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Immunology > Immunology- Immune Phase Reactants > Flashcards

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
Q

IL-4- secreted by Th2 cells

A

“E”: Induces differentiation of T cells in Th2 cells

Promotes growth of B cells and IgG and IgE class switching

26
Q

IL-5- secreted by Th2 cells

A

“A”: Promotes growth and diff of B cell- enhances class switching to IgA

Stimulate growth and diff of eosinophils

27
Q

IL-6- secreted by Mphages

A

“K”: Produces a”K”ute phase reactants and causes fever

28
Q

IL-8- secreted by Mphages

A

“Clean up on aisle 8”

Chemotactic factors for neutrophils (like C5a, and LT B4)

29
Q

Il-10- secreted by Th2 and Treg

A

A”ten”uates: Attenuates immune response (along with TGF- B)

Decreases expression of MHC Class II and Th1 cytokines, Mphages, and dendritic cells

30
Q

IL-12- secreted by Mphages

A

Stimulate differentiation in Th1 cells; activates NK cells

31
Q

TNF-alpha- secreted by Mphages

A

Mediates septic shock, activates endothelium, and causes WBC recruitment and vascular leak

Causes cachexia in malignancy

32
Q

IFN-gamma- produced by Th1 and NK cells

A

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
Q

Respiratory burst

A

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
Q

Lactoferrin

A

Protein found in secretory fluids and neutrophils that inhibits microbial growth via iron chelation

35
Q

IFN alpha and beta

A

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
Q

All nucleated cells

A

MHC I

RBCs dont have this though- makes sense because they are not nucleated!

37
Q

T cells

A

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
Q

Helper T cells

A

CD4, CD40L (used to bind to B cells)

39
Q

Cytotoxic T cells

A

CD8, CXCR4/ CCR5

40
Q

Regulatory T cells

A

CD4, CD25, FOXP3

41
Q

B cells

A

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
Q

Mphages

A

CD14 (receptor for PAMPs (e.g. LPS)), CD 40, CCR5, MHC II, B7, Fc and C3b receptors

43
Q

NK cells

A

CD16 (binds Fc of IgG)

CD56 (unique for NK cells)

44
Q

Hematopoietic stem cells

A

CD34

45
Q

Anergy

A

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
Q

Superantigens

A

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
Q

Endotoxins/ LPS

A

Directly stimulate Mphages (via binding to to CD14)

48
Q

Passive vaccinations available for:

A

“To Be Healed Very Rapidly”

Tetanus
Botulinum
HBV
Varicella
Rabies
49
Q

Live vaccines vs. inactivated vaccine

A

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
Q

Type I HS

A

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
Q

Type II HS

A

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
Q

Direct vs. Indirect Coombs

A

Direct: Tests tissue (and looks for antibody deposits)
Indirect: Tests serum for antibodies

53
Q

Type III HS

A

Immune complex mediated: Arthus reaction, SLE, Polyarteritis nodosa, PSGN, serum sickness

54
Q

Arthus reaction

A

Immune complex formation in the skin after internal injection of antigen to pre-sensitized (individual has IgG) individual

55
Q

Serum sickness

A

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
Q

Type IV HS

A

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
Q

Blood transfusion reactions- allergic rxn

A

Type I; caused by plasma proteins in blood

S&S: urticaria, wheezing, pruritis

Tx: antihistamines

58
Q

Blood transfusion reactions- anaphylaxis

A

Can be seen in people with IgA deficiency

S&S: dyspnea, brochospasm, hypotension, respiratory arrest, shock

Tx: epinephrine

59
Q

Blood transfusion reaction- febrile non-hemolytic

A

Type II HS; antibodies agains donor HLA antigens and WBCs

S&S: fever, headache, chills, flushing

60
Q

Blood transfusion reaction- acute hemolytic

A 
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

Immunology (7 decks)

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