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1.
Rev. cuba. hematol. inmunol. hemoter ; 37(1): e1310, ene.-mar. 2021.
Article in Spanish | LILACS, CUMED | ID: biblio-1251720

ABSTRACT

Introducción: Los síndromes mielodisplásicos constituyen un grupo heterogéneo de desórdenes hematológicos clonales adquiridos, que afectan la célula madre. Se caracterizan morfológicamente por: hematopoyesis ineficaz, citopenias periféricas progresivas, displasia en uno o más linajes celulares y tendencia evolutiva a leucemia aguda. Los avances recientes en la comprensión de los mecanismos genéticos y moleculares de los síndromes mielodisplásicos, han revelado la asociación entre alteraciones inmunológicas y las mutaciones recurrentes. Las células de la respuesta inmune innata y adaptativa, así como diversos mediadores solubles liberados por ellas, pueden establecer una respuesta antitumoral protectora o, por el contrario, inducir eventos de inflamación crónica que favorezcan la promoción y progresión de esta enfermedad. Objetivos: Resumir los conocimientos actuales de la relación sistema inmune-síndromes mielodisplásicos, enfatizando en las células inmunes del microambiente de la médula ósea y su importancia en la clínica de la enfermedad. Métodos: Se realizó investigación bibliográfica-documental acerca del tema. Se consultaron las bases de datos Scielo y Pubmed. Conclusiones: La comprensión de la función dual que ejerce el sistema inmune en los síndromes mielodisplásicos, constituye un desafío y son necesarios estudios clínicos rigurosos para poder establecer el valor de la manipulación del sistema inmune como una forma posible de tratamiento de esta enfermedad(AU)


Introduction: Myelodysplastic syndromes (MDS) constitute a heterogeneous group of acquired clonal hematological disorders that affect the stem cell. These are characterized morphologically and clinically by: ineffective hematopoiesis, progressive peripheral cytopenia, dysplasia in one or more cell lineages, in most of cases and evolutionary tendency to acute leukemia. Recent advances in understanding the genetic and molecular mechanisms of MDS have revealed the association between immunological alterations and recurrent mutations. Cells of the innate and adaptive immune response, as well as various soluble mediators released by them, can establish a protective antitumor response or, on the contrary, induce events of chronic inflammation that favor the promotion and progression of this disease. Objective: To summarize the current knowledge of the immune system-MDS relationship, emphasizing the immune cells of the bone marrow microenvironment and their importance in the clinic of the disease. Methods: A bibliographic-documentary research was carried out on the subject. The Scielo and Pubmed databases were consulted. Conclusions: Understanding the dual role of the immune system in MDS constitutes a challenge and rigorous clinical studies are necessary to establish the value of manipulating the immune system as a possible form of treatment of this disease(AU)


Subject(s)
Humans , Stem Cells , Myelodysplastic Syndromes/complications , Leukemia , Adaptive Immunity , Hematopoiesis/genetics , Immune System/physiopathology , Inflammation/diagnosis
2.
Washington; Organización Panamericana de la Salud; Mar. 17, 2021. 89 p. tab.
Non-conventional in Spanish | LILACS | ID: biblio-1253360

ABSTRACT

En este documento se presenta orientación provisional sobre las mejores prácticas para evaluar la efectividad de las vacunas contra la COVID-19 usando el diseño de estudio observacional. Se examinan las consideraciones esenciales del diseño, el análisis y la interpretación de las evaluaciones de la efectividad de las vacunas contra la COVID-19, dado que se pueden obtener resultados sesgados aun en entornos en los que la exhaustividad y la calidad de los datos son altas. Esta orientación se dirige principalmente a las evaluaciones realizadas en los países de ingresos bajos o medianos, pero la mayoría de los conceptos también son aplicables en entornos de ingresos altos.


Since its emergence in December 2019, SARS-CoV-2, the virus that causes coronavirus disease 2019 (COVID-19), has taken a tremendous toll globally; by 28 February 2021, there have been over 110 million cases and 2.5 million deaths worldwide from COVID-19 (1). Although most COVID-19 deaths occur among older adults and persons with chronic comorbid medical conditions, deaths have occurred in persons of all ages. Moreover, the pandemic has caused widespread morbidity and necessitated control measures that have devastated economies worldwide. In response to the pandemic, the global efforts to develop multiple vaccines to protect against COVID-19 disease have been unrivalled in the history of public health. By the end of 2020, three COVID-19 vaccines have received Emergency Use Approval/Listing (EUA/EUL) by maturity level 4 regulatory authorities, based on reaching predefined criteria for safety and efficacy, and at least several dozen more are in clinical trials.


Subject(s)
Humans , Immunization Programs/organization & administration , Vaccination Coverage/statistics & numerical data , COVID-19 Vaccines/immunology , COVID-19 Testing/methods , SARS-CoV-2/immunology , COVID-19/immunology , Data Collection , Adaptive Immunity/immunology , SARS-CoV-2/isolation & purification , SARS-CoV-2/genetics , COVID-19/genetics , COVID-19/virology
4.
Rev. Assoc. Med. Bras. (1992) ; 66(12): 1666-1672, Dec. 2020. tab, graf
Article in English | LILACS, SES-SP | ID: biblio-1143670

ABSTRACT

SUMMARY BACKGROUND: The COVID-19 pandemic has affected the entire world, posing a serious threat to human health. T cells play a critical role in the cellular immune response against viral infections. We aimed to reveal the relationship between T cell subsets and disease severity. METHODS: 40 COVID-19 patients were randomly recruited in this cross-sectional study. All cases were confirmed by quantitative RT-PCR. Patients were divided into two equivalent groups, one severe and one nonsevere. Clinical, laboratory and flow cytometric data were obtained from both clinical groups and compared. RESULTS: Lymphocyte subsets, CD4+ and CD8+ T cells, memory CD4+ T cells, memory CD8+ T cells, naive CD4+ T cells, effector memory CD4+ T cells, central memory CD4+ T cells, and CD3+CD4+ CD25+ T cells were significantly lower in severe patients. The naive T cell/CD4 + EM T cell ratio, which is an indicator of the differentiation from naive T cells to memory cells, was relatively reduced in severe disease. Peripheral CD4+CD8+ double-positive T cells were notably lower in severe presentations of the disease (median DP T cells 11.12 µL vs 1.95 µL; p< 0.001). CONCLUSIONS: As disease severity increases in COVID-19 infection, the number of T cell subsets decreases significantly. Suppression of differentiation from naive T cells to effector memory T cells is the result of severe impairment in adaptive immune functions. Peripheral CD4+CD8+ double-positive T cells were significantly reduced in severe disease presentations and may be a useful marker to predict disease severity.


RESUMO OBJETIVO: A pandemia de COVID-19 tem afetado o mundo todo, constituindo uma ameaça grave para a saúde humana. As células T desempenham um papel crítico na imunidade celular contra infecções virais. Procuramos desvendar a relação entre sub grupos de células T e a severidade da doença. MÉTODOS: Um total de 40 pacientes com COVID-19 foram aleatoriamente recrutados para o presente estudo transversal. Todos os casos foram confirmados por RT-PCR quantitativo. Os pacientes foram divididos em dois grupos equivalentes, um grave e um não-grave. Os dados da avaliação clínica, laboratorial e da citometria de fluxo foram obtidos para ambos os grupos e comparados. RESULTADOS: Os subconjuntos de linfócitos, células T CD4+ e CD8+, células T de memória CD4+, células T de memória CD8+, células T CD4+ virgens, células T efetoras CD4+, células T de memória central CD4+ e células T CD3+ CD4+ CD25+ estavam significativamente mais baixas nos pacientes graves. A razão células T virgens/células T efetoras TCD4+, que é um indicador da diferenciação entre células T virgens e células de memória, estava relativamente reduzida em casos graves da doença. As células T duplo-positivas CD4+CD8+ periféricas estavam notavelmente mais baixas em casos graves da doença (mediana das células T DP: 11,12 µL vs. 1,95 µL; p< 0,001). CONCLUSÃO: Conforme aumenta a gravidade da doença nos casos de COVID-19, o número de subconjuntos de células T diminui significativamente. A supressão da diferenciação de células T virgens para células T efetoras é o resultado do comprometimento grave das funções imunológicas adaptativas. As células T duplo-positivas CD4+CD8+ periféricas estavam notavelmente mais baixas em casos graves da doença e podem ser um marcador útil para predizer a severidade da doença.


Subject(s)
Humans , Male , Female , Adult , Aged , Aged, 80 and over , CD4-Positive T-Lymphocytes/immunology , Coronavirus Infections/immunology , CD8-Positive T-Lymphocytes/immunology , Immunologic Memory , Cell Differentiation , Cross-Sectional Studies , Coronavirus Infections/diagnosis , Adaptive Immunity , Middle Aged
5.
Frontiers of Medicine ; (4): 746-751, 2020.
Article in English | WPRIM | ID: wpr-880959

ABSTRACT

The ongoing pandemic of Coronavirus disease 19 (COVID-19) is caused by a newly discovered β Coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). How long the adaptive immunity triggered by SARS-CoV-2 can last is of critical clinical relevance in assessing the probability of second infection and efficacy of vaccination. Here we examined, using ELISA, the IgG antibodies in serum specimens collected from 17 COVID-19 patients at 6-7 months after diagnosis and the results were compared to those from cases investigated 2 weeks to 2 months post-infection. All samples were positive for IgGs against the S- and N-proteins of SARS-CoV-2. Notably, 14 samples available at 6-7 months post-infection all showed significant neutralizing activities in a pseudovirus assay, with no difference in blocking the cell-entry of the 614D and 614G variants of SARS-CoV-2. Furthermore, in 10 blood samples from cases at 6-7 months post-infection used for memory T-cell tests, we found that interferon γ-producing CD4


Subject(s)
Adaptive Immunity/physiology , Adult , Aged , Antibodies, Neutralizing/blood , COVID-19/immunology , Cohort Studies , Female , Humans , Immunoglobulin G/blood , Male , Middle Aged , SARS-CoV-2/immunology , T-Lymphocytes/physiology , Time Factors , Viral Proteins/immunology
6.
Chinese Medical Journal ; (24): 2966-2975, 2020.
Article in English | WPRIM | ID: wpr-877923

ABSTRACT

Antimicrobial peptides (AMPs) are small molecules produced by a myriad of cells and play important roles not only in protecting against infections and sustaining skin barrier homeostasis but also in contributing to immune dysregulation under pathological conditions. Recently, increasing evidence has indicated that AMPs, including cathelicidin (LL-37), human β-defensins, S100 proteins, lipocalin 2, and RNase 7, are highly expressed in psoriatic skin lesions. These peptides broadly regulate immunity by interacting with various immune cells and linking innate and adaptive immune responses during the progression of psoriasis. In this review, we summarize the recent findings regarding AMPs in the pathogenesis of psoriasis with a main focus on their immunomodulatory abilities.


Subject(s)
Adaptive Immunity , Humans , Immunity, Innate , Pore Forming Cytotoxic Proteins , Psoriasis , Skin Diseases , beta-Defensins
7.
Article in English | WPRIM | ID: wpr-762185

ABSTRACT

Improved understanding of the contribution of immune-inflammatory mechanisms in allergic diseases and asthma has encouraged development of biologicals and small molecules specifically targeting the innate and adaptive immune response. There are several critical points impacting the efficacy of this stratified approach, from the complexity of disease endotypes to the effectiveness in real-world settings. We discuss here how these barriers can be overcome to facilitate the development of implementation science for allergic diseases and asthma.


Subject(s)
Adaptive Immunity , Asthma , Biological Products , Hypersensitivity
8.
Article in English | WPRIM | ID: wpr-816636

ABSTRACT

Coccidiosis-causing Eimeria species are transmitted in poultry via the oral-fecal route and can lead to hemorrhagic diarrhea and mortality. This results in enormous economic losses in the poultry industry. Furthermore, its resistance to some currently used antibiotics is increasing. This has prompted the development of new alternative drug therapies that address the issue of chemical-free meat production. Effective management of infectious diseases in veterinary practice includes the induction of protective and adaptive immunity by treatment with an alternative agent. In this study, we evaluated the anticoccidial effects of dietary supplementation of Chosun University (CS) 32 compounds (0.1% and 1.0%) against Eimeria tenella, which was isolated and purified from the supernatant of culture broth of Bacillus strain (KCTC18250P), as well as its effect on the growth rate and feed efficiency in chickens. Overall, we observed a decrease in lesion scores and oocyte output in CS 32 compounds-treated chickens. We concluded that 0.1% CS 32 compounds displayed anticoccidial effects against E. tenella infection.


Subject(s)
Adaptive Immunity , Anti-Bacterial Agents , Bacillus , Chickens , Communicable Diseases , Diarrhea , Dietary Supplements , Drug Therapy , Eimeria tenella , Eimeria , Meat Products , Mortality , Oocytes , Poultry
9.
Article in English | WPRIM | ID: wpr-811071

ABSTRACT

Since the airways are constantly exposed to various pathogens and foreign antigens, various kinds of cells in the airways—including structural cells and immune cells—interact to form a precise defense system against pathogens and antigens that involve both innate immunity and acquired immunity. Accumulating evidence suggests that innate lymphoid cells (ILCs) play critical roles in the maintenance of tissue homeostasis, defense against pathogens and the pathogenesis of inflammatory diseases, especially at body surface mucosal sites such as the airways. ILCs are activated mainly by cytokines, lipid mediators and neuropeptides that are produced by surrounding cells, and they produce large amounts of cytokines that result in inflammation. In addition, ILCs can change their phenotype in response to stimuli from surrounding cells, which enables them to respond promptly to microenvironmental changes. ILCs exhibit substantial heterogeneity, with different phenotypes and functions depending on the organ and type of inflammation, presumably because of differences in microenvironments. Thus, ILCs may be a sensitive detector of microenvironmental changes, and analysis of their phenotype and function at local sites may enable us to better understand the microenvironment in airway diseases. In this review, we aimed to identify molecules that either positively or negatively influence the function and/or plasticity of ILCs and the sources of the molecules in the airways in order to examine the pathophysiology of airway inflammatory diseases and facilitate the issues to be solved.


Subject(s)
Adaptive Immunity , Cellular Microenvironment , Cytokines , Homeostasis , Immunity, Innate , Inflammation , Lymphocytes , Neuropeptides , Phenotype , Plastics , Population Characteristics , Respiratory Tract Diseases
10.
Rev. Assoc. Med. Bras. (1992) ; 65(2): 262-269, Feb. 2019. tab, graf
Article in English | LILACS | ID: biblio-990342

ABSTRACT

SUMMARY INTRODUCTION: Opioids interact with both innate and adaptive immune systems and have direct effects on opioid receptors located on immune cells. Research on this topic has provided evidence of the opioid influence on the immune response associated with surgical stress. The immunological effects of opioids are currently being investigated, particularly whether they influence the outcome of surgery or the underlying disease regarding important aspects like infection or cancer progression. This review addresses background research related to the influence of the opioid receptor on the immune system, the immunosuppressive effect associated with major opioids during the perioperative period, and their clinical relevance. The objective of the study was to review the effects of opioids on the immune system. Methods: A search strategy was conducted in PubMed, Embase, and the Cochrane databases using the terms "immunosuppression," "immune system," "surgical procedures," "analgesics," "opioids" and "perioperative care." Results: The immunosuppressive effect of opioids was identified over 30 years ago. They include signaling and acting directly through immune cells, including B and T lymphocytes, NK cells, monocytes, and macrophages, as well as activating the downstream pathways of the hypothalamic-pituitary-adrenal (HPA) axis leading to the production of immunosuppressive glucocorticoids in the peripheral and sympathetic nervous system.


RESUMO INTRODUÇÃO: Os opioides interagem com ambos os sistemas imunes, inato e adaptativo, através de efeitos diretos sobre os receptores dos opioides localizados nas células imunes. As pesquisas neste assunto têm fornecido evidência da influência dos opioides sobre a resposta imune associada ao estresse cirúrgico. Os efeitos imunológicos dos opioides estão sendo pesquisados na atualidade, principalmente se eles determinam o resultado da cirurgia ou doença consequente devido a fatos importantes como infecção ou progressão do câncer. Essa revisão tem como alvo ver antecedentes em pesquisa relativa à influência dos receptores dos opioides no sistema imunológico, o efeito imunossupressor associado com opioides maiores durante o período peri-operatório e sua importância clínica. O objectivo da pesquisa foi revisar os efeitos dos opioides no sistema imunológico. MÉTODOS: Uma estrategia de procura foi dirigida na mídia PubMed, e no cadastro de Embase e The Cochrane, usando os termos "imunosuppressão", "sistema imunológico", "procedimentos cirúrgicos", "analgésicos", "opioides" e "cuidado peri-operatório". RESULTADOS: O efeito imunosuppressor dos opioides foi identificado há mais de 30 anos. Os efeitos imunosupressores incluem sinalização e ação diretamente através das células imunes, mesmo com os linfócitos B e T, células NK, monócitos e macrófagos, também como ativando as vias de corrente do eixo hipotálamo- hipófise- adrenal (HPA) levando à produção de glucocorticoides imunossupresores no sistema nervoso periférico e simpático.


Subject(s)
Humans , Analgesics, Opioid/pharmacology , Immune System/drug effects , Tramadol/administration & dosage , Tramadol/pharmacology , Fentanyl/administration & dosage , Fentanyl/pharmacology , Adaptive Immunity/drug effects , Perioperative Period , Remifentanil/administration & dosage , Remifentanil/pharmacology , Analgesics, Opioid/administration & dosage , Morphine/administration & dosage , Morphine/pharmacology
11.
Immune Network ; : e31-2019.
Article in English | WPRIM | ID: wpr-764029

ABSTRACT

Asthma is one of the most common and chronic diseases characterized by multidimensional immune responses along with poor prognosis and severity. The heterogeneous nature of asthma may be attributed to a complex interplay between risk factors (either intrinsic or extrinsic) and specific pathogens such as respiratory viruses, and even bacteria. The intrinsic risk factors are highly correlated with asthma exacerbation in host, which may be mediated via genetic polymorphisms, enhanced airway epithelial lysis, apoptosis, and exaggerated viral replication in infected cells, resulting in reduced innate immune response and concomitant reduction of interferon (types I, II, and III) synthesis. The canonical features of allergic asthma include strong Th2-related inflammation, sensitivity to non-steroidal anti-inflammatory drugs (NSAIDs), eosinophilia, enhanced levels of Th2 cytokines, goblet cell hyperplasia, airway hyper-responsiveness, and airway remodeling. However, the NSAID-resistant non-Th2 asthma shows a characteristic neutrophilic influx, Th1/Th17 or even mixed (Th17-Th2) immune response and concurrent cytokine streams. Moreover, inhaled corticosteroid-resistant asthma may be associated with multifactorial innate and adaptive responses. In this review, we will discuss the findings of various in vivo and ex vivo models to establish the critical heterogenic asthmatic etiologies, host-pathogen relationships, humoral and cell-mediated immune responses, and subsequent mechanisms underlying asthma exacerbation triggered by respiratory viral infections.


Subject(s)
Adaptive Immunity , Airway Remodeling , Apoptosis , Asthma , Bacteria , Chronic Disease , Cytokines , Eosinophilia , Goblet Cells , Hyperplasia , Immunity, Innate , Inflammation , Interferons , Neutrophils , Polymorphism, Genetic , Prognosis , Respiratory Hypersensitivity , Respiratory Tract Infections , Risk Factors , Rivers
12.
Immune Network ; : 37-2019.
Article in English | WPRIM | ID: wpr-785824

ABSTRACT

Immunosenescence is characterized by a progressive deterioration of the immune system associated with aging. Multiple components of both innate and adaptive immune systems experience aging-related changes, such as alterations in the number of circulating monocytic and dendritic cells, reduced phagocytic activities of neutrophils, limited diversity in B/T cell repertoire, T cell exhaustion or inflation, and chronic production of inflammatory cytokines known as inflammaging. The elderly are less likely to benefit from vaccinations as preventative measures against infectious diseases due to the inability of the immune system to mount a successful defense. Therefore, aging is thought to decrease the efficacy and effectiveness of vaccines, suggesting aging-associated decline in the immunogenicity induced by vaccination. In this review, we discuss aging-associated changes in the innate and adaptive immunity and the impact of immunosenescence on viral infection and immunity. We further explore recent advances in strategies to enhance the immunogenicity of vaccines in the elderly. Better understanding of the molecular mechanisms underlying immunosenescence-related immune dysfunction will provide a crucial insight into the development of effective elderly-targeted vaccines and immunotherapies.


Subject(s)
Adaptive Immunity , Aged , Aging , Communicable Diseases , Cytokines , Dendritic Cells , Humans , Immune System , Immunosenescence , Immunotherapy , Inflation, Economic , Neutrophils , Vaccination , Vaccines
13.
Immune Network ; : e14-2019.
Article in English | WPRIM | ID: wpr-740214

ABSTRACT

Invariant NKT (iNKT) cells are a small subset of thymus-generated T cells that produce cytokines to control both innate and adaptive immunity. Because of their very low frequency in the thymus, in-depth characterization of iNKT cells can be facilitated by their enrichment from total thymocytes. Magnetic-activated cell sorting (MACS) of glycolipid antigen-loaded CD1d-tetramer-binding cells is a commonly used method to enrich iNKT cells. Surprisingly, we found that this procedure also dramatically altered the subset composition of enriched iNKT cells. As such, NKT2 lineage cells that express large amounts of the transcription factor promyelocytic leukemia zinc finger were markedly over-represented, while NKT1 lineage cells expressing the transcription factor T-bet were significantly reduced. To overcome this limitation, here, we tested magnetic-activated depletion of CD24⁺ immature thymocytes as an alternative method to enrich iNKT cells. We found that the overall recovery in iNKT cell numbers did not differ between these 2 methods. However, enrichment by CD24⁺ cell depletion preserved the subset composition of iNKT cells in the thymus, and thus permitted accurate and reproducible analysis of thymic iNKT cells in further detail.


Subject(s)
Adaptive Immunity , Cytokines , Leukemia , Methods , Natural Killer T-Cells , Receptors, Antigen, T-Cell , T-Lymphocytes , Thymocytes , Thymus Gland , Transcription Factors , Zinc Fingers
14.
Immune Network ; : e2-2019.
Article in English | WPRIM | ID: wpr-740212

ABSTRACT

The enhanced differentiation and activation of osteoclasts (OCs) in the inflammatory arthritis such as rheumatoid arthritis (RA) and gout causes not only local bone erosion, but also systemic osteoporosis, leading to functional disabilities and morbidity. The induction and amplification of NFATc1, a master regulator of OC differentiation, is mainly regulated by receptor activator of NF-κB (RANK) ligand-RANK and calcium signaling which are amplified in the inflammatory milieu, as well as by inflammatory cytokines such as TNFα, IL-1β and IL-6. Moreover, the predominance of CD4+ T cell subsets, which varies depending on the condition of inflammatory diseases, can determine the fate of OC differentiation. Anti-citrullinated peptide antibodies which are critical in the pathogenesis of RA can bind to the citrullinated vimentin on the surface of OC precursors, and in turn promote OC differentiation and function via IL-8. In addition to adaptive immunity, the activation of innate immune system including the nucleotide oligomerization domain leucine rich repeat with a pyrin domain 3 inflammasome and TLRs can regulate OC maturation. The emerging perspectives about the diverse and close interactions between the immune cells and OCs in inflammatory milieu can have a significant impact on the future direction of drug development.


Subject(s)
Adaptive Immunity , Antibodies , Arthritis , Arthritis, Rheumatoid , Calcium Signaling , Cytokines , Gout , Immune System , Inflammasomes , Interleukin-6 , Interleukin-8 , Leucine , Osteoclasts , Osteolysis , Osteoporosis , T-Lymphocyte Subsets , Vimentin
15.
Chinese Journal of Traumatology ; (6): 125-136, 2018.
Article in English | WPRIM | ID: wpr-691023

ABSTRACT

Traumatic injury of the central nervous system (CNS) including brain and spinal cord remains a leading cause of morbidity and disability in the world. Delineating the mechanisms underlying the secondary and persistent injury versus the primary and transient injury has been drawing extensive attention for study during the past few decades. The sterile neuroinflammation during the secondary phase of injury has been frequently identified substrate underlying CNS injury, but as of now, no conclusive studies have determined whether this is a beneficial or detrimental role in the context of repair. Recent pioneering studies have demonstrated the key roles for the innate and adaptive immune responses in regulating sterile neuroinflammation and CNS repair. Some promising immunotherapeutic strategies have been recently developed for the treatment of CNS injury. This review updates the recent progress on elucidating the roles of the innate and adaptive immune responses in the context of CNS injury, the development and characterization of potential immunotherapeutics, as well as outstanding questions in this field.


Subject(s)
Adaptive Immunity , Astrocytes , Physiology , Brain Injuries, Traumatic , Allergy and Immunology , Therapeutics , Histone Deacetylases , Therapeutic Uses , Humans , Immunity, Innate , Allergy and Immunology , Immunotherapy , Methods , Inflammasomes , Physiology , Macrophage Activation , Spinal Cord Injuries , Allergy and Immunology , Therapeutics
16.
Article in English | WPRIM | ID: wpr-713820

ABSTRACT

Systemic lupus erythematous (SLE) is a systemic autoimmune disease with multi-organ inflammation caused by the production of pathogenic autoantibodies and immune complexes reflecting a global loss of tolerance. Lupus nephritis (LN) is present in approximately 60% of SLE patients and is considered a major predictor of a poor prognosis. To date, many studies utilizing genomics, transcriptomics, epigenetics, metabolomics, and microbiome have been conducted on a range of animal models and lupus patients to understand the pathogenesis of SLE and LN. Collectively, these studies support the concept that LN is caused by increased cell death, which has not been properly dealt with; abnormal innate immunity; hyperactive adaptive immunity; and genetic variants triggered by a range of environmental factors. This review summarizes the results from studies that contributed strongly to elucidating the pathogenesis of SLE and LN, highlighting the immunological and non-immunological mechanisms.


Subject(s)
Adaptive Immunity , Allergy and Immunology , Antigen-Antibody Complex , Apoptosis , Autoantibodies , Autoimmune Diseases , Cell Death , Epigenomics , Genomics , Humans , Immunity, Innate , Inflammation , Lupus Nephritis , Lymphocytes , Metabolomics , Microbiota , Models, Animal , Prognosis , Wolves
17.
National Journal of Andrology ; (12): 452-456, 2018.
Article in Chinese | WPRIM | ID: wpr-689734

ABSTRACT

Neisseria gonorrhoeae (NG), as a pathogen of gonorrhea, is strictly limited to growth on the human host. In case of gonococcal infection, the body may recruit such inflammatory cells as neutrophils to resist the invasion of NG or initiate its adaptive immune response by antigen presentation to eliminate the pathogen. However, a series of immune escape mechanisms of NG make it difficult to clear up the infection. In the innate immune system, NG can not only secrete thermonuclease to degrade neutrophile granulocytes, inhibit respiratory burst to resist killing by neutrophils, activate NLRP3 to prompt the pyronecrosis of inflammatory cells, but also regulate the differentiation of macrophages to reduce the inflammatory response, combine with factor H to evade complement-mediated killing. NG infection can hardly give rise to effective adaptive immune response and immune memory, but can promote TGF-β production to inhibit Th1/Th2-mediated adaptive immune response, bind to CEACAM1 on the B cell surface to promote apoptosis in B cells, and combine with CEACAM1 on the T cell surface to inhibit helper T cell proliferation, which makes it difficult for B cells to produce high-affinity specific antibodies. With the increasing drug-resistance of NG, immunological studies may play a significant role in the development of novel therapies and effective vaccines against the infection.


Subject(s)
Adaptive Immunity , Antibodies , Allergy and Immunology , Antigens, CD , Allergy and Immunology , Cell Adhesion Molecules , Allergy and Immunology , Complement Factor H , Allergy and Immunology , Gonorrhea , Allergy and Immunology , Humans , Immune Evasion , Allergy and Immunology , Immunity, Innate , Allergy and Immunology , Neisseria gonorrhoeae , Allergy and Immunology
18.
Immune Network ; : e25-2018.
Article in English | WPRIM | ID: wpr-716242

ABSTRACT

γδ T cells are abundant in the gut mucosa and play an important role in adaptive immunity as well as innate immunity. Although γδ T cells are supposed to be associated with the enhancement of Ab production, the status of γδ T cells, particularly in the synthesis of IgA isotype, remains unclear. We compared Ig expression in T cell receptor delta chain deficient (TCRδ⁻/⁻) mice with wild-type mice. The amount of IgA in fecal pellets was substantially elevated in TCRδ⁻/⁻ mice. This was paralleled by an increase in surface IgA expression and total IgA production by Peyer's patches (PPs) and mesenteric lymph node (MLN) cells. Likewise, the TCRδ⁻/⁻ mice produced much higher levels of serum IgA isotype. Here, surface IgA expression and number of IgA secreting cells were also elevated in the culture of spleen and bone marrow (BM) B cells. Germ-line α transcript, an indicator of IgA class switch recombination, higher in PP and MLN B cells from TCRδ⁻/⁻ mice, while it was not seen in inactivated B cells. Nevertheless, the frequency of IgA+ B cells was much higher in the spleen from TCRδ⁻/⁻ mice. These results suggest that γδ T cells control the early phase of B cells, in order to prevent unnecessary IgA isotype switching. Furthermore, this regulatory role of γδ T cells had lasting effects on the long-lived IgA-producing plasma cells in the BM.


Subject(s)
Adaptive Immunity , Animals , B-Lymphocytes , Bone Marrow , Immunity, Innate , Immunoglobulin A , Immunoglobulin Class Switching , Lymph Nodes , Mice , Mucous Membrane , Peyer's Patches , Plasma Cells , Receptors, Antigen, T-Cell, gamma-delta , Recombination, Genetic , Spleen , T-Lymphocytes
19.
Immune Network ; : e18-2018.
Article in English | WPRIM | ID: wpr-715082

ABSTRACT

Mast cells integrate innate and adaptive immunity and are implicated in pathophysiological conditions, including allergy, asthma, and anaphylaxis. Cross-linking of the high-affinity IgE receptor (FcεRI) initiates diverse signal transduction pathways and induces release of proinflammatory mediators by mast cells. In this study, we demonstrated that hyperactivation of mechanistic target of rapamycin (mTOR) signaling using the mTOR activator MHY1485 suppresses FcεRI-mediated mast cell degranulation and cytokine secretion. MHY1485 treatment increased ribosomal protein S6 kinase (S6K) and eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) phosphorylation, which are downstream targets of mTOR complex 1 (mTORC1), but decreased phosphorylation of Akt on mTOR complex 2 (mTORC2) target site serine 473. In addition, this activator decreased β-hexosaminidase, IL-6, and tumor necrosis factor α (TNF-α) release in murine bone marrow-derived mast cells (BMMCs) after FcεRI stimulation. Furthermore, MHY1485-treated BMMCs showed significantly decreased proliferation when cultured with IL-3. These findings suggested hyperactivation of mTORC1 as a therapeutic strategy for mast cell-related diseases.


Subject(s)
Adaptive Immunity , Anaphylaxis , Asthma , Cell Degranulation , Cell Proliferation , Hypersensitivity , Immunoglobulin E , Interleukin-3 , Interleukin-6 , Mast Cells , Peptide Initiation Factors , Phosphorylation , Ribosomal Protein S6 Kinases , Serine , Signal Transduction , Sirolimus , Tumor Necrosis Factor-alpha
20.
Article in English | WPRIM | ID: wpr-766165

ABSTRACT

Inflammation is a normal physiological response to an infection or injury, such as aggression by microbes, trauma, or heat and radiation. Inflammation works to maintain homeostasis and is a highly regulated process with both pro- and anti-inflammatory components to ensure the prompt resolution of noxious conditions. In the initial stages of inflammation, macrophages destroy the abnormal stimuli, and remove the apoptotic bodies of the dead neutrophils as well as any remaining hazard factor. The macrophages then present the antigen to T lymphocytes to initiate the mechanisms of acquired immunity, which leads to the production of antibodies, cytokines and memory cells. The macrophage activity then switches from pro-inflammatory to anti-inflammatory to remove any elements of aggression, thereby achieving homeostasis. Macrophages play a key role in the innate immune response and form a bridge between the innate and acquired immune response. In certain circumstances, however, when chronic inflammation is produced, macrophages may have a harmful effect and cause lesions. Therefore, inflammation is the classic “double-edged sword”, in which macrophages cut both ways. Activated macrophages have two different phenotypes related to different stimuli: M1 (classically activated) and M2 (alternatively activated). M1 macrophages are pro-inflammatory and play a key role in the host defense mechanism, while M2 are associated with the responses to anti-inflammatory reactions and tissue remodeling. The transformation of different phenotypes of macrophages regulates the initiation, development, and cessation of inflammatory diseases. An imbalance of macrophage M1~M2 polarization is often associated with a range of diseases or inflammatory conditions, such as rheumatoid arthritis and systemic lupus erythematous.


Subject(s)
Adaptive Immunity , Aggression , Antibodies , Arthritis, Rheumatoid , Cytokines , Extracellular Vesicles , Homeostasis , Hot Temperature , Immunity, Innate , Inflammation , Macrophages , Memory , Neutrophils , Phenotype , T-Lymphocytes
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