Immunology- Immune Phase Reactants Flashcards

1
Q

Acute phase reactants

A

Factors whose serum concentrations change in response to inflammation

Produced by the liver

Induced by IL-6

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2
Q

C reactive protein

Note: not to be confused with protein C (coagulation cascade) or C-peptide (component of proinsulin)

A

Opsonin: fixes complement and facilitates phagocytosis

Clinically: used to assess ongoing inflammation

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3
Q

Ferritin

A

Binds and sequesters iron to inhibit microbial iron scavenging

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4
Q

Fibrinogen

A

Coagulation factor (1); promotes endothelial repair; correlates with ESR

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5
Q

Hepcidin

A

Decreases iron absorption by degrading ferroportin and decreasing iron release from Mphages

elevated in anemia of chronic disease

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6
Q

Serum amyloid A

A

Prolonged elevation can lead to amyloidosis

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7
Q

Factors that are DOWNregulated

A

Albumin- AAs are being used to make the unregulated reactants (CRP, ferritin, fibrinogen, hepcidin, and serum amyloid A)

Transferrin- internalized by Mphages to sequester iron

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8
Q

Complement

A

Hepatically synthesize plasma proteins that play a role in innate immunity and inflammation; MAC defends against gram - bacteria

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9
Q

Classic pathway

A

Mediated by IgG and IgM (GM makes CLASSIC cars)

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10
Q

Alternative pathway

A

Microbe surface molecules

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11
Q

Lectin pathway

A

Mannose or other sugars on microbe surface

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12
Q

C3b- role

A

opsonization; binds bacteria

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13
Q

C3a, C4a, C5a

A

anaphylaxis

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14
Q

C5a (also)

A

neutrophil chemotaxis

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15
Q

C5b-C9

A

cytolysis by MAC

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16
Q

Opsonins

A

C3b and IgG; enhance phagocytosis

C3b also helps clear immune complexes

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17
Q

Inhibitors (of complement)

A

decay-accelerating factor (DAF– aka CD55) and C1 esterase inhibit complement activation on self- cells (e..g RBCs)

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18
Q

C1 esterase inhibitor deficiency

A

Can cause hereditary angioedema (unregulated activation of kallikrein –> increases bradykinin)

ACE inhibitors are CONTRAINDICATED

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19
Q

C3 deficiency

A

Increases risk of severe, recurrent pyogenic sinus and respiratory tract infections; increased susceptibility to type III HS reactions (more things have to go down the adaptive pathway)

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20
Q

C5-C9 deficiency

A

MAC complex

Increases susceptibility to Neisseria infections/ bacteremia

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21
Q

DAF- GPI-anchored enzyme deficiency

A

Causes complement-mediated lysis of RBCs

Paroxysmal nocturnal hemoglobinuria

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22
Q

IL-1- secreted by Mphages

A

Aka osteoclast activating factor
“Hot”: causes fever
Produced by mononuclear phagocytes and stimulates WBC recruitment

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23
Q

IL-2- secreted by ALL T cells

A

“T”: Stimulates growth of ALL T cells + NK cells

IL-2 administered in melanoma to increase host NK response (and adaptive immune response- T cells)

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24
Q

IL3- secreted by ALL T cells

A

“Bone”: supports growth of bone marrow stem cells (like GM-CSF– stimulates stem cell prod of granulocytes and monocytes)

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25
IL-4- secreted by Th2 cells
"E": Induces differentiation of T cells in Th2 cells Promotes growth of B cells and IgG and IgE class switching
26
IL-5- secreted by Th2 cells
"A": Promotes growth and diff of B cell- enhances class switching to IgA Stimulate growth and diff of eosinophils
27
IL-6- secreted by Mphages
"K": Produces a"K"ute phase reactants and causes fever
28
IL-8- secreted by Mphages
"Clean up on aisle 8" Chemotactic factors for neutrophils (like C5a, and LT B4)
29
Il-10- secreted by Th2 and Treg
A"ten"uates: Attenuates immune response (along with TGF- B) Decreases expression of MHC Class II and Th1 cytokines, Mphages, and dendritic cells
30
IL-12- secreted by Mphages
Stimulate differentiation in Th1 cells; activates NK cells
31
TNF-alpha- secreted by Mphages
Mediates septic shock, activates endothelium, and causes WBC recruitment and vascular leak Causes cachexia in malignancy
32
IFN-gamma- produced by Th1 and NK cells
Stimulates Mphages to kill phagocytosed pathogen Inhibits Th2 differentiation Also activates NK cells to kill virus-infected cell Increases MHC expression and antigen presentation on ALL cells
33
Respiratory burst
Activation of phagocyte oxidase complex (in neutrophils and monocytes) NADPH: plays a key role in creating and neutralizing the ROS Myeloperoxidase: blue-green heme-containing pigment that gives sputum its color
34
Lactoferrin
Protein found in secretory fluids and neutrophils that inhibits microbial growth via iron chelation
35
IFN alpha and beta
Part of innate host defense against RNA and DNA viruses (interferons "interfere" with viruses) Prime locally uninfected cells to selectively degrade viral nucleic acid
36
All nucleated cells
MHC I RBCs dont have this though- makes sense because they are not nucleated!
37
T cells
TCR (binds antigen-MHC complex) CD3 (signal transduction) CD28 (binds to B7 on APC) CCR5- on macrophages (early)/ CXCR4 (late)- on T cells (co-receptors for HIV)
38
Helper T cells
CD4, CD40L (used to bind to B cells)
39
Cytotoxic T cells
CD8, CXCR4/ CCR5
40
Regulatory T cells
CD4, CD25, FOXP3
41
B cells
Ig (binds antigen) CD 19-21 (21- receptor for EBV), CD40 (used to bind to Th cells) MHC II, B7 (used to bind to naive T cells)
42
Mphages
CD14 (receptor for PAMPs (e.g. LPS)), CD 40, CCR5, MHC II, B7, Fc and C3b receptors
43
NK cells
CD16 (binds Fc of IgG) | CD56 (unique for NK cells)
44
Hematopoietic stem cells
CD34
45
Anergy
State during wherein T cell is made refractory to any future stim (e.g. when antigen/MHC complex binds to TCR, but does not receive T cell does not receive costimulatory signal (e.g. from B7 (on APC) to CD28 (on T cell))
46
Superantigens
Can cross-like a region on the TCR to the MHC II of APCs thereby activating CD4+ T cells and causing massive release of cytokines
47
Endotoxins/ LPS
Directly stimulate Mphages (via binding to to CD14)
48
Passive vaccinations available for:
"To Be Healed Very Rapidly" ``` Tetanus Botulinum HBV Varicella Rabies ```
49
Live vaccines vs. inactivated vaccine
Live vaccine: induce cell-mediated (T cells) and humoral (antibodies) response (BCG, Influenza (intranasal), MMR, Polio (Sabin), Rubella, Varicella, Yellow Fever) Inactivated vaccine: induces only humoral response (RIP Always- Rabies, H. Influenza, Polio, HAV)
50
Type I HS
Anaphylactic (bee sting, food allergies) and atopy (allergic hypersensitivity- rhinitis, asthma, eczema) Antigen cross links IgE --> Fc binds mast cells and basophils --> histamine release (immediate) --> leukotrienes (delayed/ long-lasting effects)
51
Type II HS
Cytotoxic (antibody-mediated against our (normal) cells): AIHA, Goodpasture, Pernicious Anemia, ITP, Erythroblastosis fetalis, Rheumatic fever Can also be complement-mediated (via opsonization and formation of MAC)
52
Direct vs. Indirect Coombs
Direct: Tests tissue (and looks for antibody deposits) Indirect: Tests serum for antibodies
53
Type III HS
Immune complex mediated: Arthus reaction, SLE, Polyarteritis nodosa, PSGN, serum sickness
54
Arthus reaction
Immune complex formation in the skin after internal injection of antigen to pre-sensitized (individual has IgG) individual
55
Serum sickness
immune complex disease in which antibodies to foreign proteins are produced (takes 5 days) Immune complexes deposit in tissue and fix complement (therby causing tissue damage)
56
Type IV HS
Delayed (T-cell mediated) HS (Transplant rejection, poison ivy/ contact dermatitis, TB test, MS) Sensitized T cells encounter antigen and release cytokines and activate Mphages
57
Blood transfusion reactions- allergic rxn
Type I; caused by plasma proteins in blood S&S: urticaria, wheezing, pruritis Tx: antihistamines
58
Blood transfusion reactions- anaphylaxis
Can be seen in people with IgA deficiency S&S: dyspnea, brochospasm, hypotension, respiratory arrest, shock Tx: epinephrine
59
Blood transfusion reaction- febrile non-hemolytic
Type II HS; antibodies agains donor HLA antigens and WBCs S&S: fever, headache, chills, flushing
60
Blood transfusion reaction- acute hemolytic
``` Type II HS; Intravascular hemolysis (donor RBCs themselves): ABO blood group incompatibility Extravascular hemolysis (foreign antigen on donor RBCs): host antibody reaction against foreign antigen on donor RBCs ``` S&S: Intravascular: fever, hypotension, tachypnea, tachycaria, hemoglobinuria (can look like ATN, but will be preceded by TRANSFUSION) Extravascular: jaundice