# data[].attributes.body
Mannose binding lectin
Binds to mannose or carbo on antigen (generally bacteria)

# data[].attributes.body
Form from Cleavage of C5 by C5 convertase
--> Initiate formation of MAC

# data[].attributes.body
C6 is a park of MAC.
C7 exposed hydrophobic site will allow it to be inserted into phospholipid bilayer of the pathogen

# data[].attributes.body
the C5 convertase that is found in the classical and lectin pathways
comprises of C4b2a (C3 convertase in these 2 pathways),  and C3b

in both pathways, after cleavage of C3 to form C3a and C3b, the increased concentration of C3b causes C3b to bind and form a complex with C4b2a to form the C5 convertase.

C4b2aC3b cleaves C5 to form C5a and C5b

# data[].attributes.body
Factor D which is a serine protease will cleave Factor B into Ba & Bb.
Bb will then bind to C3b to form C3bBb complex (also known as C3 convertase).
Ba will diffuse away

# data[].attributes.body
C3BbC3b is a C5 convertase of the alternative spontaneous pathway. The amplification of C3bBbP loop causes saturation of C3b on the surface of the cell. A molecule of C3b will bind to C3Bb to form C3BbC3b.

# data[].attributes.body
C4b is formed after C4 is cleaved by the activated C1s molecule, into 2 proteolytic fragments of C4a and C4b.

C4b is an opsonin, which assists in opsonization, (together with C3b) as they will be covalently bonded to a surface molecule of a pathogen. Once bounded, they can be recognised by the phagocytes receptors, signalling for phagocytosis.

Another role that C4b plays is in the forming of C4b2a (c3 convertase), because when C2 is cleaved into C2a and C2b, C2a will bind with C4b, hence forming the bimolecular complex is C4b2a that will cleave C3.

# data[].attributes.body
After formation of C3bBb (alternate C3 convertase), Factor P(properdin) binds to it. This stabilizes the convertase as it promotes association of C3b & Bb.

# data[].attributes.body
The Complement C5 protein is comprised of the C5 alpha and beta chains, which are linked by a disulfide bridge.

# data[].attributes.body
C3bBb is the C3 is the C3 convertase of the Spontaneous pathway. It cleaves C3 to form C3a and C3b

# data[].attributes.body
C3 gets cleaved by C3 convertase from either of the 3 pathways  to form the C3a and C3b
C3b will be used to make C5 convertase later or be used in positive loop
C3a and b will be used as chemoattractant. a for mast and basophils and b for neutrophil and macrophages

# data[].attributes.body
C8 binds to the C5b67 complex and inserts into the cell membrane
C9 molecules will bind to the complex and polymerize to form a pore in the membrane. The pore consists of 10-16 C9 molecules.

# data[].attributes.body
C4b2a is now known as C4b2b. It is C3 convertase which catalyzes the cleavage of C3 into C3a and C3b.
It can be found in both lectin and classical pathway.

# data[].attributes.body
- complex that catalyzes cleavage of C5 into C5a and C5b
- exists in all pathways: Classical + Lectin = C4b2a3b
Alternative = C3bBbC3

# data[].attributes.body
From the above explanations, we can see that there are cleaved complement fragments which are C3a, C4a and C5a.
There are anaphylatoxins and acts as chemoattractants to initiate inflammation

Their function is to activate local blood vessels to induce inflammation by vasodilation and attract immune cells, antibodies and complement proteins to site of infection

C3a and C4a attracts mast cells and basophils that induces degranulation and release inflammation mediators like histamine.

C5a activates neutrophils and macrophages. Most potent chemoattractant for neutrophils

# data[].attributes.body
formed by cleavage of C2 by C1S in classical pathway and cleaved by MASP-2 in MBL pathway
C2b will bind to c4b to form c4b2b complex  also known as c3 convertase
C2a will be diffused out which have other functions that is not yet established

# data[].attributes.body
C3b binds to complement receptors on phagocytes and opsonisation of pathogens occur.

Opsonisation is when the antibody binds to the antigen for better recognition by phagocytes to engulf and destroy the antigen. The Fc receptors (complement receptor CR1) of phagocytes will bind to the antibody.

# data[].attributes.body
After the cleavage of C5 into C5a and C5b, C5b will associate with C6, C7 and C8, producing a multimolecular complex which will disrupt the cell membrane of the pathogenic cell. C9 will bind to C8 and will polymerise, forming a large pore in the cell membrane. The pore is large enough to allow water molecules and ions to diffuse into the pathogenic cell. This will lead to cell lysis due to the osmotic pressure created by the water molecules entering the cell. The MAC can be found in all 3 pathways and the formation of the membrane attack complex is called as the terminal complement pathway.

# data[].attributes.body
C5a is cleaved by C5 molecule. C5a is potent to chemoattractant. C5a attract macrophages and neutrophils. In this case the reruitment of inflammatory cells. This will then contribute to innate immune function.

# data[].attributes.body
initiating serine protease. MASP-1 activates MASP-2. MASP-2 initiates the lectin pathway by triggering the activation of C4 & C2

# data[].attributes.body
C3 Convertase catalyses the cleavage of C3 into C3a and C3b.
Each pathways have C3 Convertase present

Classical pathway : C4b2b
Lectin pathway : C4b2b
Alternative pathway : C3bBb

# data[].attributes.body
C4 is a central protein that is used in both  the classical and lectin  pathway.
classical pathway: C4 is cleaved by the activated  C1s molecule in C1 into 2 polyteolytic fragments : small peptide, C4a and a larger fragment C4b

lectin pathway: similar to the classical pathway, after the activation of MASP- 2 will cleave to C4 and C2  to produce the C3 convertase.

# data[].attributes.body
C3 will spontaneously hydrolyze into C3(H20).
C3(H20): Has binding site for Factor B.
C3(H20)---Factor B: Will be cleaved by Factor D into 2 fragments, Bb & Ba.
Bb: Will then associate with C3(H20) to form a C3(H20)Bb (fluid phase C3 convertase) to cleave C3 into C3a & C3b.

# data[].attributes.body
-Cleaved complement fragment of C4
-Induces the effector function, inflammation
-Attracts immune cells, antibodies, mast cells and neutrophils to produce more inflammation mediators
-occurs in Classical and Lectic pathway

# data[].attributes.body
C2 is a protein encoded by the gene C2 and it is part of the complement system in the classical and lectin pathway. When C1 is activated, it will cleave C2 to form C2a and C2b.

# data[].attributes.body
C1q is involve in innate complement system. Which involves antibodies. C1q is an enzyme that recognize and bind to antibodies IgG/ IgM that are non-covalently attached to pathogens.

Activated C1q cleave C2 to C2a and C2b. C4 to C4a and C4b. Cleaved C2 and C4 form C3 convertase C4bc2b/ c4bc2a.

C1q  is important to start the classical cascade pathway.

# data[].attributes.body
When the antibodies igM or igG binds to the antigen of the pathogen, a AG-AB complex is formed where the C1 complex binds to the Fc portion of the AB with the complement protein C1q and the zymogens C1r and C1s. The binding of C1q causes conformational change in the C1 complex which activates an autocatalytic conversion of C1r. The activated C1r then cleaves the C1s into an active serine protease to cleave C2 and C4