Complement System

C3.

The target of the cytokines.

Antibody independent.

A phenomenon where white blood cells release too many cytokines into the blood too quickly, causing harm to the host.

They stimulate or inhibit activation, proliferation, and differentiation of various cells.

Secondary messengers, typically tyrosine kinases.

Picomolar concentrations of cytokines can produce physiological responses.

They direct the movement of leukocytes around the body and affect leukocyte behavior.

5 minutes.

It enhances the production of C3b, leading to a stronger immune response.

It binds to Factor B.

Keeps macrophages localized at the site of high antigen concentration.

They become leaky, filling the lungs with fluid.

Lysis of cells, bacteria, and viruses, with or without antibody.

It is continuously and spontaneously cleaved into C3a and C3b.

A cytokine that affects cells that are near the secretor.

C4b, C3b, and iC3b.

It alters the behavior of the cell, including gene expression.

They cleave proenzymes to activate them.

Signaling molecules for inflammation.

Neutrophils, basophils, eosinophils, and monocytes.

It leads to oxidative burst and increases production of hydrolytic enzymes.

Immune complexes formed in the diseases.

They damage nearby host cells.

Bacteria and some viruses.

Cytotoxic reactions towards cells and microorganisms.

mRNA real-time quantitative PCR.

The process by which chemokines affect the movement of leukocytes.

Properdin binds and stabilizes C3 convertase, extending its half-life to 30 minutes.

The lectin pathway.

Cytokines with chemotactic activities.

Because they are common and nonspecific.

Attracts monocytes and macrophages to the site of antigen concentration.

Blood clots.

It forms a complex with C1r2s2, causing it to dissociate from C1q.

A cytokine produced mainly by fibroblasts and epithelial cells that induces growth of hematopoietic cells destined to become macrophages and monocytes.

They promote platelet aggregation and activation.

A serological assay for quantitative detection.

They influence the behavior of immune cells and coordinate the immune response.

It cleaves C3 and amplifies the production of more C3b.

It is spontaneously hydrolyzed to form C3a and C3b.

Pleiotropy refers to a cytokine having different biological effects on different target cells.

c-kit Ligand.

C5a, which is 100 times more potent than C3a.

C5, C6, C7, C8, and C9.

Proteolytic cleavage of C3.

An enzymatic cascade.

They can cause lysis of 'bystander' cells, damaging host tissues.

Circulating proteins that bind to carbohydrates.

C5.

Mannose residues on glycoproteins or carbohydrates on microbial membranes.

A serine protease binds to MBL, which can activate either the C1r2s2 enzyme complex or MBL-associated serine protease (MASP).

The spontaneous hydrolysis of complement component C3.

A large group of molecules involved in signaling between cells during immune responses.

On cell membranes.

Inflammation, trauma, and acute illness such as myocardial infarction.

To facilitate phagocytosis and clearance of foreign substances.

Soluble mediators (effectors) of the Innate (Natural) Immune System.

It is an essential part of normal host defense mechanisms.

A heat labile series of 18 plasma proteins, mainly proteolytic enzymes or Serine Proteinases.

Synergy occurs when the combined effect of two cytokines on cellular activity is greater than the sum of their individual effects.

They act as signaling molecules that mediate and regulate immunity, inflammation, and hematopoiesis.

C3b covalently binding to the membrane of a foreign microorganism.

The removal of immune complexes from circulation and their deposition in the spleen and liver.

They block the formation of C3 convertase.

Emboli and damage to tiny pulmonary capillaries.

A link between the lymphoid and the hematopoietic system.

Cytokines secreted by lymphocytes that regulate the function of other cells and tissues.

One peptide binds to the immune complex and becomes a functional part of it (e.g., peptide b).

Interleukins, Interferons (IFNs), Tumor necrosis factors, and Chemokines.

Inactive form.

By the recognition of pathogens with terminal mannose groups.

Factor D cleaves Factor B after it binds to C3b to form Bb.

A structure formed by complement proteins that creates pores in the membranes of target cells.

An antibody-independent means of generating C3 convertase and activating the MAC.

Small peptides that cause increased vascular permeability, contraction of smooth muscle, and release of histamine from basophils and mast cells.

It can be fatal.

It is quickly hydrolyzed and becomes inactivated, stopping complement activation.

It acts as a mediator of inflammation.

It blocks the association between C3b and Bb, preventing the formation of C3 convertase (C3bBb).

LPS (lipopolysaccharides).

They are substances that cause prolonged contraction of smooth muscle, sometimes referred to as slow-reacting substances of anaphylaxis (SRS-A).

If all components are used up, the body cannot continue to fight infection.

IL-1 through IL-18.

It helps them acquire characteristics of specific cell lineages (e.g., Myeloid or Lymphoid).

To amplify the inflammatory response to destroy and clear foreign antigens.

Complement proteins, which are mainly produced by the liver.

Activates them to express HLA-DR molecules and produce active oxygen intermediates.

A cytokine that affects cells in distant parts of the body.

Antibodies bound to the surface of the target.

Proenzymes (zymogens).

Erythrocytes, neutrophils, and monocytes/macrophages.

C3b, B, D, and C3b.

C3bBb.

Liquid chromatography.

It is an important effector of humoral immunity, acting as the 2nd or 3rd line of defense in reference to antibody interaction.

By binding to specific complement receptors on immune system cells, triggering immune responses.

A serine protease that cleaves C4b or C3b, preventing C3 or C5 convertase from forming.

To protect the host.

Enzymes that break down proteins into shorter fragments by hydrolysis of peptide bonds.

Cytokines produced by leukocytes that affect the inflammatory process.

One event must occur before another takes place.

Tumor Necrosis Factor (TNF).

It is almost exactly like the Classical Pathway but is antibody independent.

It diffuses away and can become an inflammatory mediator by binding to a receptor (e.g., peptide a).

To cleave C3 into C3a and C3b, which are crucial for opsonization and inflammation.

C4.

TNF-γ is antagonistic to IL-4.

C1qr2s2.

It binds to the cell surface.

Regulate the intensity and duration of the immune response.

Antibodies and other cytokines.

Proteolytic cleavage by other proteases.

C3 is spontaneously hydrolyzed and C3b binds to microbial surface.

An acute phase protein.

Turns off or inhibits antibody production.

C5b, C6, C7, C8, and C9.

C3a, C4a, and C5a.

By directly killing pathogens and infected cells.

It causes neutrophils to release leukotrienes, which lead to prolonged contraction of smooth muscle.

Cascade induction is when the action of one cytokine on a target cell induces that cell to produce other cytokines, which may then induce additional target cells to produce more cytokines.

It binds soluble C5b67, preventing membrane insertion.

They bind C5b678 on autologous cells, preventing the binding of C9.

They spontaneously inactivate.

It plays a role in inflammatory responses.

No, it does not always have to proceed to lysis to accomplish its goal.

Through three main pathways: classical, alternative, and lectin pathways.

Complement components.

Source: leukocytes; Function: inhibits viral replication.

Diseases that give rise to immune complexes.

Macrophages, monocytes, B & T Cells.

A cytokine that affects the cell that is secreting it.

By binding to specific receptors on their membranes, triggering signal-transduction pathways.

C3bBb3b, which is the C5 convertase for the Alternative Pathway.

Acute respiratory distress syndrome and multiorgan failure.

The C3bBb complex, which is the C3 convertase for the Alternative Pathway.

To lyse target cells by disrupting their membrane integrity.

Properdin.

In the liver.

Antagonism refers to the effect of one cytokine inhibiting or offsetting the effects of another cytokine.

A cytokine that enhances T cell activation, produces fever, and increases acute phase reactants.

C1, C4, C2, C3, C5, C6, C7, C8, C9 (with C4 being out of order).

Interstitial pulmonary edema.

A tyrosine kinase membrane receptor (c-kit).

Small peptides secreted by monocytes that regulate the function of other cells and tissues.

It helps to opsonize pathogens, recruit inflammatory cells, and lyse pathogens.

Through the membrane attack complex (MAC).

They stimulate inflammation and activate PMNs (neutrophils) to release granules.

A pathway activated by the binding of lectins to specific carbohydrates on pathogens.

Increased circulating immune complexes (IgM or IgG) after infection are associated with decreased complement levels.

Mediator of host inflammatory response to infections and other inflammatory stimuli.

C5b (large) and C5a (small).

C5b becomes bound to the Convertase and initiates the assembly of the MAC (C5 - C9).

The initiation of MAC assembly by C5b is similar in both pathways.

Redundancy means that two or more cytokines can mediate similar functions, making it difficult to attribute a specific activity to a single cytokine.

Messengers of the immune system.

It attracts neutrophils to sites of infection or inflammation.

C3bBb3b cleaves C5.

They catalyze metabolic processes.

C1qr2s2, which binds the Fc portion of two IgG antibody molecules or one IgM.

It binds C3b for cleavage by Factor I.

To make bone marrow stem cells responsive to CSFs without causing colony formation.

It may sustain their viability and proliferative capacity.

C5 Convertase.

A part of the immune system that enhances the ability to clear microbes and damaged cells.

Classical pathway, alternative pathway, and lectin pathway.

Interfere with viral replication in an infected cell.

T cells and other cell lines.

They prevent excessive complement activation and protect host cells.

Over 200 molecules.

C2 into C2a and C2b.

It indicates ongoing activation and depletion of complement levels.

Inflammatory bone resorption, gout, and promotes Helper T Cell response.

Deficient innate immunity and acute-phase responses, lymphopenia.

A chemical messenger that causes migration of cells in a particular direction.

C4b-binding protein and C1 inhibitor.

It blocks the formation of C3 convertase (C4b2a) by binding C4b for cleavage by Factor I.

Deposition of opsonins on antigens, promoting stable adhesive contact with phagocytic cells.

It speeds the dissociation of C3 convertase.

Immature stem cells.

A cytokine produced by fibroblasts and epithelial cells that induces growth of hematopoietic stem cells destined to become granulocytes.

They can stimulate the growth and development/expansion of various leukocytes or erythroid colonies from bone marrow cells.

C3 Convertase.

TNF-α.

To enhance the ability of antibodies and phagocytic cells to clear pathogens.

Acts against virally infected cells and tumor cells.

By opsonization of microbes.

It removes immune complexes from circulation and deposits them in the spleen and liver.

Source: fibroblasts; Function: inhibits viral replication.

Helps stabilize the MAC for full lysis capability.

T Cell growth factor, enhances cytotoxicity of T cell and NK cells.

Immune suppression; decreases antigen presentation and MHC class II expression.

Multiple (~8) cytokines simultaneously in a single sample.

A cytokine produced by activated T cells and other cell lines that stimulates an increased supply of granulocytic cells and macrophages.

By stromal cells of the bone marrow.

Consumption of components through unregulated amplification.

Communication between white blood cells.

Yes, it can be regulated specifically for one particular pathway or multiple pathways.

C3b undergoes hydrolysis.

Circulating lectins binding to microbial polysaccharides.

The binding of antibodies to antigens.

It is initiated by the spontaneous hydrolysis of C3 and does not require antibodies.

IFN α, IFN β, and IFN γ.

Systemic Lupus Erythematosus (SLE).

Susceptibility to extracellular pathogens and allergic asthma.

In the beta 1 and beta 2 globulin fractions.

In the gamma fraction.

Each activated enzyme can generate multiple activated enzymes at the next step, leading to amplification of enzymatic events.

C5 - C9.

TNF-β.

Mannose-binding lectin (MBL).

A pathway that is triggered by the binding of antibodies to pathogens.

Formation of the membrane attack complex (MAC) that can lyse pathogens.

Source: T-helper (CD4), T cytotoxic (CD8), and NK cells; Function: has antiviral effects, activates macrophages, NK cells, and stimulates B-cells to make antibodies.

Binding of C1q to IgM or IgG antigen-antibody complexes.

Less than 2%.

The C3 convertase complex.

Macrophages, T Cells, fibroblasts, and others.

Impaired Helper T Cell responses and increased susceptibility to intracellular pathogens.

They may lyse, producing anemic conditions.

It results in two peptides.

Leukocytes, specifically T cells and macrophages.

They are generated early in the cascade and play a major role in destroying foreign antigens.

Cytokines.

Increases their expression.

Through various regulatory proteins that prevent damage to host cells.

It attracts and cleaves C4 into C4a and C4b.

Proliferation and differentiation of Helper T Cells; promotes IgG and IgE isotype switching.

Differentiation and proliferation; promotes Helper T Cells and cytotoxicity.

By increasing soluble factors or cells involved in the inflammatory process.

Augments the activity of many cytokines.

The binding of mannose-binding lectin (MBL) to specific carbohydrates on pathogens.

Enhancing phagocytosis, promoting inflammation, and directly lysing pathogens.

C5b-8.

The C5 convertase complex.

Lymphoproliferative disease and susceptibility to autoimmune disease.

Immune pathology due to uncontrolled inflammation.

It is identical, differing only in the initiation and activation steps.

It suggests that complement has been excessively activated, is currently being consumed, or a single component is absent due to a genetic defect.

T Cells and Mast Cells.

Macrophages, B cells, neutrophils, dendritic cells.

T, B, NK cells, and macrophages.

Differentiated T helper cells, Tregs, B cells, dendritic cells, others.

Inflammatory and co-stimulatory action; induces proliferation and differentiation.