Product Description

iC3b (inactivated C3b) is derived from C3b.Conversion of C3b to iC3b destroys almost all of the functional binding sites present on C3b.C3b itself is produced by all three pathways of complement (Law, S.K.A. and Reid, K.B.M. (1995)) when native C3 is cleaved releasing C3a.iC3b is prepared by cleavage of C3b by factor I in the presence of factor H.Cleavage by factors H and I occurs rapidly when the C3b is free in solution and is slower when it is attached to a surface.Other cofactors for factor I also permit cleavage if C3b to iC3b and these include the two membrane proteins CR1 (CD35) and MCP (CD46).Factor I can cleave C3b in two places in the alpha chain and if both sites are cleaved a small fragment (C3f, 2,000 Da) is released.Thus, iC3b may be a mixture of 176,000 and 174,000 molecular weight proteins.If the C3b precursor was attached to a surface, the iC3b remains on that surface.The iC3b sold by CompTech is made from fluid phase C3b and is not capable of attaching to a surface.Surface-bound C3b and iC3b are linked to the target through a covalent bond which may be either an ester bond or an amide bond.Ester bonds are unstable resulting in the gradual release from the particle.Most of the C3b generated during complement activation never attaches to a surface because its thioester reacts with water forming fluid phase C3b.Surface-bound iC3b and its breakdown product C3d are recognized by numerous receptors on lymphoid and phagocytic cells which use these ligands to stimulate phagocytosis and antigen presentation to cells of the adaptive immune system.Receptors for iC3b are CR2 (CD21) found on B-cells and CR3 (CD11b/CD18) found on phagocytes (Dodds, A.W. and Sim, R.B. editors (1997); Morley, B.J. and Walport, M.J. (2000)).One of the results of iC3b-receptor interaction is an expansion of target-specific B-cell and T-cell populations.

(For full product description see link...)

Complement Technology的C1是级联反应中的第一个补体成分，称为补体经典途径。C1与抗原结合的抗体（免疫复合物）结合并被其激活，从而产生引发级联反应的蛋白酶。C1实际上是钙依赖性复合物中结合在一起的三种不同蛋白质（C1q，C1r和C1s）的非共价复合物。C1q通过其六个臂中的两个或多个与IgG或IgM的Fc结构域结合。多臂与免疫复合物的结合被认为会引入压力，从而导致复合物中的两个C1r蛋白（蛋白酶酶原）自身激活，从而产生两种活性的C1r丝氨酸蛋白酶（Morikis，D.和Lambris，JD（2005））。 。这些激活的C1r亚基裂解并激活复合物中的两个C1s蛋白酶酶原。活化的C1裂解补体成分C4，释放出C4a，并启动C4b与活化表面的共价连接。活化的C1也切割C2，并且C2的较大片段结合至表面附着的C4b，形成C4b，C2a，其为经典途径的C3 / C5转化酶。