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      New insights into Trypanosoma cruzi genetic diversity, and its influence on parasite biology and clinical outcomes

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          Abstract

          Chagas disease, caused by Trypanosoma cruzi, remains a serious public health problem worldwide. The parasite was subdivided into six distinct genetic groups, called “discrete typing units” (DTUs), from TcI to TcVI. Several studies have indicated that the heterogeneity of T. cruzi species directly affects the diversity of clinical manifestations of Chagas disease, control, diagnosis performance, and susceptibility to treatment. Thus, this review aims to describe how T. cruzi genetic diversity influences the biology of the parasite and/or clinical parameters in humans. Regarding the geographic dispersion of T. cruzi, evident differences were observed in the distribution of DTUs in distinct areas. For example, TcII is the main DTU detected in Brazilian patients from the central and southeastern regions, where there are also registers of TcVI as a secondary T. cruzi DTU. An important aspect observed in previous studies is that the genetic variability of T. cruzi can impact parasite infectivity, reproduction, and differentiation in the vectors. It has been proposed that T. cruzi DTU influences the host immune response and affects disease progression. Genetic aspects of the parasite play an important role in determining which host tissues will be infected, thus heavily influencing Chagas disease’s pathogenesis. Several teams have investigated the correlation between T. cruzi DTU and the reactivation of Chagas disease. In agreement with these data, it is reasonable to suppose that the immunological condition of the patient, whether or not associated with the reactivation of the T. cruzi infection and the parasite strain, may have an important role in the pathogenesis of Chagas disease. In this context, understanding the genetics of T. cruzi and its biological and clinical implications will provide new knowledge that may contribute to additional strategies in the diagnosis and clinical outcome follow-up of patients with Chagas disease, in addition to the reactivation of immunocompromised patients infected with T. cruzi.

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          Pathogen recognition and innate immunity.

          Microorganisms that invade a vertebrate host are initially recognized by the innate immune system through germline-encoded pattern-recognition receptors (PRRs). Several classes of PRRs, including Toll-like receptors and cytoplasmic receptors, recognize distinct microbial components and directly activate immune cells. Exposure of immune cells to the ligands of these receptors activates intracellular signaling cascades that rapidly induce the expression of a variety of overlapping and unique genes involved in the inflammatory and immune responses. New insights into innate immunity are changing the way we think about pathogenesis and the treatment of infectious diseases, allergy, and autoimmunity.
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            Toll-Like Receptor Signaling Pathways

            Toll-like receptors (TLRs) play crucial roles in the innate immune system by recognizing pathogen-associated molecular patterns derived from various microbes. TLRs signal through the recruitment of specific adaptor molecules, leading to activation of the transcription factors NF-κB and IRFs, which dictate the outcome of innate immune responses. During the past decade, the precise mechanisms underlying TLR signaling have been clarified by various approaches involving genetic, biochemical, structural, cell biological, and bioinformatics studies. TLR signaling appears to be divergent and to play important roles in many aspects of the innate immune responses to given pathogens. In this review, we describe recent progress in our understanding of TLR signaling regulation and its contributions to host defense.
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              Complement: a key system for immune surveillance and homeostasis.

              Nearly a century after the significance of the human complement system was recognized, we have come to realize that its functions extend far beyond the elimination of microbes. Complement acts as a rapid and efficient immune surveillance system that has distinct effects on healthy and altered host cells and foreign intruders. By eliminating cellular debris and infectious microbes, orchestrating immune responses and sending 'danger' signals, complement contributes substantially to homeostasis, but it can also take action against healthy cells if not properly controlled. This review describes our updated view of the function, structure and dynamics of the complement network, highlights its interconnection with immunity at large and with other endogenous pathways, and illustrates its multiple roles in homeostasis and disease.
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                Author and article information

                Contributors
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                Journal
                Front Immunol
                Front Immunol
                Front. Immunol.
                Frontiers in Immunology
                Frontiers Media S.A.
                1664-3224
                09 April 2024
                2024
                : 15
                : 1342431
                Affiliations
                [1] 1 Integrated Biomarker Research Group, René Rachou Institute, Fiocruz Minas, Oswaldo Cruz Foundation , Belo Horizonte, Minas Gerais, Brazil
                [2] 2 Department of Pharmacy, Federal University of the Jequitinhonha and Mucuri Valleys , Diamantina, Minas Gerais, Brazil
                Author notes

                Edited by: Annette Dougall, Department of Agriculture, Fisheries and Forestry, Australia

                Reviewed by: Kathryn Marie Jones, Baylor College of Medicine, United States

                Angel Ramos-Ligonio, Universidad Veracruzana, Mexico

                Luisa Magalhaes, Universidade Federal de Minas Gerais, Brazil

                *Correspondence: Glaucia Diniz Alessio, glauciabiologia@ 123456yahoo.com.br ; Helen Rodrigues Martins, helen.martins@ 123456ufvjm.edu.br

                †These authors have contributed equally to this work and share first authorship

                ‡These authors share senior authorship

                Article
                10.3389/fimmu.2024.1342431
                11035809
                38655255
                af0718b6-02fc-41ad-a237-9bcaa983833e
                Copyright © 2024 Silvestrini, Alessio, Frias, Sales Júnior, Araújo, Silvestrini, Brito Alvim de Melo, Martins-Filho, Teixeira-Carvalho and Martins

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 21 November 2023
                : 26 February 2024
                Page count
                Figures: 3, Tables: 1, Equations: 0, References: 428, Pages: 32, Words: 19960
                Funding
                The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by Fundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG) (Process APQ-02434-16), Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) and Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES). The authors thank the Integrated Center for Postgraduate Studies and Research in Health at UFVJM, Diamantina, MG; Pharmacy Department and Centro René Rachou. ATC received PQ fellowships from CNPq.
                Categories
                Immunology
                Review
                Custom metadata
                Parasite Immunology

                Immunology
                chagas disease,trypanosoma cruzi,dtu,infectivity,immune response,pathogenesis
                Immunology
                chagas disease, trypanosoma cruzi, dtu, infectivity, immune response, pathogenesis

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