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Immunology 1 Flashcards

1
Q

What are the primary lymphoid organs?

A

Thymus and Bone marrow

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2
Q

What are the components of a lymph node

A

Follicle, Medulla, and paracortex

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3
Q

How many efferents and afferents for lymph node

A

many afferents, 1 or more efferents

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4
Q

What happens in the follicle

A

Site of B-cell localization and proliferation. In outer cortex. Primary follicles are dense and dormant. Secondary follicles have a pale central germinal center and are active.

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5
Q

What happens in medulla.

A

Consists of medullary cords (closely packed lymphocytes and plasma cells) and medullary sinuses. medullary sinuses communicate with efferent lymphatics and contain reticular cells and macrophages.

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6
Q

What happens in paracortex

A

Houses T cells. Region of cortex between follicles and medulla. Contains high endothelial venules through which T and B cells enter from blood. Not well developed in DiGeorge syndrome.

Paracortex enlarges in extreme cellular immune response (e.g. viral infection)

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7
Q

Sinusoids of spleen

A

Red pulp is on the outside containing RBCs and surrounds the white pulp which contains T cells, B cells.

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8
Q

Sinusoids and Lymphocytes

A

T cells in Periarterial lymphatic sheath (central arteriole is in the center of everything).

B cells in follicles within the white pulp of the spleen.

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9
Q

What is the marginal zone

A

Red pulp and white pulp, contains APCs and specialized B cells, and is where APCs present blood-borne antigens

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10
Q

What do macrophages do in the spleen

A

Remove encapsulated bacteria.

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11
Q

What does asplenia due path

A

Decreases IgM leading to decreased complement activation leading to decreased C3b opsonization and increased susceptibility to encapsulated organisms.

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12
Q

Encapsulated bacteria

A

SHiNE SKiS: Strep pneumo, HiB, Neisseria meningococcus, E. coli, Salmonella, Klebsiella, Groub B Strep

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13
Q

What results due to postsplenectomy?

A

Howell-Jolly bodies (nuclear remants); target cells; thrombocytosis

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14
Q

Thymus made from what

A

epithelium of 3rd pharyngeal pouches

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15
Q

lymphocyte cell layer

A

Mesenchymal origin

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16
Q

Thymus structure

A

Cortex is dense with immature T cells; medulla is pale with mature T cells and Hassall corpuscles containing epithelial reticular cells.

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17
Q

Where do T and B cells mature

A

Thymus: T cells

Bone marrow: B cells

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18
Q

What are the examples of innate immunity

A

PMNs, macrophages, monocytes, dendritic cells, NK cells (lymphoid origin), complement

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19
Q

How long for innate immunity to kick in

A

minutes to hours

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20
Q

Are physical barriers included in innate immunity

A

Yes, e.g. tight junctions, mucus, lysozyme, complement, CRP, defensins

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21
Q

What are toll-like receptors

A

pattern recognition receptors that recognize pathogen-associated molecular patterns (PAMPs):

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22
Q

What are examples of PAMPs

A

LPS, flagellin, ssRNA

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23
Q

How does adaptive immunity get its variation

A

Through V(D)J recombination

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24
Q

MHC-I loci

A

HLA-A, B, and C

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25
Q

MHC II locis

A

HLA-DR, DP, and DQ (P Q R)

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26
Q

What do MHC-I and II bind

A

I: TCR and CD8
II: TCR and CD4

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27
Q

MHC-I found where

A

All nucleated cells, no RBCs

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28
Q

MHC-II found where

A

Only on APCs

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29
Q

Difference between MHC-I and II

A

I reveals endogenous proteins, II reveals exogenous proteins

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30
Q

how are antigens revealed by the MHCs

A

I: antigen peptides loaded onto MHC I in RER after delivery via TAP peptide transporter

II: Antigen loaded following release of invariant chain in an acidified endosome

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31
Q

How are MHC I and II moved to the cell surface

A

I: Beta2-microglobulin
II: Unknown

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32
Q

Structure to MHC I and II

A

Both have peptide binding groove
I: alpha is main component and has the peptide binding groove, beta2-microglobulin is small
II: alpha and beta are extremely similar and together form the peptide-binding groove

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33
Q

HLA A3

A

Hemochromatosis

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34
Q

HLA B27

A

PAIR: Psoriatic arthritis, ankylosing spondylitis, IBD, Reactive arthritis (seronegative arthropathies)

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35
Q

HLA DQ2/DQ8

A

Celiac disease

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36
Q

HLA DR2

A

MS, hay fever, SLE, Goodpasture syndrome

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37
Q

HLA DR3

A

T1DM, SLE, Graves disease

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38
Q

HLA DR4

A

RA, T1DM (4 walls in a “rheum”)

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39
Q

HLA DR5

A

Pernicious anemia, hashimotos

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40
Q

NK cells MOA

A

perforin and granzymes to induce apoptosis of virally infected cells and tumor cells.

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41
Q

NK cells activated by

A 
IL-2, IL-12, IFN-beta, and IFN-alpha
Activated by nonspecific activation signal and/or absence of class I MHC on target cell surface
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42
Q

Can NK cells bind antibodies

A

Yes, antibody-dependent cell-mediated cytotoxicity (CD16 binds Fc region of bound Ig, activating NK cell)

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43
Q

What do CD4 t cells do

A

Make antibody and produce cytokines to activate other cells of immune system

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44
Q

Differentiation of T cells

A

Starts in bone marrow, then moves to thymus, then lymph nodes

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45
Q

Steps of T cell differentiation

A

T-cell precursor from bone marrow moves into thymus where CD4+CD8+ T cells are positively selected for in the cortex. Then in the medulla they are divided up into CD4+ and CD8+ cells individually. They then move into the lymph nodes to fully differentiate.

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46
Q

Positive selection

A

Thymic cortex. T cells expressing TCRs capable of binding surface self MHC molecules survive.

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47
Q

Negative selection

A

Medulla. T cells expressing TCRs with high affinity for self antigens undergo apoptosis.

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48
Q

Th1 from

A

IL-12

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49
Q

Th2 from

A

IL-4

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50
Q

Th17 cell from

A

TGF-beta and IL-6

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51
Q

Treg cell from

A

TGF-Beta

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52
Q

What are the APCs

A

B cells, macrophages, and dendritic cells

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53
Q

What are the signals for T cell activation

A

MHC II binds TCR on Thelper, MHC I binds Tc (cytotoxic) cells (signal 1)
Signal 2: Costimulatory signal given by interaction of B7 (Dendritic cell) and CD28 (T cell)

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54
Q

B cell activation and class switching

A
  1. Helper T activated (so it is already primed to the antigen?)
  2. B cell presents antigens on MHC II to TCR on Th cell
  3. CD40 on B cell binds CD40 ligand on Th cell (signal 2)
  4. Th cell secretes cytokines that determine Ig class switching of B cell. B cell activates and undergoes class switching, affinity maturation, and antibody production.
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55
Q

What do CD4 and CD8 do.

A

They bind MHC for activation from Dendritic cell, this activation does not occur with B cells.

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56
Q

Th1 function

A

Secretes IFN-gamma

Activates macrophages and cytotoxic T cells

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57
Q

What inhibits Th1 cells

A

IL-4 and IL-10 (from Th2 cell)

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58
Q

Th2 function

A

Secretes IL-4, IL-5, IL-6, IL-13

Recruits eosinophils for parasite defense and promotes IgE production by B cells

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59
Q

What inhibits Th2 cells

A

IFN-gamma from Th1 cell

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60
Q

How to macrophages interact with lymphocytes

A

Macrophages produce IL-12 to produce Th1 cells which produce IFN-gamma which stimulates macrophages

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61
Q

Must know heme synthesis

A

For BIOCHEM

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62
Q

What to CD8 T cells have

A

Cytotoxic granules with perforin; granzyme B-serine protease to activate apoptosis; granulysin: antimicrobial, induces apoptosis

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63
Q

What are Tregs

A

Suppress CD4 and CD8 T cell fector functions.

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64
Q

How to identify Tregs

A

Cell surface markers: CD3, CD4, CD25 (alpha chain of IL-2 receptor) and transcription factor FOXP3.

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65
Q

What do Tregs produce

A

Anti-inflammatory cytokines like IL-10 and TGF-beta

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66
Q

What makes up the antigen binding site of antibodies

A

The variable part of the light and heavy chains.

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67
Q

What part of antibody fixes complement

A

Fc portion of IgM and IgG fixes complement.

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68
Q

What part of antibody does complement and macrophages bind

A

Complement: CH2
Macrophages: CH2 and CH3 junction point.

69
Q

What do light and heavy chains contribute to the antibody

A

Heavy chain is Fc and Fab fractions. Light chain only contributes Fab function.

70
Q

Mnemonic for Fc region of antibody

A

4 C’s: Constant, Carboxy terminal, Complement binding, and Carbohydrate side chains. Also determines isotype (IgM, IgD)

71
Q

Recombination for the chains

A

Light (VJ)
Heavy (V(D)J)
Light and heavy chains randomly combined

72
Q

What is somatic hypermutation and when does it happen

A

Follows antigen stimulation, the DNA mutates in hypervariable regions to make a receptor with even greater antigen recognizing ability. The effect is that over the course of an infection the affinity for the antigen increases.

73
Q

What happens to DNA during recombination

A

Add nucleotides by terminal deoxynucleotidyl transferase.

74
Q

The ways antibodies do their thing

A
  1. Opsonize
  2. Neutralize
  3. Complment activation (C3b)
75
Q

What is affinity maturation?

A

Over time of an infection and with reinfection, the affinity of antibodies for a specific antigen increases. This works through Somatic Hypermutation which creates the variable antibodies. Then Clonal Selection using APCs weeds only the B cells with the most affinity, because the B cells require growth factors to survive.

76
Q

What do all mature B cells express on their surfaces

A

IgM and IgD

77
Q

What mediates isotype switching

A

gene rearrangement; mediated by cytokines and CD40 ligand

78
Q

Does IgG cross placenta?

79
Q

IgA MOA

A

blocks bacteria and viruses attaching to mucous membranes. Does not fix complement. Crosses epithelium by trancytosis. Picks up secretory component from epithelial cells before secretion.

80
Q

IgA antibody structure

A

Monomer in circulation or dimer when secreted. Most abundant overall but it is in secretions and colostrum.

81
Q

IgG prevalence

A

Most abundant isotype in serum.

82
Q

IgM MOA

A

Fixes complement but does not cross placenta. Antigen receptor on the sruface of B cells. Monomer on B cell or pentamer when secreted.

83
Q

IgD function

A

Unclear function. On B cells and in serum.

84
Q

IgE function

A

Binds mast cells and basophils; cross-links when exposed to allergen, mediating immediate (type I) hypersensitivity through release of inflammatory mediators such as histamine. mediates immunity to worms by activating eosinophils. Lowest concentration in serum.

85
Q

What are thymus independent antigens

A

Lack a peptide component, cannot be presented by MHC to T cells.

86
Q

What induces acute-phase reactants

A

IL-6, IL-1, TNF-alpha, and IFN-gamma

87
Q

What acute phase reactants are upregulated

A

Serum amyloid A, CRP, ferritin, fibrinogen, and hepcidin

88
Q

What acute phase reactants are downregulated

A

Albumin and transferrin

89
Q

Serum Amyloid A

A

Prolonged elevation can cause amyloidosis

90
Q

CRP

A

Opsonin; fixes complement and facilitates phagocytosis. Measured clinically as a sign of ongoing inflammation.

91
Q

Ferritin

A

Binds and sequesters iron to inhibit microbial iron scavenging.

92
Q

Fibrinogen

A

Coagulation factor; promotes endothelial repair; correlates with ESR

93
Q

Hepcidin

A

Prevents release of iron bound by ferritin leading to anemia of chronic disease

94
Q

Albumin

A

Reduces to conserve amino acids for positive reactants

95
Q

Transferrin

A

Internalized by macrophages to sequester iron.

96
Q

When does Membrane Attack Complex target?

A

Defends against gram-negative.

97
Q

Different pathways of Complement

A

Classic pathway: IgG or IgM mediated
Alternative pathway: Microbe surface molecules
Lectin pathway: Mannose or other sugars on microbe surface.

98
Q

C3b

A

opsonization

99
Q

C3a,C4a, and C5a

A

A for anaphylaxis

100
Q

C5a

A

Neutrophil chemotaxis

101
Q

C5b-9

A

Cytolysis by MAC

102
Q

What are the opsonins

A

C3b and IgG are the two primary opsonins in bacterial defense; C3b also helps clear immune complexes.

103
Q

What is Decay-accelerating factor

A

DAF, aka CD55 (along with C1 esterase inhibitor) prevent complement actiation on self cells like RBCs (nocturnal paroxysmal hemoglobinuria)

104
Q

C1 esterase inhibitor deficiency

A

Causes hereditary angioedema. ACE inhibitors are contraindicated

105
Q

C3 deficiency

A

Increases risk of severe, recurrent pyogenic sinus and respiratory tract infections; increases susceptibility to type III hypersensitivity reactions

106
Q

C5-C9 deficiencies

A

Increases susceptibility to recurrent Neisseria bacteremia

107
Q

DAF (CPI anchored enzyme) deficiency

A

Causes complement-mediated lysis of RBCs and paraoxsymal nocturnal hemoglobinuria

108
Q

IL-1

A

Osteoclast-activating factor, endogenous pyrogen.
Causes fever, acute inflammation. Activates endothelium to express adhesion molecules; induces chemokine secretion to recruit leukocytes.

109
Q

IL-6

A

Endogenous pyrogen. Secreted by Th2 cells. Causes fever and stimulates production of acute-phase proteins.

110
Q

IL-8

A

Major chemotactic factor for neutrophils

111
Q

IL-12

A

Induces differentiation of T cells into TH1 cells. Activates NK cells. Also secreted by B cells.

112
Q

TNF-alpha

A

Mediates septic shock. Activates endothelium. Causes leukocyte recruitment, vascular leak.

113
Q

Neutrophils need what cytokine

A

IL-8 to clear infections

114
Q

What cytokines are secreted by Macrophages

A

IL-1, IL-6, IL-8, IL-12, TNF-alpha

115
Q

What cytokines are secreted by all T cells.

A

IL-2 and IL-3

116
Q

IL-2

A

Stimulates growth of helper, cytotoxin, and regulatory T cells.

117
Q

IL-3

A

Supports the growth of differentiation of bone marrow stem cells. Functions like GM-CSF

118
Q

What acts like GM-CSF

119
Q

What does Th1 cells produce

A

Interferon-gamma

120
Q

IFN-gamma

A

Has antiviral and antitumor properties. Activates NK cells to kill virus-infected cells, increases MHC expression and antigen presentation in all cells.

121
Q

What do Th2 cells produce

A

IL-4, IL-5, IL-10

122
Q

Il-4

A

Induces differentiation into Th2 cells. Promotes growth of B cells. enhances class switching to IgE and IgG.

123
Q

IL-5

A

Promotes differentiation of B cells. Enhances class switching to IgA. Stimulates the growth and differnetiation of eosinophils.

124
Q

IL-10

A

Modulates inflammatory response. Inhibits actions of activated T cells and Th1. Also secreted by regulatory T cells.

125
Q

TGF-beta similar to

A

Similar to IL-10, because it inhibits inflammation.

126
Q

Cytokine mnemonic

A

Hot T-bone stEAK: IL-1: fever (hot), IL-2: stimulates T cells. IL-3: stimulates bone marrow, IL-4: Stimulates IgE production. IL-5: Stimulates IgA production. IL-6: stimulates aKute-phase protein protein production.

127
Q

Interferon alpha and beta

A

Innate host defense against both RNA and DNA viruses. Glycoproteins synthesized by viral-infected cells that act locally on uninfected cells, priming them for viral defense. When a virus infects primed cells, viral dsDRNA activates RNAse L which degrades viral/host mRNA and protein kinase which inhibits viral/host protein synthesis which ends up resulting in apoptosis.

128
Q

T cell surface proteins

A

TCR (binds antigen-MHC complex)
CD3 (associated with TCR for signal transduction)
CD28 (Binds b7 on APC)

129
Q

Helper T cell specific proteins

A

CD4, CD40L

130
Q

Cytotoxic T cell specific proteins

131
Q

B cell surface proteins

A

Ig
CD19, CD20, CD21 (receptor for EBV), CD40
MHC II, B7

132
Q

What receptor does EBV bind to?

A

CD21 (Beer at Barr aged 21)

133
Q

Macrophages receptors

A

CD14, CD40
MHC II, B7
Fc and C3b receptors (enhanced phagocytosis)

134
Q

NK cell receptors

A

CD16 (binds Fc of IgG), CD56 (unique marker for NK)

135
Q

Anergy

A

Without costimulatory molecule: B cells become anergic, but tolerance is less complete than in T cells.

136
Q

What are superantigens

A

S. pyogenes and S. aureus: cross-link Beta region of the TCR to MHC class II on APCs, massive release of cytokines.

137
Q

Gram negative effect on macrophages

A

Endotoxins/Lipopolysaccharides directly stimulate macrophages by binding to endotoxin receptor CD14; Th cells not involved.

138
Q

Antigenic variation examples

A 
Salmonella (2 flagellar variants), Borrelia (relapsing fever), Neisseria gonorrhoeae (pilus protein)
Influenza shift vs. drift. 
Parasites trypanosomes (programmed rearrangement)
139
Q

Type I hypersensitivity

A

anaphylactic and atopic. antigen crosslinks IgE on presensitized mast cells and basophils, releasing vasoactive amines that act at postcapillary venules. Delayed response follows due to production of arachidonic acid (leukotrienes)

140
Q

What mediates the types of hypersensitivities

A

Antibodies mediate Types I, II, and III

141
Q

Type II hypersensitivities

A

Essentially autoimmune conditions through opsonization, complement, and antibody dependent cell-mediated cytotoxicity, usually due to NK cells or macrophages

142
Q

Direct Coombs

A

Detects antibodies that HAVE adhere to patient’s RBCs (testing Rh+ infant of an Rh- mother.

143
Q

Indirect Coombs

A

Detects antibodies that CAN adhere to other RBCs (testing Rh- woman for Rh+ antibodies)

144
Q

Type III hypersensitivity

A

Immune complex-antigen-antibody (IgG) activates complement which attracts PMNs which release lysosomal enzymes. Like Rheum diseases (SLE, vasculitides)

145
Q

Type III mnemonic

A

3 things stuck together: antigen-antibody-complement

146
Q

Serum Sickness path

A

Immune complex disease (type III) in which 5 days after being exposed to drugs (formerly exogenous proteins) antibodies are made which complex with the foreign substance and deposit in membranes causing damage from fixing complement.

147
Q

Serum Sickness presentation

A

Drugs (not serum) acting as haptens. Fever, urticaria, arthralgias, proteinuria, LAD 5-10 days after antigen exposure

148
Q

Arthus reaction

A

Type III where intradermal injections of antigen lead to antigen-antibody complexes with dema, necrosis, and activation of complement

149
Q

Arthus reaction test

A

IF staining

150
Q

Example of drugs that cause Arthus reaction

151
Q

Type IV hypersensitivity

A

Sensitized T cells encoutner antigen and release lymphokines (leading to macrophage activation, no antibody involved)

152
Q

Type IV hypersensitivity mnemonic

A

4 T’s: T lymphocytes, Transplant rejections, TB skin tests, Touching (contact dermatitis)

153
Q

Type IV tests

A

Patch test, PPD

154
Q

Type IV path

A

???????????

155
Q

Hypersensitivities mnemonic

A 
ACID
Anaphylactic and Atopic (type I)
Cytotoxic (antibody mediated) Type II
Immune complex (type III)
Delayed (cell mediated ) type IV
156
Q

Know examples of each type of hypersensitivties

A

????????????

157
Q

Autograft

158
Q

Syngeneic graft

A

From identical twin or clone.

159
Q

Allograft

A

From nonidentical individual of same species

160
Q

Xenograft

A

From different species

161
Q

What kind of rejection is hyperacute?

A

Type II reaction, complement activates and the organ dies

162
Q

Acute transplant rejection path

A

Cellular: CTLs activated against donor MHCs.
Humoral: similar to hyperacute, except antibodies develop after transplant.

163
Q

Chronic path

A

Recipient T cells perceive donor MHC as recipient MHC and react against donor antigens presented. Both cellular and humoral components.

164
Q

Graft-versus-host disease

A

Grafted immunocompetent T cells proliferate in the immunocompromised host and reject host cells with “foreign” proteins leading to severe organ dysfunction

165
Q

Hyperacute rejection features

A

Widespread thrombosis of graft vessels leading to ischemia and necrosis and graft must be removed

166
Q

Acute rejection features

A

Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate. Prevent/reverse with immunosuppressants.

167
Q

Chronic rejection features

A

Irreversible. T-cell and antibody-mediated damage.
Organ specific:
Heart - atherosclerosis
Lungs - bronchiolitis obliterans
Liver - vanishing bile ducts
Kidney - vascular fibrosis, glomerulopathy

168
Q

Chronic rejection path

169
Q

Graft-Versus-host disease features

A

Maculopapular rash, jaundice, diarrhea, hepatosplenomegaly. Usually in bone marrow and liver transplants (rich in lymphocytes). Potentially beneficial in bone marrow transplant for leukemia (graft-versus-tumor effect)

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