C0009546 - The complement system of plasma proteins is an important part of the immune system that forms a cascade of factors that lyses foreign cells. There are two branches of the complement system, the classical pathway that is initiated by antibody-antigen complexes on a cell and the alternative pathway that is antibody independent. The ultimate result in either pathway is the creation of the membrane attack complex, a large pore in the cell membrane that results in cell lysis. The alternative pathway starts with the spontaneous conversion of C3 to an active protease. C3 contains a thioester group that is spontaneously hydrolyzed at a slow rate to create C3(H2O). From there, binding of factor B (Fb) and activation by factor D (Fd) cleaves factor B to create the active protease C3 convertase (AP convertase). This enzyme cleaves C3 to form C3b, which can go on to form a C5 activating convertase. At this point the alternative pathway proceeds in the same manner as the classical pathway, recruiting additional complement factors (C6, C7, C8 and C9) to ultimately form the membrane attack complex and lyse the associated cell. One question about the alternative pathway is how the spontaneous activation of C3 in plasma leads to the lysis of specific cells in the absence of antibody on the cell surface. Active C3b binds to the cell surface, particularly to complement activators like cell wall components and lipopolysaccharide. A constant low level of spontaneous C3b formation ensures that C3b can bind to invading cells and trigger the rest of the alternative complement pathway to lyse the cells even in the absence of an antibody response. The constant low level of C3b activation and potential activation of the alternative pathway is kept in check by a natural damper, factor H and factor I. Factors H and I in plasma inactivate C3b enzyme in solution. Factors H and I cannot inactivate C3b on the cell surface due to protection by properdin, ensuring that the alternative pathway is primarily inactive in plasma and specifically activated on the surface of invading. (This definition may be outdated

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Lang Dictionary CODE			LUI	preferred no	SUI	preference Yes / No	Terms, descriptions
							CUI C0009546

Russian	Medical Subject Headings Russian	D003170	L3353091	preferred	S3880551	Y	КОМПЛЕМЕНТА АКТИВАЦИЯ, АЛЬТЕРНАТИВНЫЙ ПУТЬ
Russian	Medical Subject Headings Russian	D003170	L0897286	no	S1101103	Y	KOMPLEMENTA AKTIVATSIIA, AL'TERNATIVNYI PUT'
Russian	Medical Subject Headings Russian	D003170	L1508072	no	S1803981	Y	AL'TERNATIVNYI PUT' AKTIVATSII KOMPLEMENTA
Russian	Medical Subject Headings Russian	D003170	L1537460	no	S1833369	Y	PROPERDINOVYI PUT'
Russian	Medical Subject Headings Russian	D003170	L3337763	no	S3865244	Y	АЛЬТЕРНАТИВНЫЙ ПУТЬ АКТИВАЦИИ КОМПЛЕМЕНТА
Russian	Medical Subject Headings Russian	D003170	L3365461	no	S3892945	Y	ПРОПЕРДИНОВЫЙ ПУТЬ
	Medical Subject Headings				A0041527	AT53895225	Complement activation initiated by the interaction of microbial ANTIGENS with COMPLEMENT C3B. When COMPLEMENT FACTOR B binds to the membrane-bound C3b, COMPLEMENT FACTOR D cleaves it to form alternative C3 CONVERTASE (C3BBB) which, stabilized by COMPLEMENT FACTOR P, is able to cleave multiple COMPLEMENT C3 to form alternative C5 CONVERTASE (C3BBB3B) leading to cleavage of COMPLEMENT C5 and the assembly of COMPLEMENT MEMBRANE ATTACK COMPLEX.
	Gene Ontology				A11589137	AT148901468	Any process involved in the activation of any of the steps of the alternative pathway of the complement cascade which allows for the direct killing of microbes and the regulation of other immune processes. [GOC:add, ISBN:0781735149]
	(CPTSP) CRISP Thesaurus				A4366655	AT51224156	complement activation sequence initiated by the activation of complement factor C3, which is triggered by the interaction of microbial polysaccharides and properdin without participation of an antigen-antibody reaction.
	NCI BioCarta online maps of molecular pathways, adapted for NCI use				A7568664	AT224185275	The complement system of plasma proteins is an important part of the immune system that forms a cascade of factors that lyses foreign cells. There are two branches of the complement system, the classical pathway that is initiated by antibody-antigen complexes on a cell and the alternative pathway that is antibody independent. The ultimate result in either pathway is the creation of the membrane attack complex, a large pore in the cell membrane that results in cell lysis. The alternative pathway starts with the spontaneous conversion of C3 to an active protease. C3 contains a thioester group that is spontaneously hydrolyzed at a slow rate to create C3(H2O). From there, binding of factor B (Fb) and activation by factor D (Fd) cleaves factor B to create the active protease C3 convertase (AP convertase). This enzyme cleaves C3 to form C3b, which can go on to form a C5 activating convertase. At this point the alternative pathway proceeds in the same manner as the classical pathway, recruiting additional complement factors (C6, C7, C8 and C9) to ultimately form the membrane attack complex and lyse the associated cell. One question about the alternative pathway is how the spontaneous activation of C3 in plasma leads to the lysis of specific cells in the absence of antibody on the cell surface. Active C3b binds to the cell surface, particularly to complement activators like cell wall components and lipopolysaccharide. A constant low level of spontaneous C3b formation ensures that C3b can bind to invading cells and trigger the rest of the alternative complement pathway to lyse the cells even in the absence of an antibody response. The constant low level of C3b activation and potential activation of the alternative pathway is kept in check by a natural damper, factor H and factor I. Factors H and I in plasma inactivate C3b enzyme in solution. Factors H and I cannot inactivate C3b on the cell surface due to protection by properdin, ensuring that the alternative pathway is primarily inactive in plasma and specifically activated on the surface of invading. (This definition may be outdated - see the DesignNote.)