artigo em Inglês | MEDLINE | ID: mdl-33478949

RESUMO

The molecular properties of CD8+ T cells that respond to SARS-CoV-2 infection are not fully known. Here, we report on the single-cell transcriptomes of >80,000 virus-reactive CD8+ T cells, obtained using a modified Antigen-Reactive T cell Enrichment (ARTE) assay, from 39 COVID-19 patients and 10 healthy subjects. COVID-19 patients segregated into two groups based on whether the dominant CD8+ T cell response to SARS-CoV-2 was 'exhausted' or not. SARS-CoV-2-reactive cells in the exhausted subset were increased in frequency and displayed lesser cytotoxicity and inflammatory features in COVID-19 patients with mild compared to severe illness. In contrast, SARS-CoV-2-reactive cells in the dominant non-exhausted subset from patients with severe disease showed enrichment of transcripts linked to co-stimulation, pro-survival NF-κB signaling, and anti-apoptotic pathways, suggesting the generation of robust CD8+ T cell memory responses in patients with severe COVID-19 illness. CD8+ T cells reactive to influenza and respiratory syncytial virus from healthy subjects displayed polyfunctional features and enhanced glycolysis. Cells with such features were largely absent in SARS-CoV-2-reactive cells from both COVID-19 patients and healthy controls non-exposed to SARS-CoV-2. Overall, our single-cell analysis revealed substantial diversity in the nature of CD8+ T cells responding to SARS-CoV-2.


Assuntos
Linfócitos T CD8-Positivos/imunologia , /imunologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Glicólise/imunologia , Humanos , Memória Imunológica/imunologia , Masculino , Pessoa de Meia-Idade , NF-kappa B/imunologia , Transdução de Sinais/imunologia , Análise de Célula Única/métodos , Adulto Jovem
4.
Nat Rev Immunol ; 21(2): 83-100, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33353987

RESUMO

Immunization is a cornerstone of public health policy and is demonstrably highly cost-effective when used to protect child health. Although it could be argued that immunology has not thus far contributed much to vaccine development, in that most of the vaccines we use today were developed and tested empirically, it is clear that there are major challenges ahead to develop new vaccines for difficult-to-target pathogens, for which we urgently need a better understanding of protective immunity. Moreover, recognition of the huge potential and challenges for vaccines to control disease outbreaks and protect the older population, together with the availability of an array of new technologies, make it the perfect time for immunologists to be involved in designing the next generation of powerful immunogens. This Review provides an introductory overview of vaccines, immunization and related issues and thereby aims to inform a broad scientific audience about the underlying immunological concepts.


Assuntos
Controle de Doenças Transmissíveis/métodos , Doenças Transmissíveis/imunologia , Vacinas Atenuadas/imunologia , Vacinas de Produtos Inativados/imunologia , Vacinologia/métodos , Anticorpos/imunologia , Antígenos/imunologia , Humanos , Memória Imunológica/imunologia , Linfócitos T/imunologia , Vacinação
5.
PLoS Pathog ; 16(12): e1009132, 2020 12.
Artigo em Inglês | MEDLINE | ID: mdl-33370392

RESUMO

NK cells have been shown to display adaptive traits such as memory formation akin to T and B lymphocytes. Here we show that Zika virus infection induces memory like NK cells that express CD27. Strikingly, these cells exhibit stem-like features that include expansion capacity, self-renewal pathway, differentiation into effector cells, longer telomeres and gene signature associated with hematopoietic stem cell (HSC) progenitors. This subset shared transcriptional and epigenetic changes with memory CD8 T cells, stem cells and stem like T cells. These NK cells with memory and stem cell features, which we term "NK memory stem cells", demonstrated greater antiviral potential than CD27- or naïve CD27+ NK when adoptively transferred to Zika infected mice. Our results also suggest a role for the transcription factor TCF-1 in memory and stemness features of this NK subset. This study defines a unique TCF1hi CD27+ NK subset with memory capacity and stem cell features that play a role in antiviral immunity.


Assuntos
Memória Imunológica/imunologia , Células Matadoras Naturais/imunologia , Subpopulações de Linfócitos/imunologia , Células-Tronco/imunologia , Infecção por Zika virus/imunologia , Animais , Feminino , Camundongos , Camundongos Endogâmicos C57BL , Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/imunologia
7.
Ned Tijdschr Geneeskd ; 1642020 10 07.
Artigo em Holandês | MEDLINE | ID: mdl-33331729

RESUMO

A number of clinical trials are currently underway worldwide to assess whether BCG, the old vaccine against tuberculosis, can protect against COVID-19 infection. In this Perspective, we briefly outline the background, the immunological mechanisms (in particular induction of 'innate immune memory' or 'trained immunity'), and further considerations for the potential future use of BCG against viral and other infections.


Assuntos
Vacina BCG , Reposicionamento de Medicamentos/métodos , Memória Imunológica/imunologia , Tuberculose/prevenção & controle , Vacina BCG/imunologia , Vacina BCG/uso terapêutico , /prevenção & controle , Humanos , Imunidade Inata/imunologia , Tuberculose/imunologia
8.
Front Immunol ; 11: 571481, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33362759

RESUMO

In December 2019, an outbreak of a novel coronavirus (SARS-CoV-2) in Wuhan, China resulted in the current COVID-19 global pandemic. The human immune system has not previously encountered this virus, raising the important question as to whether or not protective immunity is generated by infection. Growing evidence suggests that protective immunity can indeed be acquired post-infection-although a handful of reinfection cases have been reported. However, it is still unknown whether the immune response to SARS-CoV-2 leads to some degree of long-lasting protection against the disease or the infection. This review draws insights from previous knowledge regarding the nature and longevity of immunity to the related virus, SARS-CoV, to fill the gaps in our understanding of the immune response to SARS-CoV-2. Deciphering the immunological characteristics that give rise to protective immunity against SARS-CoV-2 is critical to guiding vaccine development and also predicting the course of the pandemic. Here we discuss the recent evidence that characterises the adaptive immune response against SARS-CoV-2 and its potential implications for the generation of memory responses and long-term protection.


Assuntos
Anticorpos Neutralizantes/imunologia , Anticorpos Antivirais/imunologia , Imunidade Celular/imunologia , Memória Imunológica/imunologia , /imunologia , Anticorpos Neutralizantes/sangue , Anticorpos Antivirais/sangue , Linfócitos T CD4-Positivos/imunologia , Linfócitos T CD8-Positivos/imunologia , /prevenção & controle , /imunologia , Humanos
9.
Int J Mol Sci ; 21(22)2020 Nov 11.
Artigo em Inglês | MEDLINE | ID: mdl-33187101

RESUMO

Immune memory is a defining characteristic of adaptive immunity, but recent work has shown that the activation of innate immunity can also improve responsiveness in subsequent exposures. This has been coined "trained immunity" and diverges with the perception that the innate immune system is primitive, non-specific, and reacts to novel and recurrent antigen exposures similarly. The "exposome" is the cumulative exposures (diet, exercise, environmental exposure, vaccination, genetics, etc.) an individual has experienced and provides a mechanism for the establishment of immune training or immunotolerance. It is becoming increasingly clear that trained immunity constitutes a delicate balance between the dose, duration, and order of exposures. Upon innate stimuli, trained immunity or tolerance is shaped by epigenetic and metabolic changes that alter hematopoietic stem cell lineage commitment and responses to infection. Due to the immunomodulatory role of the exposome, understanding innate immune training is critical for understanding why some individuals exhibit protective phenotypes while closely related individuals may experience immunotolerant effects (e.g., the order of exposure can result in completely divergent immune responses). Research on the exposome and trained immunity may be leveraged to identify key factors for improving vaccination development, altering inflammatory disease development, and introducing potential new prophylactic treatments, especially for diseases such as COVID-19, which is currently a major health issue for the world. Furthermore, continued exposome research may prevent many deleterious effects caused by immunotolerance that frequently result in host morbidity or mortality.


Assuntos
Betacoronavirus/imunologia , Linhagem da Célula/imunologia , Infecções por Coronavirus/imunologia , Imunidade Inata/imunologia , Memória Imunológica/imunologia , Pneumonia Viral/imunologia , Metilação de DNA/genética , Células Dendríticas/imunologia , Expossoma , Código das Histonas/genética , Humanos , Tolerância Imunológica/imunologia , Células Matadoras Naturais/imunologia , Macrófagos/imunologia , Pandemias
10.
Front Immunol ; 11: 2059, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33013871

RESUMO

The novel, highly contagious coronavirus SARS-CoV-2 spreads rapidly throughout the world, leading to a deadly pandemic of a predominantly respiratory illness called COVID-19. Safe and effective anti-SARS-CoV-2 vaccines are urgently needed. However, emerging immunological observations show hallmarks of significant immunopathological characteristics and dysfunctional immune responses in patients with COVID-19. Combined with existing knowledge about immune responses to other closely related and highly pathogenic coronaviruses, this could forebode significant challenges for vaccine development, including the risk of vaccine failure. Animal data from earlier coronavirus vaccine efforts indicate that elderly people, most at risk from severe COVID-19 disease, could be especially at risk from immunopathologic responses to novel coronavirus vaccines. Bacterial "new old friends" such as Bacille Calmette-Guérin (BCG) or Mycobacterium obuense have the ability to elevate basal systemic levels of type 1 cytokines and immune cells, correlating with increased protection against diverse and unrelated infectious agents, called "trained immunity." Here we describe dysfunctional immune responses induced by coronaviruses, representing potentially difficult to overcome obstacles to safe, effective vaccine development for COVID-19, and outline how trained immunity could help protect high risk populations through immunomodulation with BCG and other "new old friends."


Assuntos
Vacina BCG/imunologia , Betacoronavirus/imunologia , Infecções por Coronavirus/imunologia , Imunidade Celular , Imunidade Inata , Memória Imunológica/imunologia , Pneumonia Viral/imunologia , Vacinação , Idoso , Animais , Vacinas Anticâncer/imunologia , Infecções por Coronavirus/prevenção & controle , Infecções por Coronavirus/virologia , Humanos , Micobactérias não Tuberculosas/imunologia , Pandemias/prevenção & controle , Pneumonia Viral/prevenção & controle , Pneumonia Viral/virologia , Risco , Vacinas Virais/efeitos adversos
12.
Nat Immunol ; 21(11): 1336-1345, 2020 11.
Artigo em Inglês | MEDLINE | ID: mdl-32887977

RESUMO

The development of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines and therapeutics will depend on understanding viral immunity. We studied T cell memory in 42 patients following recovery from COVID-19 (28 with mild disease and 14 with severe disease) and 16 unexposed donors, using interferon-γ-based assays with peptides spanning SARS-CoV-2 except ORF1. The breadth and magnitude of T cell responses were significantly higher in severe as compared with mild cases. Total and spike-specific T cell responses correlated with spike-specific antibody responses. We identified 41 peptides containing CD4+ and/or CD8+ epitopes, including six immunodominant regions. Six optimized CD8+ epitopes were defined, with peptide-MHC pentamer-positive cells displaying the central and effector memory phenotype. In mild cases, higher proportions of SARS-CoV-2-specific CD8+ T cells were observed. The identification of T cell responses associated with milder disease will support an understanding of protective immunity and highlights the potential of including non-spike proteins within future COVID-19 vaccine design.


Assuntos
Antígenos Virais/imunologia , Betacoronavirus/imunologia , Linfócitos T CD4-Positivos/imunologia , Linfócitos T CD8-Positivos/imunologia , Memória Imunológica/imunologia , Infecções por Coronavirus/imunologia , Infecções por Coronavirus/patologia , Infecções por Coronavirus/prevenção & controle , Epitopos de Linfócito T/imunologia , Humanos , Epitopos Imunodominantes/imunologia , Pandemias , Pneumonia Viral/imunologia , Pneumonia Viral/patologia , Glicoproteína da Espícula de Coronavírus/imunologia , Reino Unido , Vacinas Virais/imunologia
13.
Proc Natl Acad Sci U S A ; 117(40): 24957-24963, 2020 10 06.
Artigo em Inglês | MEDLINE | ID: mdl-32963096

RESUMO

B lymphocytes acquire self-reactivity as an unavoidable byproduct of antibody gene diversification in the bone marrow and in germinal centers (GCs). Autoreactive B cells emerging from the bone marrow are silenced in a series of well-defined checkpoints, but less is known about how self-reactivity that develops by somatic mutation in GCs is controlled. Here, we report the existence of an apoptosis-dependent tolerance checkpoint in post-GC B cells. Whereas defective GC B cell apoptosis has no measurable effect on autoantibody development, disruption of post-GC apoptosis results in accumulation of autoreactive memory B cells and plasma cells, antinuclear antibody production, and autoimmunity. The data presented shed light on mechanisms that regulate immune tolerance and the development of autoantibodies.


Assuntos
Apoptose/genética , Autoimunidade/genética , Genes de Imunoglobulinas/genética , Tolerância Imunológica/genética , Animais , Anticorpos Antinucleares/imunologia , Apoptose/imunologia , Autoanticorpos/imunologia , Autoimunidade/imunologia , Linfócitos B/imunologia , Genes de Imunoglobulinas/imunologia , Centro Germinativo/imunologia , Humanos , Memória Imunológica/genética , Memória Imunológica/imunologia , Camundongos , Plasmócitos/imunologia
14.
Proc Natl Acad Sci U S A ; 117(41): 25667-25678, 2020 10 13.
Artigo em Inglês | MEDLINE | ID: mdl-32978300

RESUMO

Memory CD8 T cells provide durable protection against diverse intracellular pathogens and can be broadly segregated into distinct circulating and tissue-resident populations. Paradigmatic studies have demonstrated that circulating memory cells can be further divided into effector memory (Tem) and central memory (Tcm) populations based on discrete functional characteristics. Following resolution of infection, we identified a persisting antigen-specific CD8 T cell population that was terminally fated with potent effector function but maintained memory T cell qualities and conferred robust protection against reinfection. Notably, this terminally differentiated effector memory CD8 T cell population (terminal-Tem) was conflated within the conventional Tem population, prompting redefinition of the classical characteristics of Tem cells. Murine terminal-Tem were transcriptionally, functionally, and developmentally unique compared to Tem cells. Through mass cytometry and single-cell RNA sequencing (RNA-seq) analyses of human peripheral blood from healthy individuals, we also identified an analogous terminal-Tem population of CD8 T cells that was transcriptionally distinct from Tem and Tcm Key findings from this study show that parsing of terminal-Tem from conventionally defined Tem challenge the reported characteristics of Tem biology, including enhanced presence in lymphoid tissues, robust IL-2 production, and recall potential, greater than expected homeostatic fitness, refined transcription factor dependencies, and a distinct molecular phenotype. Classification of terminal-Tem and clarification of Tem biology hold broad implications for understanding the molecular regulation of memory cell states and harnessing immunological memory to improve immunotherapies.


Assuntos
Linfócitos T CD8-Positivos/imunologia , Diferenciação Celular/imunologia , Memória Imunológica/imunologia , Subpopulações de Linfócitos T/imunologia , Animais , Linhagem da Célula/imunologia , Células Cultivadas , Humanos , Camundongos
15.
Proc Natl Acad Sci U S A ; 117(40): 24998-25007, 2020 10 06.
Artigo em Inglês | MEDLINE | ID: mdl-32958643

RESUMO

Infections elicit immune adaptations to enable pathogen resistance and/or tolerance and are associated with compositional shifts of the intestinal microbiome. However, a comprehensive understanding of how infections with pathogens that exhibit distinct capability to spread and/or persist differentially change the microbiome, the underlying mechanisms, and the relative contribution of individual commensal species to immune cell adaptations is still lacking. Here, we discovered that mouse infection with a fast-spreading and persistent (but not a slow-spreading acute) isolate of lymphocytic choriomeningitis virus induced large-scale microbiome shifts characterized by increased Verrucomicrobia and reduced Firmicute/Bacteroidetes ratio. Remarkably, the most profound microbiome changes occurred transiently after infection with the fast-spreading persistent isolate, were uncoupled from sustained viral loads, and were instead largely caused by CD8 T cell responses and/or CD8 T cell-induced anorexia. Among the taxa enriched by infection with the fast-spreading virus, Akkermansia muciniphila, broadly regarded as a beneficial commensal, bloomed upon starvation and in a CD8 T cell-dependent manner. Strikingly, oral administration of A. muciniphila suppressed selected effector features of CD8 T cells in the context of both infections. Our findings define unique microbiome differences after chronic versus acute viral infections and identify CD8 T cell responses and downstream anorexia as driver mechanisms of microbial dysbiosis after infection with a fast-spreading virus. Our data also highlight potential context-dependent effects of probiotics and suggest a model in which changes in host behavior and downstream microbiome dysbiosis may constitute a previously unrecognized negative feedback loop that contributes to CD8 T cell adaptations after infections with fast-spreading and/or persistent pathogens.


Assuntos
Anorexia/imunologia , Antígenos CD8/imunologia , Memória Imunológica/imunologia , Coriomeningite Linfocítica/imunologia , Viroses/imunologia , Animais , Anorexia/microbiologia , Anorexia/virologia , Antígenos CD8/metabolismo , Linfócitos T CD8-Positivos/imunologia , Linfócitos T CD8-Positivos/microbiologia , Disbiose/imunologia , Disbiose/microbiologia , Disbiose/virologia , Firmicutes/imunologia , Firmicutes/metabolismo , Microbioma Gastrointestinal/imunologia , Humanos , Coriomeningite Linfocítica/microbiologia , Coriomeningite Linfocítica/patologia , Vírus da Coriomeningite Linfocítica/patogenicidade , Camundongos , Linfócitos T/imunologia , Linfócitos T/microbiologia , Verrucomicrobia/imunologia , Verrucomicrobia/patogenicidade , Viroses/microbiologia , Viroses/patologia
16.
PLoS One ; 15(8): e0237646, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32845913

RESUMO

Tumor antigen-primed CD8 T cells differentiate into effector T cells that kill tumor cells rapidly, whereas durable responses of CD8 T cells are required to cope with long-lasting tumor growth. However, it is not well known how persisting CD8 T cells are generated. In this study, we analyzed CD8 T cells primed by antigens in tumor-draining lymph nodes and found that CD8 T cells first differentiated into a CD62L-intermediate (CD62Lint) stage upon antigen stimulation. These cells gave rise to tumor-infiltrating CD62L-CD44high Bcl6- effector T cells and CD62L+CD44highBcl6+ memory-like T cells. Memory-like T cells within the tumor expressed CD127, CXCR3 and had the potential to proliferate significantly when they were transferred into tumor-bearing mice. Bcl6 expression in these T cells was critical because Bcl6-/-CD62L+CD44highCD8T cells within the tumor were defective in expansion after secondary transfer. Taken together, our findings show that CD62L+CD44highBcl6+ cells are generated from highly proliferating CD62Lint T cells and retain high proliferative potential, which contributes to replenishment of effector T cells within the tumor.


Assuntos
Linfócitos T CD8-Positivos/imunologia , Carcinoma Pulmonar de Lewis/patologia , Memória Imunológica/imunologia , Selectina L/metabolismo , Melanoma Experimental/patologia , Receptor de Morte Celular Programada 1/metabolismo , Proteínas Proto-Oncogênicas c-bcl-6/metabolismo , Animais , Carcinoma Pulmonar de Lewis/imunologia , Carcinoma Pulmonar de Lewis/metabolismo , Diferenciação Celular , Feminino , Selectina L/genética , Masculino , Melanoma Experimental/imunologia , Melanoma Experimental/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Receptor de Morte Celular Programada 1/genética , Proteínas Proto-Oncogênicas c-bcl-6/genética , Células Tumorais Cultivadas
18.
Scand J Immunol ; 92(5): e12953, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32757303

RESUMO

Psoriasis is an inflammatory disease that arises in genetically predisposed individuals. Chronic skin lesions that contain activated immune cells can persist for years. Systemic inhibition of TNF, IL-17 and IL-23 cytokines has revolutionized psoriasis care during the recent decades. Unfortunately, local relapse of disease is common at previously inflamed sites after cessation of treatment. This highlights that fundamental pathologic alterations of the affected tissues are not completely resolved during clinical remission. Here, we present arguments for a local disease memory located in both dermis and epidermis in psoriasis skin. We decipher different cellular components and intercellular crosstalk that sustain local disease memory and amplify disease relapse in human psoriasis. Decrypting the mechanisms underlying the establishment and persistence of pathogenic memory cells in resolved psoriasis may provide new therapeutic perspectives aimed at long-term remission of psoriasis.


Assuntos
Cicatriz/imunologia , Citocinas/imunologia , Interleucina-17/imunologia , Queratinócitos/imunologia , Psoríase/imunologia , Pele/imunologia , Cicatriz/metabolismo , Citocinas/metabolismo , Epiderme/imunologia , Epiderme/metabolismo , Epiderme/patologia , Humanos , Memória Imunológica/imunologia , Interleucina-17/metabolismo , Queratinócitos/metabolismo , Queratinócitos/patologia , Psoríase/metabolismo , Recidiva , Pele/metabolismo , Pele/patologia
19.
Nature ; 584(7820): 274-278, 2020 08.
Artigo em Inglês | MEDLINE | ID: mdl-32760003

RESUMO

Colonization by the microbiota causes a marked stimulation of B cells and induction of immunoglobulin, but mammals colonized with many taxa have highly complex and individualized immunoglobulin repertoires1,2. Here we use a simplified model of defined transient exposures to different microbial taxa in germ-free mice3 to deconstruct how the microbiota shapes the B cell pool and its functional responsiveness. We followed the development of the immunoglobulin repertoire in B cell populations, as well as single cells by deep sequencing. Microbial exposures at the intestinal mucosa generated oligoclonal responses that differed from those of germ-free mice, and from the diverse repertoire that was generated after intravenous systemic exposure to microbiota. The IgA repertoire-predominantly to cell-surface antigens-did not expand after dose escalation, whereas increased systemic exposure broadened the IgG repertoire to both microbial cytoplasmic and cell-surface antigens. These microbial exposures induced characteristic immunoglobulin heavy-chain repertoires in B cells, mainly at memory and plasma cell stages. Whereas sequential systemic exposure to different microbial taxa diversified the IgG repertoire and facilitated alternative specific responses, sequential mucosal exposure produced limited overlapping repertoires and the attrition of initial IgA binding specificities. This shows a contrast between a flexible response to systemic exposure with the need to avoid fatal sepsis, and a restricted response to mucosal exposure that reflects the generic nature of host-microbial mutualism in the mucosa.


Assuntos
Linfócitos B/citologia , Linfócitos B/imunologia , Imunidade nas Mucosas/imunologia , Mucosa Intestinal/imunologia , Mucosa Intestinal/microbiologia , Simbiose/imunologia , Administração Intravenosa , Administração Oral , Animais , Clostridiales/imunologia , Clostridiales/isolamento & purificação , Escherichia coli/imunologia , Escherichia coli/isolamento & purificação , Feminino , Vida Livre de Germes , Imunoglobulina A/química , Imunoglobulina A/imunologia , Imunoglobulina G/química , Imunoglobulina G/imunologia , Cadeias Pesadas de Imunoglobulinas/imunologia , Memória Imunológica/imunologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Plasmócitos/citologia , Plasmócitos/imunologia , Priming de Repetição
20.
Monoclon Antib Immunodiagn Immunother ; 39(4): 107-111, 2020 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-32762609

RESUMO

In this hypothesis, we address the biological/immunological pathway leading to severe disease or death after infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The underlying immune response is described with "original antigenic sin" (OAS) whereby previous infections influence the response to future virus encounters. We cite evidence for OAS-induced immunopathology in HIV-1 disease. We hypothesize that similar immune abnormalities can occur after infection with SARS-CoV-2. This hypothesis is supported by recent analysis of the antibodies in infected patients demonstrating serological and B cell abnormalities. The concept of symmetrical clonal regulation developed earlier for the immune network illustrates the pathway suggested by our hypothesis and may be helpful to develop strategies avoiding severe coronavirus disease 2019.


Assuntos
Anticorpos Antivirais/imunologia , Linfócitos B/imunologia , Betacoronavirus/imunologia , Infecções por Coronavirus/imunologia , Evasão da Resposta Imune/imunologia , Pneumonia Viral/imunologia , Anticorpos Monoclonais/imunologia , Infecções por Coronavirus/patologia , Reações Cruzadas/imunologia , Síndrome da Liberação de Citocina/imunologia , HIV/imunologia , HIV-1/imunologia , Humanos , Imunoglobulina G/imunologia , Imunoglobulina M/imunologia , Memória Imunológica/imunologia , Pandemias , Pneumonia Viral/patologia
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