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Immunology > Immunology: Exam 1 > Flashcards

Immunology: Exam 1 Flashcards

1
Q

First Line of Defense

A

Skin- physical barrier.

Secretions by mucosal membranes. Oil, ear wax, pH of certain fluids, tears, saliva, etc.

Normal flora- compete with pathogens for nutrients

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2
Q

Skin as a 1st line of defense

A

top layer is composed of dead cells so microbes can’t attach to it and viruses can’t live within it.
Also composed of keratin which repels water, also inhibiting microbe growth.

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3
Q

Granulocytes

A

Neutrophils- most abundant. first cells to encounter infections. phagocytosis

Eosinophils- anti-parastiic responses and allergy rxns

Basophils- allergies and inflammation

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4
Q

Monocytes/Macrophages

A

Monocytes are in blood and macrophages are in tissues. Kupfer cells are in liver.

Increase in #’s with inflammation, infections, and certain cancers. Phagocytosis and APC.

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5
Q

Lymphocytes

A

B cells- mature to produce antibodies. then they are called plasma cells

T cells- Cytoxic (kills cells infected with pathogens) & helper cells (coordinate the acquired immune response)

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6
Q

Three classes of molecules in immune system

A
  1. Pattern recognition receptors- recognize PAMPs
  2. Cytokines- cell to cell communication
  3. Complement proteins- cascade of protein response
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7
Q

Innate immunity

A

Born with.
Non-specific.
No memory.
Happens First.

Pretty much everything but T, B, and NK cells

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8
Q

Adaptive immunity

A

Allows body to recognize, remember, and respond to antigen in future.

Can be acquired (naturally or vaccination) or passive (injecting Ab or from mother)

T, B, and NK cells

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9
Q

Cellular Response

A

T cells (cytotoxic)

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10
Q

Humoral Response

A

B cells (antibodies)

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11
Q

Antibody

A

aka Immunoglobins (Ig)

produced in plasma cells. found in serum and bodily secretions

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12
Q

Antibody Structure

A

2 heavy chains and one light chain.

Intra-chain disulfide bonds and inter-chain disulfide bonds

Hinge region- points at which arms form Y. flexibility

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13
Q

Heavy/Light Chains

A

Each has a constant region and a variable region (different antigen-binding abilities)

Heavy- gives Ab its class (on constant region..also effector functions)
Light- either kappa or lambda.

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14
Q

Papain

A

Cuts Ab into three pieces (2 Fab and 1 Fc)

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15
Q

Fab region

A

involved in antigen binding.

composed of light chain and part of heavy chain

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16
Q

Fc region

A

effector functions.

only heavy chain.

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17
Q

IgG

A

Majority.
Very stable so lasts longer.
Can cross placenta..immunity for newborns

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18
Q

IgM

A

1st antibody in immune response.
J chain (10 binding sites)
Most effective at activating complement
If present, usually active infection

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19
Q

IgA

A

Predominant in secretions (protects surfaces)
Breast Milk
Opsonization and phagocytosis

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20
Q

IgD

A

on mature B cell surface

Not in serum

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21
Q

IgE

A

least abundant.
attaches to basophils and mast cells causing release of heparin and histamines
allergies/parasites

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22
Q

IgM response

A
  1. lag phase- no Ab
  2. log phase- sharp increase of Ab
  3. plateau phase- antibody levels stabilize
  4. decline phase- levels decrease
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23
Q

Primary immune response

A

Ab production due to encounter with antigen for 1st time

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24
Q

Secondary immune response

A

Much quicker response due to previous exposure

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25
Q

Polyclonal

A

Antibodies that recognize a single antigen but many different epitopes on that antigen

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26
Q

Monoclonal

A

Only recognizes one specific epitope on single antigen (very specific)

27
Q

Good immunogens characteristics

A
  1. Foriegnness (from host)
  2. Size (bigger the better..ideally bigger than 6,000 daltons)
  3. Chemical complexity (proteins make best, then polysaccharides, rarely lipids except for syphillis)
28
Q

Haptens

A

small compounds that cannot stimulate an immune response without attaching itself to a larger molecule

29
Q

Cross reactivity

A

parts of an antigen are shared by another antigen and illicit same response (can cause auto-immune diseases)

30
Q

Major Histocompatability Complex

A 
On chromosome 6.
Only class 1 and class 2 are involved in immunity.

Human Leukocyte antigen- genes that encode antigen-presenting proteins on the cell surface

31
Q

Class 1 MHC

A

proteins are expressed on all nucleated cells.

T cell receptors on CD8+ recognize antigen and will trigger apoptosis (viral infections)

32
Q

Class 2 MHC

A

on all APC (B cells, macrophages, dendritic cells <- most effective)
APC cells uptake antigen and load epitope on its membrane
T cell receptors on CD4+ recognize epitope and mediate an immune response

33
Q

affinity

A

measure of how strong an antibody binds to an epitope

34
Q

avidity

A

measure of affinity x # of binding sites

35
Q

Types of T helper cells

A

Th1 = stimulates macrophages & phagocytosis

Th2 = stimulates antibody production

36
Q

T cell Production

A

T cell precursor go from BM to thymus.
First double positive (CD4/CD8)
Then double negative
Then either CD4+ or CD8+

37
Q

Positive selection

A

if T cells recognize self MHC, they survive. if not..death

38
Q

Negative selection

A

if T cells recognize self, they die.

39
Q

APC

A
  1. dendritic cells- present in tissues
  2. macrophages- phagocytosis then present
  3. B cells- recognize surface Ig
40
Q

Quiescent

A

T or B cells that are non-dividing/non-active due to lack of antigen exposure (they are naive)

41
Q

Pleiotropic

A

the ability of a single cytokine to act on multiple cells with multiple functions

42
Q

Redundant

A

Two or more cytokines having same fuction

43
Q

Autocrine effect

A

acts on cell that secreted it

44
Q

Paracrine effect

A

acts on cells nearby

45
Q

Endocrine effect

A

acts on distal cells. travels via bloodstream

46
Q

Tumor necrosis factor

A

cytokine that acts against Gram neg bacteria and causes inflammation

47
Q

Interferons

A

interfere with viral replication. reason for viral symptoms

48
Q

Interleukins

A

regulate adaptive immunity.

IL-2 is most important

49
Q

Zymogenes

A

inactive complement proteins

50
Q

Gram Neg bacteria/RBC in Complement

A

lysed

51
Q

Gram Pos bacteria

A

opsonized

52
Q

Where are plasma proteins made?

A

Most in liver.

Exceptions: C1 in intestinal epithelial cells and Factor D in adipose tissue.

53
Q

4 outcomes of complement

A
  1. local vasodilation/vascular permeability
  2. attraction of immune cells
  3. opsonization (tagging)
  4. membrane attack complex
54
Q

Complement regulators

A

Try to prevent C3 -> C3B (pivotal step in all pathways)

C1 inhibitor- inhibits classical pathway by stopping dissociation of C1r and Cls from Clq.

Factor H- inhibits alternative pathway by preventing binding of factor B by binding to C3b

55
Q

Complement tests

A

antigenic assays- quantifies amount of protein using ELISAs

functional assays- lytic function is measure

56
Q

CH50

A

looks at integrity of classical pathway

57
Q

AH50

A

looks at integrity of alternative pathway

58
Q

Classical Pathway

A

triggered by antigen-antibody combo (usually IgG & IgM)
proteins are C#
Recognition: C1
C3 convertase: C4b2a

59
Q

Alternative Pathway

A

activated by bacteria (usually LPS)
proteins are factor B, D
Recognition: C3 on microbe
C3 convertase- Bb (fragment of Factor B that was cleaved by Factor D) attached to C3

60
Q

Lectin Pathway

A

activated by PAMP (usually MBL)
Proteins start with M
Recognition: MBL binding to carb on pathogen
C3 convertase: MASP

61
Q

Inflammation

A

C4a
C3a
C5a

62
Q

Opsonization

A

C3b

63
Q

MAC

A

C5b, C6-C9

Immunology (2 decks)

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