Group A Streptococcal Infections as Related to Rheumatic Fever

Kawakita, Seiichi; Takeuchi, Tsune; Uemura, Yoshio; Onishi, Toyohiko; Saito, Koichi; Nagami, Hideo; Watanabe, Taketoshi; Watanabe, Tetsujiro

doi:10.1536/ihj.17.592

Cited by 4 publications

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“…It is already known that some viral and bacterial infections can promote the development of autoimmunity by inducing the breakdown of T cell tolerance and development of effector T cells reactive with the self-antigens or by the phenomenon called molecular mimicry, where a foreign antigen shares sequence or structural similarities with self-antigens [6] , [7] . For instance, acute rheumatic fever, where antibodies attack the heart, can occur after the body makes immune responses against Group A β-hemolytic streptococci [8] , [9] . In addition, it has been proposed that the prematurely egressed DP-T cells observed during Trypanosoma cruzi infection play an important role in the autoimmune cardio-inflammation [10] .…”

Section: Introductionmentioning

confidence: 99%

Exacerbation of Autoimmune Neuro-Inflammation in Mice Cured from Blood-Stage Plasmodium berghei Infection

et al. 2014

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The thymus plays an important role shaping the T cell repertoire in the periphery, partly, through the elimination of inflammatory auto-reactive cells. It has been shown that, during Plasmodium berghei infection, the thymus is rendered atrophic by the premature egress of CD4+CD8+ double-positive (DP) T cells to the periphery. To investigate whether autoimmune diseases are affected after Plasmodium berghei NK65 infection, we immunized C57BL/6 mice, which was previously infected with P.berghei NK65 and treated with chloroquine (CQ), with MOG35–55 peptide and the clinical course of Experimental Autoimmune Encephalomyelitis (EAE) was evaluated. Our results showed that NK65+CQ+EAE mice developed a more severe disease than control EAE mice. The same pattern of disease severity was observed in MOG35–55-immunized mice after adoptive transfer of P.berghei-elicited splenic DP-T cells. The higher frequency of IL-17+- and IFN-γ+-producing DP lymphocytes in the Central Nervous System of these mice suggests that immature lymphocytes contribute to disease worsening. To our knowledge, this is the first study to integrate the possible relationship between malaria and multiple sclerosis through the contribution of the thymus. Notwithstanding, further studies must be conducted to assert the relevance of malaria-induced thymic atrophy in the susceptibility and clinical course of other inflammatory autoimmune diseases.

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Section: Introductionmentioning

confidence: 99%

Exacerbation of Autoimmune Neuro-Inflammation in Mice Cured from Blood-Stage Plasmodium berghei Infection

et al. 2014

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“…Conhecidamente, infecções virais e bacterianas podem promover o desenvolvimento de autoimunidade por meio da (i) quebra da tolerância periférica de células T, (ii) pelo desenvolvimento de linfócitos T efetores reativos a auto-antígenos ou (iii) pelo fenômeno conhecido por mimetismo molecular, onde um antígeno exógeno compartilha sequencias ou estruturas semelhantes a proteínas próprias (Gilden, 2005;Herrmann et al, 2006). Neste último caso, a febre reumática aguda, onde anticorpos atacam cardiomiócitos, pode se desenvolver após a geração de resposta imune contra Streptococcus β-hemolítico do grupo A (Read et al, 1974;Kawakita et al, 1976)…”

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Efeito da infecção por Plasmodium berghei sobre a encefalomielite autoimune experimental

Thomé¹,

Verinaud²

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Malaria remains as the most frequent infectious disease in the world, where half of the world population is at risk. Destruction of the causative agent, protozoan of the Plasmodium gender, is essential for the resolution of the disease and this is mediated by the coordinated action of both T and B lymphocytes. It has been demonstrated that malariabearing patients possess auto-antibodies, e in some cases, the worsening of autoimmune diseases such as lupus and multiple sclerosis. Studies, conducted by our group, have shown that P. berghei NK65 infection promoted thymic atrophy and the subsequent migration of CD4 + CD8 + (DP) T cells towards the peripheral immune system. Since the thymus is the primary lymphoid organ responsible for the generation and maturation of T cells, playing a major role in the shaping of T cells repertoire, the present study aimed to investigate the influence of P. berghei infection in the clinical course of Experimental Autoimmune Encephalomyelitis (EAE), the mouse model for multiple sclerosis, and also over the maturation/activation status of dendritic cells. Results showed that malaria-cured mice developed a more severe EAE clinical course compared with control mice. The worsening in EAE score was related to the migration of DP-T cells towards the Central Nervous System (CNS), where these cells produced high amounts of inflammatory cytokines. Interestingly, EAE-resistant BALB/c mice developed the disease after plasmodia infection, indicating that the thymic atrophy induced by the infection is able to alter the susceptibility to autoimmune diseases. On the other hand, treatment of dendritic cells (DCs) with P.berghei extracts (PbX) modified their activation/maturation status towards a tolerogenic profile. The adoptive transfer of DC-PbX was able to suppress the development of EAE, as well as neuro-inflammation, through the reduction in cellular immune responses towards neuro-antigens. Taken together, the results collected in this study show that Plasmodium berghei NK65 infection promotes significant alterations in the immune system that aid the development of autoimmune neuro-inflammation. On the other hand, the use of plasmodia extracts may become an interesting approach to modulate inflammation through the adoptive transfer of tolerogenic dendritic cells. xiv xv Sumário Página Dedicatória xvii Agradecimentos xix Introdução 1 O desenvolvimento de linfócitos T e a geração de repertório 4 O comprometimento tímico nas infecções 7 A infecção por plasmódio e as alterações tímicas na malária 11 A influência mútua entre malária e doenças autoimunes 15 Células dendríticas: elementos-chave na malária e sua modulação para fins terapêuticos 19 Objetivo 23 Material e Métodos 27 Capítulo 1 -Desenvolvimento de modelo não letal de infecção por Plasmodium berghei NK65 37 Capítulo 2 -Efeito da infecção por Plasmodium berghei NK65 sobre o curso da Encefalomielite Autoimune Experimental 55 Capítulo 3 -Modulação de células dendríticas por extratos de plasmódio e terapia de Encefalomielite Autoimune Experimen...

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Immune Response to Streptococcal Antigens in Rheumatic Fever

Williams

1985

Immunology of Rheumatic Diseases

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Group A Streptococcal Infections as Related to Rheumatic Fever

Cited by 4 publications

References 7 publications

Exacerbation of Autoimmune Neuro-Inflammation in Mice Cured from Blood-Stage Plasmodium berghei Infection

Exacerbation of Autoimmune Neuro-Inflammation in Mice Cured from Blood-Stage Plasmodium berghei Infection

Efeito da infecção por Plasmodium berghei sobre a encefalomielite autoimune experimental

Immune Response to Streptococcal Antigens in Rheumatic Fever

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