LUIZA GUILHERME GUGLIELMI
Projetos de Pesquisa
Unidades Organizacionais
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina
LIM/19 - Laboratório de Histocompatibilidade e Imunidade Celular, Hospital das Clínicas, Faculdade de Medicina - Líder
LIM/19 - Laboratório de Histocompatibilidade e Imunidade Celular, Hospital das Clínicas, Faculdade de Medicina - Líder
5 resultados
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- Rheumatic Fever: How Streptococcal Throat Infection Triggers an Autoimmune Disease(2015) GUILHERME, L.; KALIL, J.Molecular mimicry between streptococcal and human proteins has been proposed as the triggering factor leading to autoimmunity in rheumatic fever (RF) and rheumatic heart disease (RHD). Punctual genetic polymorphisms related to both innate and adaptive immune responses are involved in the development of RF/RHD. Some adhesion molecules and chemokines facilitate the monocytes and macrophages and T and B cell infiltration to the heart-tissue. Here we presented data on molecular mimicry mediated by B and T cell responses of peripheral blood and T cell clones infiltrating heart lesions from RHD patients against streptococcal antigens and human tissue proteins. The molecular analysis of T cell recognition is assessed by the definition of heart-cross reactive antigens. Degenerate patterns of T cell receptor (TCR) recognition in which intralesional T cell clones presenting the same TCR-BVJB and AVJB and recognized different antigens are described. The production of inflammatory cytokines such as TNFa, IL-2, IL-17, IL-23 and IFNg from peripheral and heart-infiltrating mononuclear cells, suggested that Th-1 and Th-17 type cytokines are the mediators of RHD heart lesions. All the results presented here delineate the mechanisms involved in RF/RHD and can certainly be a model for other autoimmune diseases. © 2015 Elsevier B.V. All rights reserved.
- Rheumatic fever: From pathogenesis to vaccine perspectives(2023) GUILHERME, L.; BRANCO, C. E.; BARROS, S. F. De; KALIL, J.Rheumatic fever (RF) is considered a model of autoimmune disease due to untreated throat infection by S. pyogenes that affects children and teenagers. The autoimmune process is believed to be the basis of all of the clinical manifestations; for instance, arthritis by immune complex deposition, chorea by antibody binding to neuronal cells, skin and subcutaneous manifestations that are mediated by a delayed hypersensitivity reaction, and carditis that is caused by cross-reactive antibodies and T cells. This chapter presents an overview of the mechanisms leading to the tissue lesions, treatment, and future possibilities of a vaccine against S. pyogenes. © 2023 Elsevier Inc. All rights reserved.
- Rheumatic Fever and Rheumatic Heart Disease(2017) GUILHERME, L.; SAMPAIO, R. O.; BARROS, S. Freschi de; KöHLER, K. F.; SPINA, G. S.; TARASOUTCHI, F.; KALIL, J.Rheumatic fever (RF) is the prototype of postinfectious autoimmune diseases. Similarities of structure and/or spatial conformation between Streptococcus pyogenes and human tissue proteins lead to autoimmune reactions due to molecular mimicry. The activation of T and B lymphocytes involves several genetically controlled molecules that act in both the innate and adaptive immune response. In this chapter, we describe the strains of bacteria that are more commonly involved in the development of RF worldwide as well as the genetic predisposition of diverse ethnic groups. The disease manifests in susceptible children and teenagers, usually starting as polyarthritis or Sydenham's chorea. This condition generally occurs several months after streptococcal infection. Erythema marginatum and subcutaneous nodules are rare cutaneous manifestation, and carditis is the most serious sequelae and can lead to severe valve damage and rheumatic heart disease (RHD). The immune mechanisms that lead to the diverse manifestations mentioned above are discussed. The diagnosis and treatment, particularly the revision of Jones Criteria in the era of Doppler echocardiography, as well as the perspective of vaccine development, are also presented. © 2017 Elsevier Inc. All rights reserved.
- Rheumatic fever and rheumatic heart disease(2019) GUILHERME, L.; KALIL, J.Rheumatic heart disease is a sequel of rheumatic fever that follows an untreated group A streptococcal infection of young susceptible individuals. The disease is mediated by inflammatory and autoimmune reactions. Several genes related to both innate and adaptive immune responses are involved. Human leukocytes antigens class II alleles have been associated with the disease. Both cellular and humoral immune responses are involved with the autoimmune reactions, and Th1 and Th17 inflammatory cytokines are the mediators of rheumatic heart lesions. Although humans are unique hosts for Streptococcus pyogenes infections, several studies have been done to find a suitable animal model and numerous different species (mice, rats, hamsters, rabbits, and primates). The in vitro analysis of tissue-infiltrating T cells showed their ability of recognizing several streptococcal-M protein peptides and self-antigens by molecular mimicry mechanism and demonstrated the involvement of CD4+ T cells in the pathogenesis of the disease. © 2020 Elsevier Inc. All rights reserved.
- Rheumatic Fever and Rheumatic Heart Disease(2014) GUILHERME, L.; KALIL, J.Rheumatic heart disease is a sequel of rheumatic fever that follows an untreated group A streptococcal infection of young susceptible individuals. The disease is mediated by inflammatory and autoimmune reactions. Several genes related to both innate and adaptive immune responses are involved and HLA class II alleles have also been associated with the disease. Both cellular and humoral immune responses take part in the autoimmune reactions, in which Th1 and Th17 inflammatory cytokines are mediators of the rheumatic heart lesions. Since humans are unique hosts for S. pyogenes infections, several studies have been done to find a suitable animal model in numerous different species including mice, rats, hamsters, rabbits, and primates. The in vitro analysis of heart tissue infiltrating T cells showed their ability to recognize several streptococcal-M protein peptides as well as self antigens by molecular mimicry mechanisms and demonstrated the contribution of CD4+ T cells in the pathogenesis of the disease.