Immune evasion strategies of major tick-transmitted bacterial pathogens

Rana, Vipin Singh; Kitsou, Chrysoula; Dumler, J. Stephen; Pal, Utpal

doi:10.1016/j.tim.2022.08.002

Cited by 10 publications

(7 citation statements)

References 110 publications

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“…However, how pathogens evade different protective pathways and persist in the vector need to be explored. Tick-borne pathogens such as Anaplasma , Borrelia burgdorferi sensu lato , Ehrlichia , Francisella , and relapsing fever spirochetes have evolved various immune evasion strategies such as altering surface components, complement inhibition, antimicrobial molecule blocking, and inhibiting cytokines ( 108 ). Several tick-borne microbes modulate their outer-surface constituents via differential expression of various surface proteins through transcriptional regulation and intragenic recombination.…”

Section: Arthropod Vectors Viruses and Innate Immune Responsesmentioning

confidence: 99%

“…Certain pathogens, for example Francisella tularensis mask their surfaces (to evade immune sensing) by synthesizing a carbohydrate-based capsule that inhibits the antibody and complement deposition on the cell wall, and provide protection against microbicidal host responses (for instance, opsonization) ( 111 ). Some bacteria, for example, B. burgdorferi and Anaplasma use host lipids (as a building block for the biogenesis of their membranes) that helps in bypassing host immune responses by avoiding the immune cells ( 108 , 112 ). The cytokines play crucial roles in the integration of the innate and adaptive immune responses that are important for host defense against pathogens; various tick-borne microbes inhibit or enhance cytokine expression ( 108 ).…”

Section: Arthropod Vectors Viruses and Innate Immune Responsesmentioning

confidence: 99%

“…Some bacteria, for example, B. burgdorferi and Anaplasma use host lipids (as a building block for the biogenesis of their membranes) that helps in bypassing host immune responses by avoiding the immune cells ( 108 , 112 ). The cytokines play crucial roles in the integration of the innate and adaptive immune responses that are important for host defense against pathogens; various tick-borne microbes inhibit or enhance cytokine expression ( 108 ). For example, Anaplasma phagocytophilum infection leads to disruption of the IFN-γ (interferon-gamma) signaling pathways and downstream phagocytosis events by neutrophils ( 113 ).…”

Section: Arthropod Vectors Viruses and Innate Immune Responsesmentioning

confidence: 99%

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Host-pathogen interaction in arthropod vectors: Lessons from viral infections

et al. 2023

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Haematophagous arthropods can harbor various pathogens including viruses, bacteria, protozoa, and nematodes. Insects possess an innate immune system comprising of both cellular and humoral components to fight against various infections. Haemocytes, the cellular components of haemolymph, are central to the insect immune system as their primary functions include phagocytosis, encapsulation, coagulation, detoxification, and storage and distribution of nutritive materials. Plasmatocytes and granulocytes are also involved in cellular defense responses. Blood-feeding arthropods, such as mosquitoes and ticks, can harbour a variety of viral pathogens that can cause infectious diseases in both human and animal hosts. Therefore, it is imperative to study the virus-vector-host relationships since arthropod vectors are important constituents of the ecosystem. Regardless of the complex immune response of these arthropod vectors, the viruses usually manage to survive and are transmitted to the eventual host. A multidisciplinary approach utilizing novel and strategic interventions is required to control ectoparasite infestations and block vector-borne transmission of viral pathogens to humans and animals. In this review, we discuss the arthropod immune response to viral infections with a primary focus on the innate immune responses of ticks and mosquitoes. We aim to summarize critically the vector immune system and their infection transmission strategies to mammalian hosts to foster debate that could help in developing new therapeutic strategies to protect human and animal hosts against arthropod-borne viral infections.

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Section: Arthropod Vectors Viruses and Innate Immune Responsesmentioning

confidence: 99%

Section: Arthropod Vectors Viruses and Innate Immune Responsesmentioning

confidence: 99%

Section: Arthropod Vectors Viruses and Innate Immune Responsesmentioning

confidence: 99%

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Host-pathogen interaction in arthropod vectors: Lessons from viral infections

et al. 2023

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“…Once within a tick, the spirochetal bacteria remain dormant in the midgut until a second blood meal taken during the nymphal stage, after which B. burgdorferi migrates to the salivary glands where it is deposited into the skin of an impending host. Perpetuation of B. burgdorferi ’s enzoonotic cycle and persistence within vertebrate reservoirs is contingent on the spirochete’s ability to evade innate and adaptive immunity (Di et al, 2022; Rana et al, 2022). Although humans are incidental (“dead end”) hosts for B. burgdorferi , the spirochetes have the capacity to disseminate and colonize distal tissues, which contributes to the clinical manifestations commonly associated with Lyme disease, including erythema migrans, neuroborreliosis, carditis, and Lyme arthritis (Radolf et al, 2021; Steere et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Structural Elucidation of a Protective B cell Epitope on Outer Surface Protein C (OspC) of the Lyme disease spirochete,Borreliella burgdorferi

Rudolph

Davis

Haque

et al. 2022

Preprint

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Outer surface protein C (OspC) plays a pivotal role in mediating tick-to-host transmission and infectivity of the Lyme disease spirochete, Borreliella burgdorferi. OspC is a helical-rich homodimer that interacts with tick salivary proteins, as well as components of the mammalian immune system. Several decades ago, it was shown that the OspC-specific monoclonal antibody, B5, was able to passively protect mice from experimental tick-transmitted infection by B. burgdorferi strain B31. However, B5's epitope has never elucidated, despite widespread interest in OspC as a possible Lyme disease vaccine antigen. Here we report the crystal structure of B5 antigen-binding fragments (Fabs) in complex with recombinant OspC type A (OspCA). Each OspC monomer within the homodimer was bound by a single B5 Fab in a side-on orientation, with contact points along OspC's a-helix 1 and a-helix 6, as well as interactions with the variable loop between a-helices 5 and 6. In addition, B5's complementarity-determining region (CDR) H3 bridged the OspC-OspC' homodimer interface, revealing the quaternary nature of the protective epitope. To provide insight into the molecular basis of B5 serotype specificity, we solved the crystal structures of recombinant OspC types B and K and compared them to OspCA. This study represents the first structure of a protective B cell epitope on OspC and will aid in the rational design of OspC-based vaccines and therapeutics for Lyme disease.

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Bridging the gap: Insights in the immunopathology of Lyme borreliosis

Snik,

Stouthamer,

Hovius

et al. 2024

Eur J Immunol

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Lyme borreliosis (LB), caused by Borrelia burgdorferi sensu lato (Bbsl) genospecies transmitted by Ixodes spp. ticks, is a significant public health concern in the Northern Hemisphere. This review highlights the complex interplay between Bbsl infection and host–immune responses, impacting clinical manifestations and long‐term immunity. Early localized disease is characterized by erythema migrans (EM), driven by T‐helper 1 (Th1) responses and proinflammatory cytokines. Dissemination to the heart and CNS can lead to Lyme carditis and neuroborreliosis respectively, orchestrated by immune cell infiltration and chemokine dysregulation. More chronic manifestations, including acrodermatitis chronica atrophicans and Lyme arthritis, involve prolonged inflammation as well as the development of autoimmunity. In addition, dysregulated immune responses impair long‐term immunity, with compromised B‐cell memory and antibody responses. Experimental models and clinical studies underscore the role of Th1/Th2 balance, B‐cell dysfunction, and autoimmunity in LB pathogenesis. Moreover, LB‐associated autoimmunity parallels mechanisms observed in other infectious and autoimmune diseases. Understanding immune dysregulation in LB provides insights into disease heterogeneity and could provide new strategies for diagnosis and treatment.

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Immune evasion strategies of major tick-transmitted bacterial pathogens

Cited by 10 publications

References 110 publications

Host-pathogen interaction in arthropod vectors: Lessons from viral infections

Host-pathogen interaction in arthropod vectors: Lessons from viral infections

Structural Elucidation of a Protective B cell Epitope on Outer Surface Protein C (OspC) of the Lyme disease spirochete,Borreliella burgdorferi

Bridging the gap: Insights in the immunopathology of Lyme borreliosis

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