Analysis of complement deposition and processing on Chlamydia trachomatis

Lausen, Mads; Thomsen, Mikkel Eggert; Christiansen, Gunna; Karred, Nichlas; Stensballe, Allan; Bennike, Tue Bjerg; Birkelund, Svend

doi:10.1007/s00430-020-00695-x

Cited by 9 publications

(3 citation statements)

References 77 publications

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“…These include monoclonal antibodies, peptides and small molecules, but complement specific nanobodies thus far represent an underexplored modality for complement inhibition. While mAbs are widely applied as therapeutics only one nanobody, caplacizumab, a dimeric nanobody against Von Willebrand factor, is clinically approved [124]. Both nanobodies and mAbs bind with high affinity and specificity to their antigen, but nanobodies lack an Fc-fragment and consequently do not engage Fc-receptors and C1q.…”

Section: Nanobodies As Complement Therapeuticsmentioning

confidence: 99%

Nanobodies Provide Insight into the Molecular Mechanisms of the Complement Cascade and Offer New Therapeutic Strategies

et al. 2021

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The complement system is part of the innate immune response, where it provides immediate protection from infectious agents and plays a fundamental role in homeostasis. Complement dysregulation occurs in several diseases, where the tightly regulated proteolytic cascade turns offensive. Prominent examples are atypical hemolytic uremic syndrome, paroxysmal nocturnal hemoglobinuria and Alzheimer’s disease. Therapeutic intervention targeting complement activation may allow treatment of such debilitating diseases. In this review, we describe a panel of complement targeting nanobodies that allow modulation at different steps of the proteolytic cascade, from the activation of the C1 complex in the classical pathway to formation of the C5 convertase in the terminal pathway. Thorough structural and functional characterization has provided a deep mechanistic understanding of the mode of inhibition for each of the nanobodies. These complement specific nanobodies are novel powerful probes for basic research and offer new opportunities for in vivo complement modulation.

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Section: Nanobodies As Complement Therapeuticsmentioning

confidence: 99%

Nanobodies Provide Insight into the Molecular Mechanisms of the Complement Cascade and Offer New Therapeutic Strategies

et al. 2021

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“…Consequent to infection of the upper genital tract, infiltration of neutrophils and monocytes that are responsible for potentially deleterious inflammation along with the bystander T cells both with the potential to cause immunopathology ( 19 ). Highly potent antibodies may also cause corresponding immunopathology through mechanisms such as activation of complement ( 20 ), ADCC (antibody-dependent cellular cytotoxicity) ( 21 ), and the emergence of a type IV hypersensitivity reaction ( 22 ). In addition, immune escape of Chlamydia is also an important reason for chronic recurrent infections, which will be described primarily in this review.…”

Section: Introductionmentioning

confidence: 99%

Insights into innate immune cell evasion by Chlamydia trachomatis

Wang,

Wu,

Fang

et al. 2024

Front. Immunol.

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Chlamydia trachomatis, is a kind of obligate intracellular pathogen. The removal of C. trachomatis relies primarily on specific cellular immunity. It is currently considered that CD4+ Th1 cytokine responses are the major protective immunity against C. trachomatis infection and reinfection rather than CD8+ T cells. The non-specific immunity (innate immunity) also plays an important role in the infection process. To survive inside the cells, the first process that C. trachomatis faces is the innate immune response. As the “sentry” of the body, mast cells attempt to engulf and remove C. trachomatis. Dendritic cells present antigen of C. trachomatis to the “commanders” (T cells) through MHC-I and MHC-II. IFN-γ produced by activated T cells and natural killer cells (NK) further activates macrophages. They form the body’s “combat troops” and produce immunity against C. trachomatis in the tissues and blood. In addition, the role of eosinophils, basophils, innate lymphoid cells (ILCs), natural killer T (NKT) cells, γδT cells and B-1 cells should not be underestimated in the infection of C. trachomatis. The protective role of innate immunity is insufficient, and sexually transmitted diseases (STDs) caused by C. trachomatis infections tend to be insidious and recalcitrant. As a consequence, C. trachomatis has developed a unique evasion mechanism that triggers inflammatory immunopathology and acts as a bridge to protective to pathological adaptive immunity. This review focuses on the recent advances in how C. trachomatis evades various innate immune cells, which contributes to vaccine development and our understanding of the pathophysiologic consequences of C. trachomatis infection.

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“…This C3 convertase cleaves C3 to C3a, a potent pro-inflammatory mediator, and C3b, which via its thioester domain can covalently bind to nearby surfaces containing amino or hydroxyl groups [9,112,124]. After C3b binding to a surface, factor B binds, which is then cleaved by Factor D to Bb and Ba, in the same manner as the fluid phase convertase [9,125]. This yields a surface bound C3 convertase, C3bBb, which has a short half-life of 90s [110].…”

Section: The Alternative Pathwaymentioning

confidence: 99%

Serum and antibiotic resistance of Klebsiella pneumoniae blood isolates

Opstrup¹

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Analysis of complement deposition and processing on Chlamydia trachomatis

Cited by 9 publications

References 77 publications

Nanobodies Provide Insight into the Molecular Mechanisms of the Complement Cascade and Offer New Therapeutic Strategies

Nanobodies Provide Insight into the Molecular Mechanisms of the Complement Cascade and Offer New Therapeutic Strategies

Insights into innate immune cell evasion by Chlamydia trachomatis

Serum and antibiotic resistance of Klebsiella pneumoniae blood isolates

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