CHAPTER 5 Flashcards
1
Q
The immune system is composed of what two systems?
A
the phylogenetically oldest highly diversified innate immune system and the adaptive immune system
2
Q
What are discussed in previous chapters?
A
Some components of the innate or natural immune system (e.g. phagocytosis)
3
Q
What does this chapter discuss?
A
the other components of the innate immune system: the complement system and other circulating effector proteins of innate immunity including cytokines and acute-phase reactants
4
Q
What are finely balanced?
A
Regulatory mechanisms of complement
5
Q
What is the activation of complement focused on?
A
the surface of invading microorganisms with limited complement deposited on normal cells and tissues
6
Q
What may the complement system cause if the mechanisms that regulate its delicate balance malfunction?
A
injury to cells tissues and organs such as destruction of the kidneys in systemic lupus erythematosus or hemolytic anemias
7
Q
What is complement?
A
a heat-labile series of 18 plasma proteins many of which are enzymes or proteinases
8
Q
Collectively what are these proteins?
A
a major fraction of the beta-1 and beta-2 globulins
9
Q
How are the complement system proteins named?
A
with a capital C followed by a number
10
Q
What does a small letter after the number indicate?
A
that the protein is a smaller protein resulting from the cleavage of a larger precursor by a protease
11
Q
What happens to several complement proteins during activation of the complement system?
A
they are cleaved
12
Q
How are the fragments designated?
A
with lower case suffixes such as C3a and C3b
13
Q
Usually how is the larger fragment designated?
A
as “b”
14
Q
Usually how is the smaller fragment designated?
A
as “a”
15
Q
What is the exception to this rule?
A
the designation of the C2 fragments
16
Q
How is the larger fragment of C2 designated?
A
C2a
17
Q
How is the smaller fragment of C2 designated?
A
C2b
18
Q
What are proteins of the alternative activation pathway called?
A
factors
19
Q
How are proteins of the alternative activation pathway symbolized?
A
by letters such as B
20
Q
What do control proteins include?
A
the inhibitor of C1 (C1 INH) factor I and factor H
21
Q
What does the complement system display?
A
three overarching physiologic activities
22
Q
These are initiated in various ways through what three pathways?
A
Classic pathway Alternative pathway and Mannose-binding lectin pathway
23
Q
The three pathways converge at what point?
A
the point of cleavage of C3 to C3b
24
Q
What is the central event of the common final pathway?
A
the cleavage of C3 to C3b
25
The common final pathway in turn leads to what?
the activation of the lytic complement sequence C5 through C9 and cell destruction
26
Normally how are complement components present in the circulation?
in an inactive form
27
In addition what is normally present to inhibit uncontrolled complement activation?
the control proteins C1 INH factor I factor H and C4-binding protein (C4-bp)
28
Under normal physiologic conditions what probably also happens?
activation of one pathway probably also leads to the activation of another pathway
29
How is the classic pathway initiated?
by the bonding of the C1 complex consisting of C1q C1r and C1s to antibodies bound to an antigen on the surface of a bacterial cell
30
How is the alternative pathway initiated?
by contact with a foreign surface such as the polysaccharide coating of a microorganism and the covalent binding of a small amount of C3b to hydroxyl groups on cell surface carbohydrates and proteins
31
What happens to the pathway by low-grade cleavage of C3 in plasma?
it is activated
32
How is the mannose-binding lectin pathway initiated?
by binding of the complex of mannose-binding lectin and associated serine proteases (MASP1 and MASP2) to arrays of mannose groups on the surface of a bacterial cell
33
After complement is initially activated what happens to each enzyme precursor?
it is activated by the previous complement component or complex which is a highly specialized proteinase
34
What does this convert the enzyme precursor to?
its catalytically active form by limited proteolysis
35
The pathways leading to the cleavage of C3 are what?
triggered enzyme cascades
36
During this activation process what is cleaved?
a small peptide fragment is cleaved a membrane-binding site is exposed and the major fragment binds
37
As a consequence what is formed?
the next active enzyme of the sequence is formed
38
Because each enzyme can activate many enzyme precursors what happens?
each step is amplified until the C3 stage
39
Therefore what does the whole system form?
an amplifying cascade
40
What do various cell types express?
surface membrane glycoproteins that react with one or more of the fragments of C3 produced during complement activation and degradation
41
What do the functions of these receptors depend on?
the type of cell
42
What does CR1 enhance?
phagocytosis
43
What is also important in these host defense mechanisms?
CR3
44
What does Plasmodium falciparum adhesin PfRh4 bind to?
complement receptor type-1 (CR1) on human erythrocytes
45
What is CR1?
a complement regulator and immune adherence receptor on erythrocytes
46
What is CR1 required for?
shuttling C3bC4b-opsonized particles to the liver and spleen for phagocytosis
47
What do the activation of complement and the products formed during the complement cascade have?
a variety of physiologic and cellular consequences
48
What do physiologic consequences include?
blood vessel dilation and increased vascular permeability
49
What do cellular consequences include?
Cell activation Cytolysis or hemolysis and Opsonization
50
What is the most important biologic role of complement in blood group serology?
the production of cell membrane lysis of antibody-coated targets
51
What does opsonization render cells?
vulnerable to phagocytosis
52
In addition to the function of complement as a major effector of antigen-antibody interaction what have physiologic concentrations of complement been found to induce?
profound alterations in the molecular weight composition and solubility of immune complexes
53
The activation of complement may also play a role in what?
mediating hypersensitivity reactions
54
This process may occur from what?
direct alternative pathway activation by immunoglobulin E (IgE)–antigen complexes or through a sequence initiated by the activated Hageman coagulation factor that causes the generation of plasmin which subsequently activates the classic pathway
55
In either case what does activation of complement components from C3 onward lead to?
the generation of anaphylatoxins in an immediate-hypersensitivity reaction
56
Although the principal source of synthesis of complement in vivo is debatable where are the majority of the plasma complement components made?
in hepatic parenchymal cells
57
What is one of the major effector mechanisms of antibody-mediated immunity?
Classical complement pathway
58
Which complement pathway is activated by antigen-antibody complexes?
Classical complement pathway
59
What are the principal components of the classical pathway?
C1 through C9
60
What is the activation sequence of the classical pathway components?
C1
61
Which complement component is most abundant in plasma?
C3
62
What is the major quantitative reaction of the complement cascade?
C3 fixation
63
Where are most plasma complement components synthesized?
Hepatic parenchymal cells
64
Where is the C1 complex primarily synthesized?
Gastrointestinal and urogenital tract epithelium
65
What are the three major stages of the classical pathway?
Recognition
66
What is the recognition unit of the classical pathway?
C1 complex (C1q
67
How many IgG molecules are required to activate C1?
At least two
68
Which antibody class can activate C1 with a single molecule?
IgM
69
What ion is essential for C4bC2 complex formation?
Magnesium (Mg²⁺)
70
What enzyme cleaves C4 and C2 in the classical pathway?
C1s protease
71
What complex serves as the C3 convertase in the classical pathway?
C4bC2a
72
Which fragment contains the catalytic site of C3 convertase?
C2a
73
What happens to the C2b fragment after cleavage?
Released into the environment
74
What are the products of C3 cleavage?
C3a (inflammatory) and C3b (opsonin)
75
What complex cleaves C5 in the classical pathway?
C4bC2aC3b (C5 convertase)
76
What are the products of C5 cleavage?
C5a (chemotactic) and C5b (MAC initiator)
77
What pore-forming complex causes cell lysis?
C5b-9 (Membrane Attack Complex/MAC)
78
Besides antibodies
what else can activate C1q directly?
79
What clinical condition involves classical pathway activation by β-amyloid?
Alzheimer’s disease
80
How does classical pathway activation combat HIV?
Antibodies trigger MAC formation on infected cells
81
What role does C3b play in immunity?
Opsonization and immune complex clearance
82
What regulates classical pathway activation to prevent host damage?
C1 inhibitor (C1INH) and Decay-Accelerating Factor (DAF)
83
Which complement pathway links adaptive and innate immunity?
Classical pathway
84
What happens when C1q binds to antigen-antibody complexes?
Conformational change activates C1r/C1s proteases
85
Why is C4b restricted to pathogen surfaces?
Its reactive thioester bond rapidly deactivates in fluid phase
86
How does classical pathway activation influence transplant rejection?
Promotes antibody-mediated injury and T-cell alloreactivity
87
What phenomenon allows grafts to survive despite DSA and C4d deposition?
Accommodation
88
Which complement receptor amplifies B-cell responses?
CR2 (binds C3d)
89
What therapeutic peptide activates classical pathway against tumors?
Tachyplesin
90
How does obesity relate to classical pathway activation?
Increased C1 production causes tissue inflammation
91
What role does C5a play in inflammation?
Recruits and activates phagocytes
92
Which pathway converges with the classical pathway at C3 convertase?
Lectin and alternative pathways
93
What structural feature enables C1q to bind multiple targets?
Six globular heads connected by collagen-like tails
94
How does classical pathway activation enhance adaptive immunity?
Promotes antigen presentation and B-cell memory
95
What happens to C4b not attached to pathogens?
Hydrolyzed and inactivated by water
96
Which autoimmune disease involves classical pathway activation by immune complexes?
Systemic Lupus Erythematosus (SLE)
97
What complement deficiency strongly correlates with lupus-like symptoms?
C1q deficiency
98
How does IgM combat methicillin-resistant Staphylococcus aureus?
Activates classical pathway for bacterial lysis
99
What role does C1q play in immune education?
Facilitates antigen presentation via immune complex trafficking
100
What triggers the amplification of the proteolytic complement cascade?
Activation of C1s by antigen-antibody complexes
101
What components are sequentially cleaved during amplification?
Complement factors C3
102
What complex is formed on the cell membrane during amplification?
C5b
103
At which stage does the complement cascade reach full amplitude?
C3 cleavage stage
104
What is the role of the C4bC2a complex?
Acts as the classic pathway C3 convertase
105
How does the C4bC2a complex activate C3?
Splits C3a (anaphylatoxin) from the N-terminal end of C3
106
What is exposed on the C3b fragment after cleavage?
A reactive binding site
107
Where do C3b molecules bind after activation?
Near the C4bC2a complex on the cell surface
108
How many C3b molecules can one catalytic site bind?
Several hundred
109
Why is the C3 cleavage reaction highly efficient?
C3 is present in high plasma concentration
110
What complex forms when C3b combines with C4bC2a?
C4bC2aC3b (C5 convertase)
111
What initiates C5b fixation and MAC formation?
C3b-mediated cleavage of C5 into C5a and C5b
112
What happens to C3b molecules not part of the C5 convertase?
Form an opsonic coat for immune adherence
113
What mediates immune adherence of opsonized targets?
C3b receptors on phagocytic cells
114
What proteins form the initial MAC complex?
C5b
115
What property allows C5b-7 to bind membranes?
Hydrophobic regions from C7
116
What phenomenon occurs when C5b-7 binds non-target cells?
Reactive lysis of bystander cells
117
What stabilizes the membrane-bound C5b-7 complex?
Interaction with C8 and C9
118
How does polymerized C9 contribute to MAC?
Forms a transmembrane tubule (pore)
119
What is the structure of the MAC pore?
Hollow cylinder spanning the membrane
120
What physical effect does the MAC pore have?
Allows free ion flow across the membrane
121
Which ions flow out due to the MAC pore?
Intracellular ions (K+
122
Why does water flood into cells with MAC pores?
Osmotic imbalance from retained large molecules
123
What is the final consequence of MAC formation?
Cell lysis via osmotic disruption
124
What is the alternative complement pathway?
A non-antibody-initiated pathway activated by microbial surfaces and foreign materials
125
How does the alternative pathway differ from the classical pathway?
Omits C1
126
What activates the alternative pathway?
Microbial surfaces
127
What is the key feature of alternative pathway activation?
Does not require antigen-antibody complexes
128
Which components are excluded in the alternative pathway?
C1
129
What is the counterpart of C2a in the alternative pathway?
C3a
130
What structural similarity exists between the pathways?
Factor B resembles C2
131
What complex initiates C3 activation in the alternative pathway?
C3b
132
How is the C3b
Bb complex formed?
133
What is the role of factor D?
Cleaves factor B into Bb (active) and Ba (inactive)
134
What stabilizes the C3b
Bb convertase?
135
What controls the alternative pathway feedback loop?
Factor H displaces factor B from C3b
136
How does factor H regulate C3b?
Blocks C3b
137
What determines factor B vs. H binding to C3b?
Surface type: activator surfaces (e.g.
138
What is the final C5 convertase in the alternative pathway?
C3b
139
How does the alternative pathway connect to MAC formation?
Cleaves C5 to initiate C5b-9 assembly
140
What role does properdin play?
Stabilizes C3b
141
What disease involves alternative pathway activation by erythrocytes?
Paroxysmal nocturnal hemoglobinuria (PNH)
142
What is the physiological advantage of the alternative pathway?
Provides immediate defense before antibody production
143
What activates the mannose-binding lectin pathway?
Mannose-binding lectin binding to terminal mannose groups on bacteria
144
What are MASP enzymes?
Mannose-binding lectin-associated serine proteases (MASP1/MASP2)
145
How does mannose-binding lectin structurally relate to C1q?
Homologous collagenous lectin structure
146
What causes mannose-binding lectin deficiency?
Three point mutations reducing lectin levels
147
Which pathway does mannose-binding lectin activation resemble?
Classical pathway via serine protease activation
148
What is the role of collectins?
Pattern recognition molecules in innate immunity (e.g.
149
How does C3b tagging differ between pathways?
Alternative pathway uses spontaneous hydrolysis (tickover) for initial C3b
150
What happens to C3b on non-activator surfaces?
Bound by factor H and inactivated by factor I
151
Why is properdin critical for amplification?
Prevents C3b
152
What is Ba’s physiological role?
Glycine-rich α2-globulin fragment considered inert
153
What are the two primary biological functions of the complement system?
Cell lysis by the membrane attack complex (MAC) and biological effects of proteolytic fragments
154
How does the MAC cause cell lysis?
Creates pores in cell membranes
155
What role do proteolytic fragments of complement play?
Mediate immune/inflammatory effects by binding to receptors on phagocytes or endothelium
156
What happens if complement components are deficient?
Decreased activation leads to impaired immunity (e.g.
157
What causes elevated complement levels?
Inflammation
158
What does low complement indicate?
Excessive activation
159
Which deficiencies increase susceptibility to pyogenic infections?
Opsonic defects
160
Why are MAC deficiencies linked to Neisseria infections?
MAC is critical for lysing Neisseria meningitidis
161
How does mannose-binding lectin deficiency affect immunity?
Increases infection risk in young children due to impaired innate defense
162
What is the role of regulatory proteins like Factor H?
Prevent excessive complement activation on host cells
163
How does complement contribute to thrombosis?
Activation damages endothelium
164
Why is hypocomplementemia common in SLE?
Immune complexes consume complement components (e.g.
165
How do complement levels recover after activation?
Rapid synthesis restores normal levels within 1-2 days
166
What is the role of C5a?
Acts as a chemoattractant and activates mast cells to release histamine
167
Why is C3 elevation nonspecific clinically?
It occurs in many inflammatory conditions without diagnostic specificity
168
How does opsonization work?
C3b coats pathogens for phagocyte recognition via CR1/CR3 receptors
169
How does complement cause autoimmune damage?
Uncontrolled activation lyses host cells and drives inflammation
170
Why are infants vulnerable with mannose-binding lectin deficiency?
They lack maternal antibodies and mature adaptive immunity
171
How does the lectin pathway recognize pathogens?
Mannose-binding lectin binds terminal mannose groups on microbes
172
What happens to C3b on host cells?
Factor H and Factor I inactivate it to prevent self-attack
173
How does the alternative pathway differ from the classical?
Activated by microbial surfaces (not antibodies) and uses Factor B instead of C2
174
What is reactive lysis?
C5b-7 binds bystander cells
175
C1q deficiency associated diseases?
SLE-like syndrome
176
C1r deficiency associated diseases?
SLE-like syndrome
177
C1s deficiency associated diseases?
SLE
178
C1 INH deficiency associated diseases?
Hereditary angioedema
179
C2 deficiency associated diseases?
Recurrent pyogenic infections
180
C3 deficiency associated diseases?
Recurrent pyogenic infections
181
C3 inactivator deficiency associated diseases?
Recurrent pyogenic infections
182
C4 deficiency associated diseases?
SLE-like syndrome
183
C5 deficiency associated diseases?
Neisseria infections
184
C5 dysfunction associated diseases?
Leiner’s disease
185
C6 deficiency associated diseases?
Neisseria infections
186
C7 deficiency associated diseases?
Neisseria infections
187
C8 deficiency associated diseases?
Neisseria infections
188
What does C1 esterase inhibitor deficiency cause?
Hereditary angioedema (HAE)
189
What diseases are linked to C1r deficiency?
SLE-like syndrome
190
What disorders are associated with C1s deficiency?
SLE
191
What does C2 deficiency cause?
Recurrent infections (S. pneumoniae
192
What does C3 deficiency lead to?
Recurrent pyogenic infections
193
What is C3b inactivator deficiency associated with?
Recurrent infections
194
What diseases link to C4 deficiency?
SLE
195
What does C5 deficiency cause?
Neisseria infections
196
What is C5 dysfunction linked to?
Leiner’s disease
197
What does C6 deficiency cause?
Neisseria infections
198
What does C7 deficiency lead to?
Neisseria infections
199
What does C8 deficiency cause?
Neisseria infections
200
What does properdin deficiency lead to?
Meningococcemia (X-linked recessive)
201
What are C4 allotypes used for?
Disease susceptibility markers (with HLA)
202
How is SLE diagnosed via complement?
Low C4 + elevated anti-DNA/ANA
203
What does low C3 + normal C4 indicate?
Alternative pathway activation (e.g.
204
What does low C3 + low C4 indicate?
Classic pathway activation (e.g.
205
What is measured in hereditary angioedema?
C1 inhibitor activity and antigen levels
206
What is familial Mediterranean fever?
Chromosome 16 defect causing recurrent fever/inflammation
207
What test identifies immune complex activation?
C1q binding assay
208
What is C3PA (factor B) used to assess?
Alternative pathway activation (low C3PA = alternative pathway consumption)
209
Substances that modulate immune responses via antibodies
cytokines
210
Antibody-secreting cells contributing to BRMs
B lymphocytes
211
Cells secreting IL-2
GM-CSF
212
Cells secreting IFN-α as BRMs
Natural Killer (NK) lymphocytes
213
Cells secreting IFN-α
IL-1
214
Immunotherapy using microbial/chemical adjuvants
Active immunotherapy
215
Immunotherapy using soluble mediators like ILs
Adoptive immunotherapy
216
Immunotherapy transferring preformed antibodies
Passive immunotherapy
217
Immunotherapy applying IFNs for disease treatment
Restorative immunotherapy
218
First discovered cytokine (T cell-derived
immobilizes macrophages)
219
Polypeptides regulating immune responses (e.g.
ILs
220
Cytokines produced by activated lymphocytes
Lymphokines
221
Cytokines acting on leukocytes
Interleukins (ILs)
222
CSF/IL-regulated blood cell production process
Hematopoiesis
223
Signaling pathway using Janus kinase/STAT proteins
JAK/STAT pathway
224
TNF receptor-associated signaling proteins
TRAFs
225
Signaling pathway using TNF death domains
TNF receptor signaling by death domains
226
Innate immunity pathway activated by microbial patterns
Toll receptor signaling
227
Signaling via membrane-bound tyrosine kinases
Receptor-associated tyrosine kinases
228
Signaling via GTP-binding proteins
G-protein signaling
229
Multiple cytokines producing identical effects
Redundancy
230
Single cytokine acting on multiple cell types
Pleiotropy
231
Cytokines acting locally on same/nearby cells
Autocrine/Paracrine action
232
Cytokine-mediated receptor up/downregulation
Receptor regulation
233
Cytokine-driven amplification/feedback loops
Amplification/Negative feedback
234
Leukocyte-derived cytokines regulating immunity
Interleukins (ILs)
235
IFN type mediating early antiviral responses
Type I Interferons (IFN-α/β)
236
Principal macrophage-activating cytokine
IFN-γ
237
TNF gene location in HLA region
TNF-α
238
Primary mediator of gram-negative septic shock
TNF-α
239
Factor stimulating granulocyte-monocyte production
GM-CSF
240
Factor stimulating monocyte production
M-CSF
241
Transmembrane proteins binding cytokines
Cytokine receptors
242
Cytokine that activates c-kit receptor on immature stem cells
Stem Cell Factor (c-kit Ligand)
243
Cytokine enabling bone marrow stem cell responsiveness to CSFs
Stem Cell Factor
244
Factor sustaining immature T-cell viability in thymus
Stem Cell Factor
245
Factor supporting mucosal mast cell proliferation
Stem Cell Factor
246
CSF regulating granulocyte/monocyte production
GM-CSF
247
CSF specific to granulocyte development
G-CSF
248
CSF measured by colony formation in semisolid medium
Colony-Stimulating Factor (CSF)
249
Cytokine group inhibiting IL-1-induced T-cell proliferation
Transforming Growth Factor-β (TGF-β)
250
TGF-β's primary immune function
Inhibition of lymphocyte/macrophage activation
251
Cytokine family guiding leukocyte migration
Chemokines
252
CC chemokine attracting monocytes to chronic inflammation
Monocyte Chemoattractant Protein 1 (MCP-1)
253
CXC chemokine recruiting neutrophils to acute inflammation
IL-8 (CXCL8)
254
CX3 chemokine acting as adhesion receptor
CX3CL1
255
Chemokine function increasing leukocyte integrin affinity
Chemokines
256
Traditional cytokine measurement method
Bioassays
257
High-sensitivity ELISA variant for cytokines
Biotrak Assay
258
Simultaneous multi-cytokine quantification method
Multiplexed FlowMetrix Assay
259
Inhibitor of IL-1-driven T-cell responses
TGF-β
260
Factor used post-chemotherapy to boost leukocytes
GM-CSF
261
HSC surface receptor for c-kit ligand
c-kit Receptor (Tyrosine Kinase)
262
Cytokine critical for erythrocyte production
Erythropoietin (EPO)
263
Factor stimulating megakaryocyte/platelet production
Thrombopoietin (TPO)
264
Cytokine inducing B-cell differentiation
IL-6
265
Interleukin driving T-cell proliferation
IL-2
266
Factor regulating eosinophil activity
IL-5
267
Cytokine supporting mast cell/stem cell growth
Stem Cell Factor (SCF)
268
TGF-β's cellular sources
Macrophages/Platelets
269
Chemokine maintaining lymphoid tissue trafficking
Chemokines
270
Assay detecting cytokine-secreting single cells
ELISPOT
271
Real-time PCR application in cytokine studies
Lymph node/spleen mRNA analysis
272
Enzyme cleaving CX3CL1 from membranes
TNF-α–Converting Enzyme (TACE)
273
Cytokine inhibiting Th1/Th2 polarization
TGF-β
274
Factor used in AIDS-related leukopenia
GM-CSF
275
CSF stimulating macrophage colonies
M-CSF
276
Cytokine promoting dendritic cell development
Flt-3 Ligand
277
Factor suppressing leukemic cell clonogenicity
Leukemia Inhibitory Factor (LIF)
278
Key transcription factor in neutrophil development
C/EBPα
279
PU.1's role in hematopoiesis
Myeloid Lineage Commitment
280
MicroRNA regulating NF-κB in hematopoiesis
miR-125b
281
Model where cytokines directly dictate differentiation
Instructive Model
282
Model where cytokines support pre-programmed cells
Stochastic Model
283
Proteins altering serum concentration by >25% during inflammation
Acute-Phase Proteins (APPs)
284
Innate immune response involving IL-1
IL-6
285
APP increasing 100–1000-fold (e.g.
Serum Amyloid A)
286
APP increasing 5–10-fold (e.g.
Haptoglobin)
287
APP increasing 50–100% (e.g.
Ceruloplasmin)
288
Liver-synthesized APP regulated by IL-6
C-Reactive Protein (CRP)
289
APP used to monitor postoperative infections
C-Reactive Protein (CRP)
290
APP predicting cardiovascular events better than LDL cholesterol
C-Reactive Protein (CRP)
291
Negative APP decreasing during inflammation
Albumin
292
Transport protein binding hemoglobin during hemolysis
Haptoglobin
293
Protease inhibitor elevated in chronic inflammation
α1-Antitrypsin
294
APP modulating immune cell adhesion and drug binding
α1-Acid Glycoprotein (Orosomucoid)
295
Coagulation factor increasing plasma viscosity
Fibrinogen
296
Copper-transport APP rising days after inflammation
Ceruloplasmin
297
Complement components rising in later inflammation stages
C3/C4
298
APP with 5–7 hour half-life for rapid inflammation tracking
C-Reactive Protein (CRP)
299
APP remaining normal in SLE despite active inflammation
C-Reactive Protein (CRP)
300
APP distinguishing bacterial from viral infections
C-Reactive Protein (CRP)
301
APP used to monitor rheumatoid arthritis therapy response
C-Reactive Protein (CRP)
302
Electrophoresis pattern showing α-globulin spikes
Acute-Phase Response
303
Systemic reaction causing fever
anorexia
304
Cytokine group including IL-1
IL-6
305
Cytokine binding protein mitigating inflammation
IL-1 Receptor Antagonist
306
Marker influenced by anemia or hypergammaglobulinemia
Erythrocyte Sedimentation Rate (ESR)
307
Assay quantifying multiple cytokines simultaneously
Multiplexed FlowMetrix
308
Method detecting cytokine-secreting cells
ELISPOT
309
APP synthesis impaired in liver failure
Acute-Phase Proteins
310
Protein reduced in DIC or hemolysis
Fibrinogen/Haptoglobin
311
Exercise-induced inflammation marker elevation
Acute-Phase Proteins
312
Chronic APR complication causing intestinal villus atrophy
Systemic Inflammatory Response
313
APP category including serum amyloid A and CRP
Positive Acute-Phase Reactants
314
APP category including albumin and transferrin
Negative Acute-Phase Reactants
315
Cytokine triggering hypothalamic-pituitary-adrenal axis
IL-1β
316
Condition with normal CRP but elevated other APPs
Systemic Lupus Erythematosus (SLE)
317
Assay measuring high-sensitivity CRP
Biotrak ELISA
318
Protein influencing erythrocyte sedimentation rate
Fibrinogen
319
APP used in neonatal sepsis diagnosis
C-Reactive Protein (CRP)
320
Marker rising faster than ESR in inflammation
C-Reactive Protein (CRP)
321
Cytokine inducing prostaglandin-mediated fever
TNF-α
322
Protein reduced during starvation or malnutrition
Acute-Phase Proteins
323
APP with anti-inflammatory effects in chronic states
Serum Amyloid A
324
Method assessing mRNA in lymphoid tissues
Real-Time PCR
325
Protease inhibitor elevated in acute inflammation
α1-Antitrypsin
326
α1-antitrypsin deficiency mechanism in vasculitis
Immune complex-mediated elimination
327
Deficiency causing recurrent serious infections
C3a/C5a deficiency
328
Opsonin critical for bacterial phagocytosis
C3b
329
Complement consumption marker in immune complex disease
C3/C4 reduction
330
More reliable indicator of complement activation than total C3
C3 breakdown products
331
Elevated C1 esterase inhibitor with minimal other changes
Lymphoma-associated response
332
Serum copper-associated APP monitoring Hodgkin’s disease
Ceruloplasmin
333
APP used to detect non-Hodgkin’s lymphoma relapse
Ceruloplasmin
334
Diagnostic marker for intravascular hemolysis
Haptoglobin reduction
335
Iron storage protein elevated in inflammation
Ferritin
336
Negative APP indicating nutritional status
Transferrin
337
Negative APP with reduced synthesis during inflammation
Albumin
338
Negative APP marker of malnutrition
Prealbumin (Transthyretin)
339
Hepcidin-regulated iron metabolism during inflammation
Hepcidin
340
Cytokine binding protein mitigating IL-1 effects
IL-1 Receptor Antagonist
341
Cytokine driving hepatic APP synthesis
IL-6
342
Test detecting neutrophil band forms
Peripheral blood smear differential
343
Nonspecific inflammation marker using RBC sedimentation
Erythrocyte Sedimentation Rate (ESR)
344
Phagocyte function assessment method
Nitroblue tetrazolium (NBT) test
345
APP rising 1000-fold in bacterial infections
C-Reactive Protein (CRP)
346
Major APP chemotactic for inflammatory cells
Serum Amyloid A (SAA)
347
Moderate APP binding hemoglobin for bacterial iron limitation
Haptoglobin
348
Minor APP with copper-dependent oxidase activity
Ceruloplasmin
349
Complement component elevated in later inflammation stages
C3/C4
350
Cytokine stimulating prostaglandin-mediated fever
IL-1β
351
Cytokine enhancing IL-6 receptor expression in hepatocytes
Cortisol
352
Acute-phase reactant masking anemia in chronic disease
Hepcidin
353
Negative APP reduced in nephrotic syndrome
Albumin
354
Negative APP indicating iron deficiency
Transferrin elevation
355
APP used to assess peritonitis/pancreatitis activity
C3 breakdown products
356
Test distinguishing bacterial vs. viral infections
Procalcitonin
357
Marker of thyroid origin elevated in sepsis
Procalcitonin
358
Cytokine binding protein inhibiting TNF-α
TNF-α Binding Protein
359
Cytokine antagonist reducing IL-1 bioavailability
Soluble IL-1 Receptor
360
Acute-phase reactant involved in lipid metabolism
Serum Amyloid A (SAA)
361
APP inhibiting myeloperoxidase release
Serum Amyloid A (SAA)
362
Cytokine promoting CRP synthesis in hepatocytes
IL-6
363
Marker of acute inflammation with 5-7h half-life
C-Reactive Protein (CRP)
364
Negative APP serving as retinol transporter
Retinol-Binding Protein
365
APP rising post-MI for cardiac risk stratification
C-Reactive Protein (CRP)
366
APP used to monitor rheumatoid arthritis therapy
C-Reactive Protein (CRP)
