BackgroundThere is evidence that the adaptive or acquired immune system is one of the crucial variables in differentiating the course of coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This work aimed to analyze the immunopathological aspects of adaptive immunity that are involved in the progression of this disease.MethodsThis is a systematic review based on articles that included experimental evidence from in vitro assays, cohort studies, reviews, cross-sectional and case-control studies from PubMed, SciELO, MEDLINE, and Lilacs databases in English, Portuguese, or Spanish between January 2020 and July 2022.ResultsFifty-six articles were finalized for this review. CD4+ T cells were the most resolutive in the health-disease process compared with B cells and CD8+ T lymphocytes. The predominant subpopulations of T helper lymphocytes (Th) in critically ill patients are Th1, Th2, Th17 (without their main characteristics) and regulatory T cells (Treg), while in mild cases there is an influx of Th1, Th2, Th17 and follicular T helper cells (Tfh). These cells are responsible for the secretion of cytokines, including interleukin (IL) - 6, IL-4, IL-10, IL-7, IL-22, IL-21, IL-15, IL-1α, IL-23, IL-5, IL-13, IL-2, IL-17, tumor necrosis factor alpha (TNF-α), CXC motivating ligand (CXCL) 8, CXCL9 and tumor growth factor beta (TGF-β), with the abovementioned first 8 inflammatory mediators related to clinical benefits, while the others to a poor prognosis. Some CD8+ T lymphocyte markers are associated with the severity of the disease, such as human leukocyte antigen (HLA-DR) and programmed cell death protein 1 (PD-1). Among the antibodies produced by SARS-CoV-2, Immunoglobulin (Ig) A stood out due to its potent release associated with a more severe clinical form.ConclusionsIt is concluded that through this study it is possible to have a brief overview of the main immunological biomarkers and their function during SARS-CoV-2 infection in particular cell types. In critically ill individuals, adaptive immunity is varied, aberrantly compromised, and late. In particular, the T-cell response is also an essential and necessary component in immunological memory and therefore should be addressed in vaccine formulation strategies.
COVID-19 is a multisystemic disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The immunopathogenic conditions of the hyperinflammatory response that cause systemic inflammation are extremely linked to its severity. This research sought to review the immunopathological elements that contribute to its progression. This is a systematic review using the PUBMED, LILACS, MEDLINE, and SCIELO databases using articles between May 2020 and July 2022 with the following search terms in conjunction with “AND”: “SARS-CoV-2”; “COVID-19”; “ARDS” and “Cytokine Storm”. The quality appraisal and risk of bias were assessed by the JBI checklists and the Cochrane Collaboration’s RoB 2.0 and ROBINS-I tools, respectively, and the risk of bias for in vitro studies by a pre-defined standard in the literature. The search resulted in 39 articles. The main actors in this response denote SARS-CoV-2 Spike proteins, cellular proteases, leukocytes, cytokines, and proteolytic cascades. The “cytokine storm” itself brings several complications to the host through cytokines such as IL-6 and chemokines (such as CCL2), which influence tissue inflammation through apoptosis and pyroptosis. The hyperinflammatory response causes several unfavorable outcomes in patients, and systemic inflammation caused largely by the dysregulation of the immune response should be controlled for their recovery.
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, first notified in China, has spread around the world causing high morbidity and mortality, which is due to factors such as the subversion of the immune response. The aims of the study are to summarise and present the immunopathological relationship of COVID-19 with innate immunity. This is a systematic review conducted by the National Library of Medicine -National Institutes of Health, USA (PUBMED), Latin American and Caribbean Literature on Health Sciences (LILACS), Medical Literature Analysis and Retrieval System Online (MEDLINE) and Scientific Electronic Library Online (SCIELO) databases with clinical trials, in vitro assays, case-controls, cohort studies, systematic reviews and meta-analyses between February 2020 and July 2021. The version 2 of the Cochrane risk-of-bias tool for RCTs (RoB 2), Joana Briggs Institute (JBI) Critical Appraisal (for the review articles) and the Risk of Bias in Non-randomised Studies of Interventions (ROBINS-I) tools were used to evaluate the quality and the risk of bias of the studies included in this review. The innate immune response through the generation of interferons, alternative pathways and complement system lectins and the joint action of innate immune cells and cytokines and chemokines lead to different clinical outcomes, taking into account the exacerbated inflammatory response and pathogenesis. Then, in addition to interacting as a bridge for adaptive immunity, the innate immune response plays an essential role in primary defense and is one of the starting points for immune evasion by SARS-CoV-2.
A paracoccidioidomicose é uma micose sistêmica prevalente na América Latina. É causada pelo Paracoccidioides brasiliensis e Paracoccidioides lutzii, que são fungos termodimórficos, a fase filamentosa está presente no solo de forma saprofítica. O objetivo deste trabalho é apresentar dados ecoepidemiológicos associando a fatores ecológicos e socioambientais da doença. Foi realizada uma revisão narrativa, por meio dos bancos de dados PubMed, Scielo, LILACS, MEDLINE e Google Scholar onde foram selecionados artigos, teses e dissertações que abordassem o tema entre 2000 e 2021. Foram encontrados 35 artigos, 2 dissertações, 2 teses e 1 monografia com foco de pesquisa no tema de interesse. Foi descrita a existência de outros hospedeiros, além do homem, principalmente tatus da espécie Dazypus novemcinctus auxiliando a analisar a situação de territorialidade, e delimitar as características do ecossistema do fungo. As mudanças socioambientais também influenciam na incidência da doença. Há uma forte associação no padrão epidemiológico e o ecossistema do Paracoccidioides, por essa análise é possível prever possíveis surtos e controlar a doença.
A asma é uma doença crônica e heterogênea das vias aéreas que tem início na infância e persiste em muitos casos até a vida adulta. A doença é resultado de interações ambientais, epigenéticas e genéticas. Este trabalho tem como objetivo revisar sobre os polimorfismos descritos na literatura no gene IL-4 associados à susceptibilidade ou proteção ao desenvolvimento da asma. Trata-se de uma revisão sistemática da literatura, feita nos bancos de dados PubMed, MEDLINE e Science Direct no corte temporal de 2000 a julho de 2021, ressaltando os seguintes pontos-chave: IL-4, Polimorfismos e Asma. A pesquisa resultou em 29 artigos, sendo em sua totalidade em língua inglesa. Apesar de alguns estudos divergentes, o SNP rs2243250, que foi o mais estudado em populações de diversos países, também foi o que mais encontrou correlações de susceptibilidade com a doença. Conclui-se que, apesar de haver dados controversos sobre os SNPs de IL-4 relacionados à doença, a associação dos estudos pangenômicos tem trazido uma lista de genes e variações deles associados com o risco de desenvolver a asma, como o SNP rs2243250 que foi bem relacionado em populações de vários países analisados.
As the host’s first line of defense against pathogens, Toll-like receptors (TLRs), such as the TLR3, are genes encoding transmembrane receptors of the same name. Depending on their expression, TLRs cause a pro- or anti-inflammatory response. The purpose of the article was to determine whether there is an association between the Toll-like receptor 3 (TLR3) rs3775291 Single Nucleotide Polymorphism—SNP and susceptibility to infections. This review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines and was registered in PROSPERO under the code CRD42023429533. A systematic search for relevant studies was performed using PubMed, Scopus, SciELO, Google Scholar, and Science Direct by the MeSH descriptors and the Boolean Operator “AND”: “Infections”; “TLR3”; “SNP”, between January 2005 and July 2022. Summary odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were calculated for genotypic comparison assuming a dominant genetic model (CT + TT vs. CC). A meta-analysis of 18 studies consisting of 3118 cases and 4368 controls found a significant association for risk between the presence of the TLR3 SNP rs3775291 and infections as part of the general analysis (OR = 1.16, 95% CI = 1.04–1.28, p = 0.004). In the subgroups of continents, the SNP had a protective role in Europe for 1044 cases and 1471 controls (OR = 0.83, 95% CI = 0.70–0.99, p = 0.04); however, the Asian (for 1588 patients and 2306 controls) and American (for 486 patients and 591 controls) continents had an increase in infectious risk (OR = 1.37, 95% CI = 1.19–1.58, p < 0.001; OR = 1.42, 95% CI = 1.08–1.86, and p = 0.01, respectively). Heterogeneity between studies was detected (I2 = 58%) but was explained in meta-regression by the subgroup of continents itself and publication bias was not evident. The results of the meta-analysis suggest a significant association between the TLR3 rs3775291 polymorphism and susceptibility to infections. Thus, when analyzing subgroups, the Asian and American continents showed that this SNP confers a higher risk against infections in a dominant genotypic model. Therefore, more studies are necessary to fully elucidate the role of TLR3 rs3775291 in infections.
Polymorphisms in genes that are responsible for encoding cytokines and receptors involved in the immune response, such as Toll-like Receptor (TLR) 2 in leprosy, are of great interest for immunogenetic studies. This work aimed to analyze the possible association of single nucleotide polymorphism (SNP), synonymous, rs3804100 of the TLR2 gene with leprosy. The study was conducted in Bacteriology and Mycology section of Evandro Chagas Institute, Brazil between August 2020 and July 2021.The scope of the study consisted of 122 subjects from cities of Goianésia, Rondon, Curionópolis, Altamira, Parauapebas and Redenção of the State of Pará, Brazil. Genotyping was performed by conventional PCR and sequencing in the ABI 3130 Genetic Analyzer (Applied Biosystems®) using primer nucleotides designed by the Primer3Plus program from the genomic region “Homo sapiens toll like receptor 2 (TLR2) transcript variant X6, mRNA”, deposited in GenBank with reference XM_011532216.2. The analyzes were performed based on Fisher's exact test. It was managed in accordance with Helsinki Declaration and the Brazilian National Health Council and with approval of the ethics committee at Evandro Chagas Institute, under opinion number: 3.950.570. No associations between gender and leprosy were possible (P> 0.05). However, associations were observed between age groups, which were significant between those over 46 years old (P=0.004) and the 2nd dose of BCG as a more protective agent between the groups analyzed (P=0.004). For the subjects with the typed genotypes, 68 contacts had T/T genotype and only 4 T/C genotypes, while in multibacillary (MB) group only 1 T/C genotype was found and none in paucibacillary (PB) (P> 0.05). We conclude that there is no association between the TLR2 SNP rs3804100 and leprosy in the Pará population, which still indicates the need for new immunogenetic studies with other genes involved in the immune response and a greater number of polymorphisms.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.