[LEC/LAB] Complement System Flashcards
3 PATHWAYS OF THE COMPLEMENT SYSTEM
CLASSICAL
ALTERNATIVE
MANNAN BINDING LECTIN
ORIGINAL NAME OF THE ALTERNATIVE PATHWAY
PROPERDIN SYSYTEM
WHAT USED TO BE DEEMED AS THE MAIN INITIATOR OF THE ALTERNATIVE PATHWAY
PROPERDIN
WHERE ARE MOST PLASMA COMPLEMENT PROTEINS SYNTHESIZED
LIVER
WHAT COMPLEMENT COMPONENT IS NOT SYNTHESIZED BY THE LIVER
C1
WHERE IS C1 SYNTHESIZED
INTESTINAL EPITHELIAL CELLS
SERUM PROTEIN THAT IS SYNTHESIZED IN THE ADIPOSE TISSUE
FACTOR D
ADDITIONAL SOURCE OF EARLY COMPLEMENT COMPONENTS
MONOCYTES
MACROPHAGES
[TRUE OR FALSE]
MOST OF THE PROTEINS INVOLVED IN THE COMPLEMENT SYSTEM ARE ACTIVE PRECURSORS
FALSE
INACTIVE PRECURSORS OR ZYMOGENS
[FUNCTION OF THE SERUM PROTEIN]
C1q
BINDS TO FC REGION OF IGM AND IGG
[FUNCTION OF THE SERUM PROTEIN]
C1r
ACTIVATES C1s
[FUNCTION OF THE SERUM PROTEIN]
C1s
CLEAVES C4 AND C2
[FUNCTION OF THE SERUM PROTEIN]
C4
PART OF THE C3 CONVERTASE
[PROTEIN COMPONENTS]
C3 CONVERTASE
C4b2a
[FUNCTION OF THE SERUM PROTEIN]
C2
BINDS TO C4B
FORMS C3 CONVERTASE
[FUNCTION OF THE SERUM PROTEIN]
C3
KEY INTERMEDIATE IN ALL PATHWAYS
[FUNCTION OF THE SERUM PROTEIN]
C5
INITIATES MAC
[FUNCTION OF THE SERUM PROTEIN]
C6
BINDS TO C5b IN MAC
[FUNCTION OF THE SERUM PROTEIN]
C7
BINDS TO C5bC6 IN MAC
[FUNCTION OF THE SERUM PROTEIN]
C8
STARTS PORE FORMATION ON MEMBRANE
[FUNCTION OF THE SERUM PROTEIN]
C9
POLYMERIZES TO CAUSE CELL LYSIS
[PROTEIN COMPONENT]
C5 CONVERTASE
C4b2a3b
[PROTEIN COMPONENT]
MAC
C5b6789
[FUNCTION OF THE SERUM PROTEIN]
FACTOR B
BINDS TO C3B TO FORM C3 CONVERTASE
[FUNCTION OF THE SERUM PROTEIN]
FACTOR D
CLEAVES FACTOR B
[FUNCTION OF THE SERUM PROTEIN]
PROPERDIN
STABILIZES C3 CONVERTASE
ALTERNATIVE PATHWAY — C3bBb
[FUNCTION OF THE SERUM PROTEIN]
MBL
BINDS TO MANNOSE
[FUNCTION OF THE SERUM PROTEIN]
MASP-1
UNKNOWN
[FUNCTION OF THE SERUM PROTEIN]
MASP-2
CLEAVES C4 AND C2
MAIN ANTIBODY DIRECTED MECHANISM
CLASSICAL
ARE ALL IMMUNOGLOBULINS ABLE TO ACTIVATE THE CLASSICAL PATHWAY
NO
IG CLASSES THAT CAN ACTIVATE THE CLASSICAL PTW
IGM
IGG1
IGG2
IGG3
IG CLASSES THAT CANNOT ACTIVATE THE CLASSICAL PATHWAY
IGG4
IGA
IGE
IG CLASS THAT IS MOST EFFICIENT IN ACTIVATING THE COMPLEMENT AND WHY
IGM
MULTIPLE BINDING SITES
WHO WON A NOBEL PRIZE FOR DESCRIBING THE COMPLEMENT SYSTEM
JULES BORDET
IS THE COMPLEMENT CONSIDERED AS AN ACUTE PHASE REACTANT
WHY OR WHY NOT
YES
LEVELS RISE DURING AN INFECTION
IS THE COMPLEMENT SYSTEM HEAT LABILE
YES
SERUM IS HEATED TO 56C FOR 30 MINS
WILL THE COMPLEMENT SYSTEM BE ACTIVATED EVEN IF EPITOPES ARE FAR FROM EACH OTHER
NO
MOST EFFECTIVE IGG SUBUNIT FOR COMPLEMENT ACTIVATION
IGG3
IGG3>IGG1>IGG2
3 MAIN STAGES OF COMPLEMENT ACTIVATION
RECOGNITION — C1
ACTIVATION — C4, C2, C3
MAC — C56789
UNIT THAT COMPLETES THE LYSIS OF FOREGN PARTICLES
MAC
C56789
WHAT IS MAINTAINS THE STRUCTURE OF THE RECOGNITION UNIT
CALCIUM
C1 UNIT THAT BINDS TO AB MOLECULES
C1Q
C1 SUBUNITS THAT GENERATE ENZYME ACTIVITY TO BEGIN THE CASCADE
C1R
C1S
WHAT HAPPENS WHEN CALCIUM IS NOT PRESENT IN SERUM
C1R AND C1S DISSOCIATE FROM C1Q
WHAT REGION OF THE AB DOES C1Q RECOGNIZE
FC REGION
SERINE PROTEASE PROENZYMES
C1R
C1S
STRUCTURAL REQUIREMENT FOR C1 TO BE BOUND TO THE FC REGION
AT LEAST TWO OF THE GLOBULAR HEADS OF C1Q
AS BINDING OCCURS, WHAT ARE C1R AND C1S CONVERTED TO
ACTIVE ENZYMES
THEY ARE ORIGINALLY ZYMOGENS
WHAT IS A ZYMOGEN
INACTIVE ENZYME
WHY IS ACTIVATED C1R EXTREMELY SPECIFIC
ITS ONLY KNOWN SUBSTRATE IS C1S
DOES C1S HAVE LIMITED SPECIFICITY
WHY OR WHY NOT
YES
ITS ONLY SUBSTRATES ARE C4 AND C2
WHEN DOES THE RECOGNITION STAGE END
ONCE C1S IS ACTIVATED
WHEN DOES THE ACTIVATION STAGE START
WHEN C1S CLEAVES C4
WHEN DOES THE ACTIVATION STAGE END
WHEN C5 CONVERTASE IS PRODUCED
SECOND MOST ABUNDANT COMPLEMENT PROTEIN
C4
WHAT HAPPENS TO C4B WHEN IT FAILS TO BIND WITH A PROTEIN WITHIN A FEW SECONDS
IT REACTS WITH WATER
iC4B IS FORMED
iC4B IS RAPIDLY DEGRADED
COMPLEMENT CANNOT PROCEED
RATIO OF C1 TO C4 MOLECULES
1 C1 MOLECULE : 30 C4 MOLECULES (TO BE SPLIT)
BASIS OF NAMING COMPLEMENT PROTEINS
ORDER OF DISCOVERY
THE C2 GENE IS CLOSELY ASSOCIATED WITH THE GENE THAT CODES FOR THIS SERUM PROTEIN
FACTOR B
THE ONLY SERUM PROTEIN THAT BINDS “A”
C2a
C3B CAN ALSO SERVE AS WHAT KIND OF PROTEIN
OPSONIN
WHY ARE A LARGE NUMBER OF C3 MOLECULES NEEDED IN THE AMPLIFICATION STAGE
TO INCREASE THE CHANCES OF C3 BINDING
C3 HAS A SHORT HALF LIFE
C3 NEEDS TO BE BOUND IMMEDIATELY
IF NOT THEN IT BECOMES HYDROLYZED
POLYPEPTIDE CHAINS IN C5
ALPHA
BETA
WHERE DOES C5b ATTACH
TO THE CELL MEMBRANE
FUNCTION OF C8’S HYDROPHOBIC PART
ANCHOR THE MAC WITHIN THE TARGET MEMBRANE
PATHWAY ACTIVATED BY THE RECOGNITION OF SURFACE MOIETIES FOUND ON PATHOGENS
LECTIN
PATHWAY THAT PROVIDES AN ADDITIONAL LINK BETWEEN THE INNATE AND ACQUIRED IMMUNE RESPONSE
LECTIN PATHWAY
WHY IS THE LECTIN PATHWAY A LINK BETWEEN THE INNATE AND ACQUIRED IMMUNE RESPONSE
IT INVOLVES THE NONSPECIFIC RECOGNITION OF CARBOHYDRATES THAT ARE COMMON CONSTITUENTS OF MICROBIAL CELL WALLS
ARE THE LECTIN PATHWAY MOLECULES STRUCTURALLY SIMILAR TO THOSE OF THE CLASSICAL
YES
COMPLEMENT PROTEINS SHARED BY THE LECTIN AND CLASSICAL PATHWAYS
C4
C2
THREE CLASSES OF MOLECULES FOUND IN THE LECTIN PATHWAY
LECTINS
FOLINS
CL-K1
PROTEIN CLASS OF LECTINS, FOLINS, CL-K1, AND C1Q
COLLECTINS
IS MBL BINDING CALCIUM DEPENDENT
YES
WHERE IS MANNOSE FOUND
GLYCOPROTEINS OR CARBOHYDRATES OF MICROORGANISMS
WHY IS MBL CONSIDERED AS AN ACUTE PHASE PROTEIN
PRODUCED IN THE LIVER
NORMALLY PRESENT IN THE SERUN
INCREASES DURING AN INITIAL INFLAMMATORY RESPONSE
PATHWAY THAT PLAYS A ROLE IN INFANT’S DEFENSE MECHANISM
LECTIN PATHWAY
PATHWAY THAT FUNCTIONS AS AN AMPLIFICATION LOOP
ALTERNATIVE PATHWAY
TRIGGERING SUBSTANCES FOR THE ALTERNATIVE PATHWAY
BACTERIAL CELL WALLS
ROLE OF FACTOR B IS ANALOGOUS TO WHAT COMPLEMENT COMPONENT
C2
MAJOR FUNCTIONS OF THE COMPLEMENT SYSTEM
OPSONIZATION
INFLAMMATION
CYTOTOXICITY
[COMPLEMENT NOMENCLATURE]
i
INDICATED INACTIVATION
[COMPLEMENT NOMENCLATURE]
HORIZONTAL BAR
COMPLEMENT PROTEIN IS AN ACTIVE ENZYME
HEATING CONDITION AFTER 4 HOURS DELAY IN COMPLEMENT TESTING
RE-INACTIVATE SERUM AT 56C FOR 10 MINS
[PATHWAY ACTIVATED BY GIVEN INITIATOR]
IMMUNE COMPLEXES
CLASSICAL
[PATHWAY ACTIVATED BY GIVEN INITIATOR]
APOPTOTIC CELLS
COMPLEMENT
[PATHWAY ACTIVATED BY GIVEN INITIATOR]
GRAM NEGATIVE BACTERIA
CLASSICAL
[PATHWAY ACTIVATED BY GIVEN INITIATOR]
CRP
CLASSICAL
[PATHWAY ACTIVATED BY GIVEN INITIATOR]
BACTERIA, FUNGI, VIRUSES
ALTERNATE
[PATHWAY ACTIVATED BY GIVEN INITIATOR]
TUMOR CELLS
ALTERNATE
[PATHWAY ACTIVATED BY GIVEN INITIATOR]
MICROBES WITH TERMINAL MANNOSE GROUPS
MBL
[SIMILAR FUNCTION]
[MBL AND CLASSICAL]
MBL
C1Q
[SIMILAR FUNCTION]
[MBL AND CLASSICAL]
MASP-1
C1R
[SIMILAR FUNCTION]
[MBL AND CLASSICAL]
MASP-2
C1S
[FUNCTION OF THE SERUM PROTEIN]
C1-INH
DISSOCIATES C1R AND C1S FROM C1Q
[FUNCTION OF THE SERUM PROTEIN]
FACTOR I
CLEAVES C3B AND C4B
[FUNCTION OF THE SERUM PROTEIN] FACTOR H
COFACTOR WITH I TO INACTIVATE C3B
PREVENTS BINDING OF B TO C3B
[FUNCTION OF THE SERUM PROTEIN] C4BP
ACTS AS A COFACTOR WITH I TO INACTIVATE C4B
[FUNCTION OF THE SERUM PROTEIN] S PROTEIN
VITRONECTIN
PREVENTS ATTACHMENT OF C5B67 COMPLEX TO CELL MEMBRANES
CR1 IS ALSO KNOWN AS
CD35
[FUNCTION OF THE SERUM PROTEIN]
DAF
DISSOCIATES C3 CONVERTASE
[FUNCTION OF THE SERUM PROTEIN]
HRF
INHIBITS MAC
[FUNCTION OF THE SERUM PROTEIN]
MIRL OR CD59
INHIBITS MAC
SUBSTANCE THAT PROMOTES THE PRODUCTION OF HISTAMINE
ANAPHYLOTOXINS
PROTEINS THAT CAN PROMOTE VASODILATION
KININS
SHOULD IMMUNE COMPLEXES REMAIN IN THE BODY
NO
[COMPLEMENT COMPONENT/SERUM PROTEIN]
PROKININ
C2B
[COMPLEMENT COMPONENT/SERUM PROTEIN]
ANAPHYLOTOXIN
C3A
C4A
C5A
[COMPLEMENT COMPONENT/SERUM PROTEIN]
OPSONIN
C3B
C4B
[COMPLEMENT COMPONENT/SERUM PROTEIN]
CHEMOTACTIC FACTOR
C5A
[COMPLEMENT COMPONENT/SERUM PROTEIN]
CHEMOTOXIN
C5B67
ABILITY OF CELLS TO BIND COMPLEMENT COATED PARTICLES
IMMUNE ADHERENCE
MOST EFFICICENT COFACTOR FOR FACTOR I-MEDIATED CLEAVAGE OF C3B
MCP
CD46
PROTECTS THE HOST CELLS FROM BYSTANDER LYSIS
DAF
[COMPLEMENT COMPONENT/SERUM PROTEIN]
IMMUNE ADHERENCE
C3B
[ASSOCIATED DISEASE]
C1QRS
LUPUS ERYTHRMATOUS-LIKE SYNDROME
RECURRENT INFECTIONS
[ASSOCIATED DISEASE]
C2
LUPUS ERYTHEMATOUS-LIKE SYNDROME
RECURRENT INFECTIONS
ATHEROSCLEROSIS
[ASSOCIATED DISEASE]
C3
SEVERE RECURRENT INFECTIONS
[ASSOCIATED DISEASE]
C4
LUPUS LIKE SYNDROME
[ASSOCIATED DISEASE]
C5678
NEISSERIA INFECTION
[ASSOCIATED DISEASE]
C9
NONE
[ASSOCIATED DISEASE]
C1-INH
HEREDITARY ANGIOEDEMA
[ASSOCIATED DISEASE]
DAF
PAROXYSMAL NOCTURNAL HEMOGLOBINURIA
[ASSOCIATED DISEASE]
HRF
PAROXYSMAL NOCTURNAL HEMOGLOBINURIA
[ASSOCIATED DISEASE]
FACTOR H OR I
RECURRENT BACTERIAL INFECTIONS
[ASSOCIATED DISEASE]
MBL
PNEUMOCOCCAL DISEASE
SEPSIS
NEISSERIA INFECTIONS
WHAT DECREASES THE DIAMETER OF BLOOD VESSELS VIA IMMUNE COMPLEXES
MICROCLOTS
INHIBITOR THAT LEADS TO FRAGMENTOCYTES
ANTIFACTOR H
DIFFERENCE OF CH50 VS AH50
CH50
Sheep RBC
AH50
Rabbit RBC
[COMPLEMENT ASSAY INTERPRETATION]
CH50 LOW
AH50 NORMAL
MISSING C1QRS
MISSING C4
[COMPLEMENT ASSAY INTERPRETATION]
CH50 NORMAL
AH50 LOW
MISSING PROPERDIN
MISSING FACTOR B OR D
[COMPLEMENT ASSAY INTERPRETATION]
CH50 LOW
AH50 LOW
MISSING C3
MISSING C56789
[COMPLEMENT ASSAY INTERPRETATION]
LATE COMPONENTS LOW
MISSING FACTOR H OR I
WHAT HOLDS C1QRS TOGETHER
CALCIUM
BETA GLOBULIN THAT ORIGINATES FROM PROC4
C4
WILL A PRIMITIVE MECHANISM REQUIRE C1, C2, AND C4
NO
C3Bb IS DEPENDENT ON WHAT ION
MAGNESIUM