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1.
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)
Adult , Aged , Female , Humans , Male , Middle Aged , Adaptive Immunity/physiology , Antibodies, Neutralizing/blood , COVID-19/immunology , Cohort Studies , Immunoglobulin G/blood , SARS-CoV-2/immunology , T-Lymphocytes/physiology , Time Factors , Viral Proteins/immunology
2.
Mem. Inst. Oswaldo Cruz ; 110(8): 945-955, Dec. 2015. graf
Article in English | LILACS | ID: lil-769829

ABSTRACT

Asymptomatic Plasmodium infection carriers represent a major threat to malaria control worldwide as they are silent natural reservoirs and do not seek medical care. There are no standard criteria for asymptomaticPlasmodium infection; therefore, its diagnosis relies on the presence of the parasite during a specific period of symptomless infection. The antiparasitic immune response can result in reducedPlasmodium sp. load with control of disease manifestations, which leads to asymptomatic infection. Both the innate and adaptive immune responses seem to play major roles in asymptomatic Plasmodiuminfection; T regulatory cell activity (through the production of interleukin-10 and transforming growth factor-β) and B-cells (with a broad antibody response) both play prominent roles. Furthermore, molecules involved in the haem detoxification pathway (such as haptoglobin and haeme oxygenase-1) and iron metabolism (ferritin and activated c-Jun N-terminal kinase) have emerged in recent years as potential biomarkers and thus are helping to unravel the immune response underlying asymptomatic Plasmodium infection. The acquisition of large data sets and the use of robust statistical tools, including network analysis, associated with well-designed malaria studies will likely help elucidate the immune mechanisms responsible for asymptomatic infection.


Subject(s)
Humans , Asymptomatic Infections , Antigens, Protozoan/immunology , Carrier State/immunology , Malaria, Falciparum/immunology , Malaria, Vivax/immunology , Plasmodium/immunology , Adaptive Immunity/physiology , Biomarkers , Carrier State/parasitology , Disease Reservoirs/parasitology , Ferritins/immunology , Haptoglobins/immunology , Heme Oxygenase-1/immunology , Immunity, Innate/physiology , /immunology , JNK Mitogen-Activated Protein Kinases/immunology , Malaria, Falciparum/prevention & control , Malaria, Vivax/prevention & control , Parasitemia/immunology , Plasmodium/isolation & purification , Transforming Growth Factor beta/immunology
3.
Mem. Inst. Oswaldo Cruz ; 110(8): 966-973, Dec. 2015.
Article in English | LILACS | ID: lil-769837

ABSTRACT

Fungal infections are emerging as a major problem in part due to high mortality associated with systemic infections, especially in the case of immunocompromised patients. With the development of new treatments for diseases such as cancer and the acquired immune deficiency syndrome pandemic, the number of immunosuppressed patients has increased and, as a consequence, also the number of invasive fungal infections has increased. Several studies have proposed new strategies for the development of effective fungal vaccines. In addition, better understanding of how the immune system works against fungal pathogens has improved the further development of these new vaccination strategies. As a result, some fungal vaccines have advanced through clinical trials. However, there are still many challenges that prevent the clinical development of fungal vaccines that can efficiently immunise subjects at risk of developing invasive fungal infections. In this review, we will discuss these new vaccination strategies and the challenges that they present. In the future with proper investments, fungal vaccines may soon become a reality.


Subject(s)
Humans , Fungal Vaccines/immunology , Host-Pathogen Interactions/immunology , Immunocompromised Host/immunology , Mycoses/prevention & control , Vaccination/methods , Adaptive Immunity/physiology , Clinical Trials as Topic , Immunity, Innate/physiology , Technology, Pharmaceutical , Vaccination/trends
4.
Rev. cuba. hematol. inmunol. hemoter ; 30(4): 332-345, oct.-dic. 2014.
Article in Spanish | LILACS | ID: lil-735294

ABSTRACT

El proceso de envejecimiento provoca cambios en el sistema inmune que afectan su funcionamiento y desarrollo. Estos cambios pueden manifestarse desde la linfopoyesis hasta la respuesta que orquesta el sistema inmune frente a determinada enfermedad o agente infeccioso. Ambas ramas de la inmunidad, innata y adaptativa, se afectan en este proceso, lo que genera un impacto negativo en la respuesta inmune de los ancianos y los predispone a padecer enfermedades infecciosas, cáncer, autoinmunidad y a desarrollar respuestas pobres tras la administración de vacunas...


The aging process produces functional and developmental changes in the immune system. Those changes may appear from lymphopoiesis up to the final response of the immune system facing a certain disease. Both branches of immunity, innate and adaptive, are affected by the aging process; hence these changes can have a negative impact on the immune response of elderly patients and increase their susceptibility to infectious diseases, cancer and decreased vaccine efficacy...


Subject(s)
Humans , Aged , Aged, 80 and over , Aging/immunology , Immunity, Active/physiology , Adaptive Immunity/physiology , Immunity, Innate/physiology , Lymphopoiesis/immunology
5.
Arq. bras. endocrinol. metab ; 56(9): 597-607, Dec. 2012. ilus, tab
Article in English | LILACS | ID: lil-660273

ABSTRACT

Leptin, the adipokine produced mainly by the white adipose tissue, plays important roles not only in the regulation of food intake, but also in controlling immunity and inflammation. It has been widely demonstrated that the absence of leptin leads to immune defects in animal and human models, ultimately increasing mortality. Leptin also regulates inflammation by means of actions on its receptor, that is widely spread across different immune cell populations. The molecular mechanisms by which leptin determines its biological actions have also been recently elucidated, and three intracellular pathways have been implicated in leptin actions: JAK-STAT, PI3K, and ERK 1/2. These pathways are closely regulated by intracellular proteins that decrease leptin biological activity. In this review, we discuss the molecular mechanisms by which leptin regulates immunity and inflammation, and associate those mechanisms with chronic inflammatory disorders. Arq Bras Endocrinol Metab. 2012;56(9):597-607.


A leptina, uma adipocina produzida principalmente pelo tecido adiposo branco, tem um papel importante não somente na regulação da ingestão alimentar, mas também no controle da imunidade e da inflamação. Já foi amplamente demonstrado que a ausência de leptina causa deficiências imunológicas em modelos animais e em humanos, levando ao aumento da mortalidade. A leptina também regula a inflamação por meio da ação em seu receptor, amplamente distribuído em diversos tipos de células do sistema imunológico. Os mecanismos moleculares pelos quais a leptina determina suas ações biológicas foram recentemente elucidados, e três cascatas intracelulares são ativadas pela leptina: JAK-STAT, PI3K e ERK 1/2. Essas cascatas são reguladas por proteínas intracelulares, reduzindo as ações da leptina. Nesta revisão, são discutidos os mecanismos moleculares pelos quais a leptina regula a imunidade e a inflamação, associando-os a enfermidades inflamatórias crônicas. Arq Bras Endocrinol Metab. 2012;56(9):597-607.


Subject(s)
Animals , Humans , Inflammation/immunology , Leptin/immunology , Adaptive Immunity/physiology , Chronic Disease , Cytokines/physiology , Disease Models, Animal , Immunologic Factors/physiology , Inflammation Mediators/physiology , Inflammation/metabolism , Leptin/physiology , Receptors, Leptin/physiology
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