Prediction of molecular mimicry between antigens from Leishmania sp. and human: Implications for autoimmune response in systemic lupus erythematosus

Múnera, Marlon; Farak, Juan Carlos Peralta; Perez, Mariana; Rojas, José M.; Villero, J.; Sánchez, Andrés; Sánchez, Jorge; Emiliani, Yuliana

doi:10.1016/j.micpath.2020.104444

Cited by 16 publications

(9 citation statements)

References 22 publications

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“…Although current literature has not shown unspecific cytokine release for SLA antigen in blood from autoimmune patients, molecular mimicry exists between antigens from Leishmania sp. and patients with systemic lupus erythematosus [ 28 ], consequently new studies are need in order to clarify this complex issue.…”

Section: Discussionmentioning

confidence: 99%

Leishmaniasis: A new method for confirming cure and detecting asymptomatic infection in patients receiving immunosuppressive treatment for autoimmune disease

et al. 2021

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Visceral leishmaniasis (VL) in patients receiving immunosuppressant drugs for autoimmune disease has been on the rise. It is important—but difficult—to know when cure has been achieved in these patients since the withdrawal of immunosuppressants during antileishmania treatment is commonly required, and there is a risk of relapse when immunosuppression is restored. The prevalence of asymptomatic infection among those immunosuppressed for autoimmune disease is also uncertain. The present work describes how cytokine release assays can be used to confirm the cure of VL, and to determine the prevalence of asymptomatic infection, in such patients. After collection of blood from volunteers (n = 108), SLA-stimulation of peripheral blood mononuclear cell cultures and of whole blood was found to induce the production of different combinations of cytokines that served to confirm recovery from VL, and asymptomatic Leishmania infection. Indeed, cure was confirmed in 14 patients, all of whom showed a specific Th1 immune response against Leishmania, and the prevalence of asymptomatic infection was determined as 21.27%. Cytokine profiles could be used to manage VL in patients with autoimmune disease, and to identify and better protect those with asymptomatic infection who are at risk of developing this disease.

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Section: Discussionmentioning

confidence: 99%

Leishmaniasis: A new method for confirming cure and detecting asymptomatic infection in patients receiving immunosuppressive treatment for autoimmune disease

et al. 2021

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“…One hypothesis is that, while autoreactive T cells are cleared in the thymus gland, those with a double TCR on the surface may be able to escape [111]. A TCR double receptor T cell could recognize an exogenous antigen from an antigen presenting cell (APC), activating it and attacking the epitopes in the body due to the second receptor (Figure 3) [112]. The correlation between the environment and its effect on the onset of autoimmune diseases is not a new theory; for example, considering the emergence of allergic rhinitis in children who have many siblings.…”

Section: Molecular Mimicrymentioning

confidence: 99%

Biomolecular Mechanisms of Autoimmune Diseases and Their Relationship with the Resident Microbiota: Friend or Foe?

et al. 2022

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The use of innovative approaches to elucidate the pathophysiological mechanisms of autoimmune diseases, as well as to further study of the factors which can have either a positive or negative effect on the course of the disease, is essential. In this line, the development of new molecular techniques and the creation of the Human Genome Program have allowed access to many more solutions to the difficulties that exist in the identification and characterization of the microbiome, as well as changes due to various factors. Such innovative technologies can rekindle older hypotheses, such as molecular mimicry, allowing us to move from hypothesis to theory and from correlation to causality, particularly regarding autoimmune diseases and dysbiosis of the microbiota. For example, Prevotella copri appears to have a strong association with rheumatoid arthritis; it is expected that this will be confirmed by several scientists, which, in turn, will make it possible to identify other mechanisms that may contribute to the pathophysiology of the disease. This article seeks to identify new clues regarding similar correlations between autoimmune activity and the human microbiota, particularly in relation to qualitative and quantitative microbial variations therein.

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“…T cell activation is one of the major pathogenic mechanisms in the immune-dysregulation observed in lupus patients (reviewed in Mountz et al, 2019 ). Lupus patients have an elevated number of T effector cells, indicating a continued pathogenic response triggered either by pathogens that may mimic self-antigen ( Zhao et al, 2019a ; Múnera et al, 2020 ; Munroe et al, 2020 ), uncleared self-antigen from dying cells (reviewed in Muñoz et al, 2010 ; Prechl et al, 2016 ), or altered cytokine milieu contributing to effector cell bias (reviewed in Bengtsson and Rönnblom, 2017 ; Paquissi and Abensur, 2021 ). The role of complement proteins in LN is quite complex, where tissue damage is induced by complement deposition, and hypocomplementemia of C3 and C4 is pronounced in active disease, suggesting that complement-mediated clearance of autoantigen and IC play a central role in pathogenesis (reviewed in Li et al, 2021 ).…”

Section: Immune-dysregulation In Lupus Nephritismentioning

confidence: 99%

Targeting Regulatory T Cells for Therapy of Lupus Nephritis

et al. 2022

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Lupus glomerulonephritis (LN) is a complex autoimmune disease characterized by circulating autoantibodies, immune-complex deposition, immune dysregulation and defects in regulatory T cell (Tregs). Treatment options rely on general immunosuppressants and steroids that have serious side effects. Approaches to target immune cells, such as B cells in particular, has had limited success and new approaches are being investigated. Defects in Tregs in the setting of autoimmunity is well known and Treg-replacement strategies are currently being explored. The aim of this minireview is to rekindle interest on Treg-targeting strategies. We discuss the existing evidences for Treg-enhancement strategies using key cytokines interleukin (IL)-2, IL-33 and IL-6 that have shown to provide remission in LN. We also discuss strategies for indirect Treg-modulation for protection from LN.

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Prediction of molecular mimicry between antigens from Leishmania sp. and human: Implications for autoimmune response in systemic lupus erythematosus

Cited by 16 publications

References 22 publications

Leishmaniasis: A new method for confirming cure and detecting asymptomatic infection in patients receiving immunosuppressive treatment for autoimmune disease

Leishmaniasis: A new method for confirming cure and detecting asymptomatic infection in patients receiving immunosuppressive treatment for autoimmune disease

Biomolecular Mechanisms of Autoimmune Diseases and Their Relationship with the Resident Microbiota: Friend or Foe?

Targeting Regulatory T Cells for Therapy of Lupus Nephritis

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