The complement system

2010 ◽  
pp. 213-224
Author(s):  
Marina Botto ◽  
Mark J. Walport
Keyword(s):  
Immune System ◽  
Complement System ◽  
Immune Complexes ◽  
Innate Immune System ◽  
Inflammatory Responses ◽  
Antibody Responses ◽  
Host Defence ◽  
System P ◽  
Dying Cells ◽  
The Complement System

The complement system consists of over 20 distinct proteins and is an essential component of the innate immune system. It is a major effector mechanism of host defence against infection and inflammatory responses, has an important role in the physiological removal of immune complexes and dying cells, and plays an accessory role in the induction of antibody responses....

The complement system

2020 ◽  
pp. 315-324
Author(s):  
Marina Botto ◽  
Matthew C. Pickering
Keyword(s):  
Complement System ◽  
Inflammatory Responses ◽  
Membrane Integrity ◽  
Membrane Attack Complex ◽  
Cell Membrane Integrity ◽  
Biological Responses ◽  
Target Cell Membrane ◽  
Membrane Bound ◽  
Dying Cells ◽  
The Complement System

The complement system, consisting of soluble and membrane-bound proteins, is a major effector mechanism of host defence against infection and inflammatory responses. It has an important role in the removal of immune complexes and dying cells, and also modulates humoral and cell-mediated immune responses. Complement activation occurs through three pathways, each generating enzyme complexes, termed C3 convertases. These cleave native C3 to form C3b and C3a. C3b can covalently attach to surfaces (e.g. pathogen surfaces) where it triggers biological responses following interaction with membrane-bound receptors and can also trigger cleavage of native C5 to C5b and C5a. C5b triggers the formation of the membrane attack complex, which disrupts target cell membrane integrity and may result in cell lysis.

scholarly journals Interactions of the innate immune system with carbon nanotubes

2017 ◽  
Vol 2 (4) ◽  
pp. 174-186 ◽  
Author(s):  
Kirsten M. Pondman ◽  
Carolina Salvador-Morales ◽  
Basudev Paudyal ◽  
Robert B. Sim ◽  
Uday Kishore
Keyword(s):  
Carbon Nanotubes ◽  
Immune System ◽  
Complement System ◽  
Innate Immune System ◽  
Innate Immune ◽  
Therapeutic Targeting ◽  
The Complement System

The complement system can interact with nanoparticles and alter the intended therapeutic targeting.

scholarly journals Insidious pathogen-mimicking properties of nanoparticles in triggering the lectin pathway of the complement system

2015 ◽  
Vol 7 (3) ◽  
Author(s):  
S. Moein Moghimi ◽  
Peter P. Wibroe ◽  
Linping Wu ◽  
Z. Shadi Farhangrazi
Keyword(s):  
Immune System ◽  
Complement System ◽  
Innate Immune System ◽  
Innate Immune ◽  
Engineered Nanoparticles ◽  
Lectin Pathway ◽  
Structural Motifs ◽  
Polymeric Surface ◽  
The Complement System ◽  
Independent Reaction

AbstractThe lectin pathway of the complement system is an integral component of the innate immune system recognizing pathogens through patterns of sugar moieties displayed on their surfaces and neutralizing them through an antibody-independent reaction cascade. Many engineered nanoparticles incite complement through the lectin pathway, but these nanoparticles inherently do not express surface-exposed sugars. However, the projected polymeric surface architecture of nanoparticles may transiently resemble structural motifs of peptidoglycan constituents of pathogens and trigger the lectin pathway. We discuss these issues in relation to nanomedicine design and immune safety.

Das Komplementsystem

2012 ◽  
Vol 32 (04) ◽  
pp. 276-285 ◽  
Author(s):  
V. Frauenknecht ◽  
V. Schroeder
Keyword(s):  
Coronary Artery Disease ◽  
Complement System ◽  
Innate Immune System ◽  
Innate Immune ◽  
The Other ◽  
Atherosclerotic Plaques ◽  
Inflammatory Processes ◽  
Artery Disease ◽  
The Complement System ◽  
Novel Therapeutic

SummaryAtherosclerotic diseases such as coronary artery disease and ischaemic stroke are caused by chronic inflammation in arterial vessel walls. The complement system is part of the innate immune system. It is involved in many processes contributing to onset and development of atherosclerotic plaques up to the final stage of acute thrombotic events. This is due to its prominent role in inflammatory processes. In addition, there is increasing evidence that interactions between complement and coagulation provide a link between inflammation and thrombosis. On the other hand, the complement system also has an atheroprotective function through the clearance of apoptotic material.The knowledge of these complex mechanisms will become increasingly important, also for clinicians, since it may lead to novel therapeutic and diagnostic options. Therapies targeting the complement system have the potential to reduce tissue damage caused by acute ischaemic events. Whether early anti-inflammatory and anti-complement therapy may be able to prevent atherosclerosis, remains a hot topic for research.

scholarly journals Effect of Hypoglycemia on Inflammatory Responses and the Response to Low-Dose Endotoxemia in Humans

2018 ◽  
Vol 104 (4) ◽  
pp. 1187-1199 ◽  
Author(s):  
Ahmed Iqbal ◽  
Lynne R Prince ◽  
Peter Novodvorsky ◽  
Alan Bernjak ◽  
Mark R Thomas ◽  
...  
Keyword(s):  
Cardiovascular Risk ◽  
Immune System ◽  
Innate Immune System ◽  
Low Dose ◽  
Inflammatory Responses ◽  
Platelet Reactivity ◽  
Innate Immune ◽  
Endotoxin Challenge ◽  
Intermediate Monocytes

Abstract Context Hypoglycemia is emerging as a risk for cardiovascular events in diabetes. We hypothesized that hypoglycemia activates the innate immune system, which is known to increase cardiovascular risk. Objective To determine whether hypoglycemia modifies subsequent innate immune system responses. Design and Setting Single-blinded, prospective study of three independent parallel groups. Participants and Interventions Twenty-four healthy participants underwent either a hyperinsulinemic-hypoglycemic (2.5 mmol/L), euglycemic (6.0 mmol/L), or sham-saline clamp (n = 8 for each group). After 48 hours, all participants received low-dose (0.3 ng/kg) intravenous endotoxin. Main Outcome Measures We studied in-vivo monocyte mobilization and monocyte-platelet interactions. Results Hypoglycemia increased total leukocytes (9.98 ± 1.14 × 109/L vs euglycemia 4.38 ± 0.53 × 109/L, P < 0.001; vs sham-saline 4.76 ± 0.36 × 109/L, P < 0.001) (mean ± SEM), mobilized proinflammatory intermediate monocytes (42.20 ± 7.52/μL vs euglycemia 20.66 ± 3.43/μL, P < 0.01; vs sham-saline 26.20 ± 3.86/μL, P < 0.05), and nonclassic monocytes (36.16 ± 4.66/μL vs euglycemia 12.72 ± 2.42/μL, P < 0.001; vs sham-saline 19.05 ± 3.81/μL, P < 0.001). Following hypoglycemia vs euglycemia, platelet aggregation to agonist (area under the curve) increased (73.87 ± 7.30 vs 52.50 ± 4.04, P < 0.05) and formation of monocyte-platelet aggregates increased (96.05 ± 14.51/μL vs 49.32 ± 6.41/μL, P < 0.05). Within monocyte subsets, hypoglycemia increased aggregation of intermediate monocytes (10.51 ± 1.42/μL vs euglycemia 4.19 ± 1.08/μL, P < 0.05; vs sham-saline 3.81± 1.42/μL, P < 0.05) and nonclassic monocytes (9.53 ± 1.08/μL vs euglycemia 2.86 ± 0.72/μL, P < 0.01; vs sham-saline 3.08 ± 1.01/μL, P < 0.05), with platelets compared with controls. Hypoglycemia led to greater leukocyte mobilization in response to subsequent low-dose endotoxin challenge (10.96 ± 0.97 vs euglycemia 8.21 ± 0.85 × 109/L, P < 0.05). Conclusions Hypoglycemia mobilizes monocytes, increases platelet reactivity, promotes interaction between platelets and proinflammatory monocytes, and potentiates the subsequent immune response to endotoxin. These changes may contribute to increased cardiovascular risk observed in people with diabetes.

The complement system: a pathway linking host defence and adipocyte biology

1999 ◽  
Vol 29 (8) ◽  
pp. 653-656 ◽  
Author(s):  
Esterbauer ◽  
Krempler ◽  
Oberkofler ◽  
Patsch
Keyword(s):  
Complement System ◽  
Host Defence ◽  
System A ◽  
The Complement System

Search for Circulating Immune Complexes and Activation of the Complement System in Relation to Estrogen Treatment

1987 ◽  
Vol 66 (8) ◽  
pp. 703-708
Author(s):  
Anne Bukh ◽  
Hakon Kaalund Jensen ◽  
Hans Jakob Andersen ◽  
Peter Bonne Eriksen ◽  
Niels Peter ◽  
...  
Keyword(s):  
Complement System ◽  
Immune Complexes ◽  
Circulating Immune Complexes ◽  
Estrogen Treatment ◽  
The Complement System

scholarly journals Binding of phosphatidylserine-positive microparticles by PBMCs classifies disease severity in COVID-19 patients

2021 ◽  
Author(s):  
Lisa Rausch ◽  
Konstantin Lutz ◽  
Martina Schifferer ◽  
Elena Winheim ◽  
Rudi Gruber ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Disease Severity ◽  
Inflammatory Responses ◽  
Immune Dysfunction ◽  
Coagulation Cascade ◽  
Activated Platelets ◽  
Programmed Death ◽  
Dying Cells ◽  
The Complement System

Infection with SARS-CoV-2 is associated with thromboinflammation, involving thrombotic and inflammatory responses, in many COVID-19 patients. In addition, immune dysfunction occurs in patients characterized by T cell exhaustion and severe lymphopenia. We investigated the distribution of phosphatidylserine (PS), a marker of dying cells, activated platelets, and platelet-derived microparticles (PMP), during the clinical course of COVID-19. We found an unexpectedly high amount of blood cells loaded with PS+ PMPs for weeks after the initial COVID-19 diagnosis. Elevated frequencies of PS+PMP+ PBMCs correlated strongly with increasing disease severity. As a marker, PS outperformed established laboratory markers for inflammation, leucocyte composition, and coagulation, currently used for COVID-19 clinical outcome prognosis. PS+ PMPs preferentially bound to CD8+ T cells with gene expression signatures of proliferating effector rather than memory T cells. As PS+ PMPs carried programmed death-ligand 1 (PD-L1), they may affect T cell expansion or function. Our data provide a novel marker for disease severity and show that PS, which can trigger the blood coagulation cascade, the complement system, and inflammation, resides on activated immune cells. Therefore, PS may serve as a beacon to attract thromboinflammatory processes toward lymphocytes and cause immune dysfunction in COVID-19.

scholarly journals Pathologies of the complement system

2020 ◽  
Vol 19 (1) ◽  
pp. 131-138
Author(s):  
A. A. Butilin ◽  
A. E. Filippova ◽  
S. S. Shakhidzhanov ◽  
F. I. Ataullakhanov
Keyword(s):  
Immune System ◽  
Complement System ◽  
The Complement System

Complement system is a part of the immune system that provides organism cells with protection against foreign pathogens. Various kinds of defects in the complement system can induce development of serious diseases. This review summarizes different malfunctions of the complement system and also shows how these defects can result in development of severe diseases.

scholarly journals Adjuvant Lineage-Negative Cell Therapy as a Potential Silencer of the Complement-Mediated Immune System in ALS Patients

2021 ◽  
Vol 10 (22) ◽  
pp. 5251
Author(s):  
Anna Sobuś ◽  
Bartłomiej Baumert ◽  
Monika Gołąb-Janowska ◽  
Piotr Kulig ◽  
Edyta Paczkowska ◽  
...  
Keyword(s):  
Immune System ◽  
Cell Therapy ◽  
Complement System ◽  
Autologous Bone Marrow ◽  
Medical Intervention ◽  
Complement Components ◽  
Inflammatory Reactions ◽  
Sporadic Als ◽  
Als Patients ◽  
The Complement System

ALS remains a fatal, neurodegenerative motor neuron disease. Numerous studies seem to confirm that innate immune system is involved in the pathophysiology of ALS. Hence, the assessment of the complement system and attempts to modify its activity remain the target of medical intervention in ALS. In the present study, three intrathecal administrations of autologous bone marrow-derived lineage-negative (Lin–) cells were performed every 6 weeks in 20 sporadic ALS patients. The concentrations of various complement components in the cerebrospinal fluid and plasma at different time points after cell injection were quantified using a Luminex multiplex. The results of the complement system were correlated with the level of leukocytes, neutrophils, lymphocytes, fibrinogen and CRP in the peripheral blood and the functional status of ALS patients using Norris and ALS-FRSr scales. The study showed a statistically significant decrease in plasma C3b concentration in all 7th days after cell application. In parallel, a peak decrease in neutrophil count and CRP level was observed on days 5–7, with a simultaneous maximum clinical improvement on days 7–28 of each Lin– cell administration. Adjuvant Lin– cell therapy appears to have the silencing potential on the complement-mediated immune system and thus suppress pro-inflammatory reactions responsible for neurodegeneration. However, further in-depth studies are necessary to address this issue.

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