Unit 4 + Final Flashcards

1
Q

What is the lingo?

A
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2
Q

What causes transplant rejection?

A
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3
Q

How are antigens recognized?

A
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4
Q

What immune mechanisms lead to rejection?

A
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5
Q

What is hyperacute rejection and what is its cause?

A
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6
Q

What is acute rejection and what is its cause?

A
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7
Q

What is chronic rejection and what is its cause?

A
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8
Q

Donor APC are also presenting with _____ ___

A

donor MHC

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9
Q

What is graft rejection?

A

activation of immune response against donor tissue

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10
Q

What is the greatest barrier to transplantation as a therapeutic option for organ failure?

A

availability of organs

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11
Q

What methods can be used to reduce the immunogenicity of allografts?

A

sourcing transplants and minimize allogeneic differences between donor and recipient we test for compatibility

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12
Q

HLA genes code for what?

A

MHC

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13
Q

What is hematopoietic stem cell transplantation used for?

A

treat lethal diseases caused by intrinsic defects in one or more hematopoietic lineages in a patient

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14
Q

What is immunodeficiency?

A

doesn’t make the immune cells (or lack thereof)

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15
Q

What are the three strategies in development to induce donor-specific tolerance?

A

costimulatory blockade, hematopoietic chimerism, and transfer or induction of Tregs

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16
Q

What is costimulatory blockade?

A

All T cells will not be activated to react to self-antigen (peripheral tolerance)

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17
Q

What is hematopoietic chimerism?

A

take donor cells and mix it in culture. Those cells are put into recipient (peripheral tolerance)

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18
Q

________________ can be used to prevent or treat allograft rejection

A

immunosuppression

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19
Q

What are the two instances when graft versus host disease (GVHD) occurs?

A

the host is immunocompromised and therefore unable to reject the allogenic cells in the graft and solid organs that contain significant numbers of T cells are transplanted

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20
Q

What is transplantation?

A

process of taking cells, tissues, or organs from one individual and placing them into a different individual

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21
Q

What is a graft?

A

the cells, tissue, or organs you are transplanting

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22
Q

What is a donor?

A

the individual who provides the graft

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23
Q

What is a recipient?

A

the individual who receives the graft

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24
Q

What is orthotopic transplantation?

A

graft is placed in its normal anatomical site

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25
Q

What is heterotopic transplantation?

A

graft is placed in a different anatomical site

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26
Q

What is transfusion?

A

the transfer of circulating blood cells or plasma from one individual to another

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27
Q

What is autologous graft?

A

graft transplanted from one individual to the same individual

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28
Q

What is syngenic graft?

A

graft transplanted between two genetically different individuals

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29
Q

What is allogenic graft (or allograft)?

A

graft transplanted between two genetically different individuals of the same species

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30
Q

What is xenogenic graft (xenograft)?

A

graft transplanted between individuals of different species

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31
Q

What are alloantigens or xenoantigens?

A

molecules that are recognized as foreign in allografts or xenografts

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32
Q

What is alloreactive or xenoreactive?

A

lymphocytes and antibodies that react with alloantigens or xenoantigens

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33
Q

What are the 3 ways alloantigens are recognized by T cells?

A

direct presentation, indirect presentation, and antibody mediated recognition

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34
Q

When does direct recognition occur?

A

when the T cell of the host recognizes that the MHC of the donor is not the same

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35
Q

Every APC found in the transplanted tissue is going to be ________ ___, which explains why MHC is so important for transplant

A

non-self MHC

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36
Q

Intact MHC molecules displayed by cells in the graft are recognized by _________ _ _____ without a need for process by host APCs

A

recipient T cells

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37
Q

Why are T cell responses very strong?

A

because there is a high frequency of T cells that can directly recognize any single allogenic MHC molecule

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38
Q

What is indirect recognition of alloantigens?

A

picks up antigens from the donor and presents antigen on surface to the self T cell to recognize the foreign antigen from donor tissue

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39
Q

Each allogenic MHC molecule can have _______ ________ that are foreign for the host, each recognized by different clones of T cells

A

multiple peptides

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40
Q

True or False: T cell rejection can happen even if the MHCs are matched really well

A

True

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41
Q

The direct pathway is….

A

the APC from the donor presenting to the TCR of the recipient

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42
Q

What two things are required for triggering the T cell response for the direct pathway?

A

antigen itself and MHC

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43
Q

The indirect pathway is when…

A

the APC of the host is presenting foreign antigen only to the host T cell

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44
Q

If the MHC is matched really closely between donor and host, then the direct pathway is…

A

unlikely to stimulate donor rejection, but the indirect pathway is almost impossible to avoid

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45
Q

What APCs transport alloantigens to the lymph node?

A

dendritic cells

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46
Q

What types of cells cause rejection by distinct mechanisms?

A

Alloreactive CD4+ and CD8+ T cells that are activated by graft alloantigens

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47
Q

What is the outcome of sensitization in activation of alloreactive T cells?

A

activation of T cells, generation of effector T cells by direct and indirect antigen presentation

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48
Q

CTLA-4 induces what?

A

an inhibitory signal that downregulates T cell activation and is the target of induction regiments

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49
Q

Leukocyte depletion strategies use what?

A

antibodies such as thymoglobulin designed to bind to peripheral alloreactive lymphocytes allowing an allograft to settle in

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50
Q

Most of the antibodies produced in graft recipients that undergo rejection are usually target at what?

A

foreign MHC proteins (MHC mismatch), leading to strong antigen stimulation of B cells, T cells, and rejection

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51
Q

What is the most significant factor for why there is rejection in transplants?

A

MHC matching

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52
Q

High affinity alloantibodies are mostly produced by what types of cells?

A

helper T cell-dependent activation of alloreactive B cells

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53
Q

Label the rejection stages of allograft rejection in order

A

hyperacute → acute → chronic

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54
Q

What happens during hyperacute rejection?

A

once graft is put in, there are antibodies already there that react to it. Then, those antibodies will bind to their antigen and activate complement and platelets leading to blood clots

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55
Q

What is vascular occlusion?

A

blood clots will prevent blood flow to the new organ and grafted organ will suffer ischemic necrosis

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56
Q

What is ischemic necrosis?

A

no blood flow and no oxygen so tissue will die

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57
Q

What is acute cellular rejection?

A

activation of CD4+ helper T cells and CD8+ CTLs and cytokines produced by helper T cells that lead to inflammation and CTL-mediated killing of graft cells

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58
Q

What is acute antibody-mediated rejection?

A

activation of B cells with T cell help with high affinity antibodies specific to that donor tissue lead to binding of tissue and complement activation

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59
Q

B cells with high-affinity antibodies are targeted at what in acute antibody-mediated rejection?

A

a donor tissue that results in loss of the graft tissue

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60
Q

When does chronic rejection happen?

A

when we don’t have preexisting antibodies

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61
Q

What is chronic rejection?

A

accumulation of chronic inflammatory responses

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62
Q

In chronic rejection, alloantigen-specific CD4+ T cell start interacting with APCs. This results in what?

A

The APCs present antigens on self MHC and over time there are some antigens that cause a small response leading to release of some proinflammatory cytokines causing muscle cells to proliferate reducing O₂ capacity to the organ

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63
Q

What immune mechanism mediates blood transfusion reactions?

A

complement

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64
Q

Which individual’s immune cells are responsible for GVHD?

A

the donor

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65
Q

Which protein is tested when recipients are looking for a “match” for organ or stem cell transplantation?

A

HLA genes

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66
Q

What is the main challenge in xenotransplantation?

A

human immune cells and antibodies react to antigens from other species

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67
Q

What is an allograft?

A

tissue from an individual is transferred into another of the same species

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68
Q

If a transplant recipient already has antibodies against the donor tissue when the transplant occurs, what type of rejection would you expect?

A

hyperacute

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69
Q

In mice, if a donor mouse is genetically identical to the recipient mouse, what is the result of a transplant?

A

no rejection

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70
Q

If a donor mouse gives a tissue transplant to a recipient mouse that is 1/2 the same strain and 1/2 a different strain, what is the result of the transplant?

A

no rejection

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71
Q

What are the general characteristics of the microenvironment?

A
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72
Q

How can the immune system recognize cancer?

A
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73
Q

What T cell types are important for cell-mediated

A
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74
Q

How to target cancer cells if they are “self”?

A

mutations lead to a change in proteins to form neoantigens, which are cancer-specific and exempt from central tolerance

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75
Q

______ ____ ________ can also be detected along with neoantigens

A

normal self antigens

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76
Q

What is the main mechanism for killing tumors?

A

CD8+ CTLs

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77
Q

Antibody significance may kill tumor cells by what two methods?

A

activating complement and ADCC

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78
Q

What innate cells can contribute to immune surveillance against cancers and kill tumor cells?

A

NK cells

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79
Q

What are two ways innate immune cells can promote tumor growth

A

M2 macrophages and innate cells generate free radicals causing DNA damage and leading to mutations

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80
Q

What adaptive immune cells can contribute to tumor growth?

A

Increase in Tregs and Th1

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81
Q

What are the different ways your immune system fights tumors?

A

blocking T cell inhibitory pathways, vaccination with tumor antigens, adoptive cellular therapy with antitumor cells, passive immunotherapy with antibodies, cytokine therapy, and non-specific inflammatory stimuli

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82
Q

What happens in blocking T cell inhibitory pathways?

A

Inhibiting the inhibitor to activate the cell

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83
Q

What is the goal of inhibiting inhibitors?

A

activate T cells in site of the anti-activation environment around tumors

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84
Q

Vaccines with tumor antigens are composed of what?

A

killed tumor cells, recombinant tumor antigens, or dendritic cells incubated with tumor antigens

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85
Q

What is the process of personalized tumor

A
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86
Q

What are the three types of adoptive cellular therapies?

A

tumor infiltrating lymphocyte therapy (TIL), chimeric antigen receptor (CAR) T-cell therapy, and endogenous T-cell (ETC) Therapy

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87
Q

What happens in chimeric antigen receptor (CAR) T-cell therapy?

A

design a specific receptor that binds to a specific antigen and T cells react strongly against that antigen which are infused back into patient and those T cells bind to cancer cells and kill them

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88
Q

What is the drawback of CAR T cell therapy?

A

potential off target toxicity effects if CAR T cell can bind to other things besides the cancer cell

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89
Q

What are the three ways to develop passive immunotherapy with antibodies?

A

direct tumour cell killing, immune-mediated tumuor cell killing, vascular and stromal cell ablation

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90
Q

T cells cannot proliferate without what cytokine?

A

IL-2

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91
Q

High doses of ___ is clinically approved treatment for advanced melanoma and renal cell carcionoma

A

IL-2

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92
Q

___ and ____ are effector antitumor agents in animal models

A

TNF; IFN-ɣ

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93
Q

What is the mechanism responsible for hypersensitivity disorders?

A
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94
Q

How soon after the exposure of hypersensitivity disorders does the response occur?

A
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95
Q

What is immunodeficiency?

A

underactivation of the immune system

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96
Q

Type I is an ______ type of reaction and based on ___ mediation

A

allergic; IgE

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97
Q

Type II involves ___, ___, and ________ cells

A

IgG; IgM; Cytotoxic

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98
Q

Type III is an _____ ______-_______ , in which antibodies and antigens are stuck together causing inflammation

A

immune complex-mediated

99
Q

Type __ results in production of cytokines?

A

IV

100
Q

_____ ________ happens when you don’t have a response, but you will have antibodies the next time you’re exposed

A

First exposure

101
Q

When __-______ happens, ____ binds causing release of histamines

A

re-exposure; IgE

102
Q

IgE antibodies respond to what types of organisms?

A

helminths

103
Q

What are the two ways antibody-mediated diseases are produced?

A
  1. antibodies bind to antigens on particular cells or in extracellular tissues 2. antigen-antibody complexes that form in the circulation and are deposited in cell walls
104
Q

Immune complexes that can cause disease may be composed of what?

A

antibodies bound to either self antigens or foreign antigens

105
Q

Many systemic immunological diseases in humans are caused by what?

A

the deposition of immune complexes in blood vessels

106
Q

Type __ is the only type of hypersensitivity that does not involve antibodies

A

IV

107
Q

Type IV is a classic _________ response

A

autoimmunity

108
Q

_______-____ ________________ is another type of type IV hypersensitivity

A

Delayed-Type Hypersensitivity (DTH)

109
Q

In tuberculosis, T cells can only be activated if…

A

you have previously encountered that pathogen

110
Q

chronic DTH reactions happen when

A

innate immune cells throw themselves on top of the phagocytosed microbes

111
Q

granulomatous inflammation is caused by what?

A

prolonged cytokine signals

112
Q

What antibody isotype is associated with Type I hypersensitivity?

A

IgE

113
Q

Which Hypersensitivity type is associated with antibody immune complexes?

A

Type III

114
Q

How do T cells mediate hypersensitivity reactions?

A

CD8 T cell direct killing, CD4 T cells produce cytokines, and induce inflammation

115
Q

Will a delayed type hypersensitivity response occur in an individual the first time they are exposed to an antigen?

A

No

116
Q

Which hypersensitivity type is associated with IgM and IgG antibodies that attach to cells and induce complement and cytotoxic responses?

A

Type II

117
Q

Cytochrome c is present in the ___________ _____________ _____ during normal cell function and is released into the _________ when apoptosis is initiated

A

mitochondrial intermembrane space; cytoplasm

118
Q

What is the basic mechanism of general anti-inflammatory drugs (NSAIDS and SAIDS)?

A

inhbiit the secretion of cytokines and other mediators of inflammation

119
Q

What type of hypersensitivity do general anti-inflammatory drugs target?

A

Bring down the inflammation and reduce symptoms (not sure abt this one)

120
Q

What are the four the basic mechanisms of anti-cytokine therapy?

A

soluble cytokine receptor, anti-cytokine antibodies, cytokine receptor antagonists, and small molecule inhibitors (JAK kinases)

121
Q

What type of hypersensitivity does anti-cytokine therapy target?

A

Type IV

122
Q

What is the basic mechanism of depletion of cells/antibodies?

A

CD20 (depletes B cells), CD3 (depletes T cells), and CD52 (depletes B and T cells)

123
Q

What type of hypersensitivity does depletion of cells/antibodies target?

A
124
Q

What are the three basic mechanisms of other biologic agents (anti-receptor anti-integrin antibody treatment)?

A

Blocks B7 costimulators (CTLA-4-IG), inhibits leukocyte migration into tissues (Anti-c4 integrin), and block T cell-mediated activation of B cells and macrophages (Anti-CD40)

125
Q

What type of hypersensitivity does other biologic agents (anti-receptor anti-integrin antibody treatment)?

A
126
Q

What are the five basic mechanisms of intravenous Ig (IVIG) therapy?

A
  • inhibits activation and function of -DCs, monocytes, macrophages, neutrophils, and NK cells
  • neutralizes activated complement components
  • modulates B-cell functions and plasma cells
  • reciprocally regulates Treg cells and effector T cells, such as Th2 and Th17 subsets
  • downregulates the production of inflammatory cytokines
127
Q

What type of hypersensitivity does intravenous Ig (IVIG) therapy target?

A
128
Q

What is the basic mechanism of tolerance inducing therapies?

A

induce tolerance in disease-producing T cells (promote activation of regulatory cells without activating effector cells)

129
Q

What type of hypersensitivity do tolerance inducing therapies target?

A
130
Q

What are the two functions of integrins?

A

help cytotoxic T cells bind to their antigens and help with cells get to the place via diapedesis

131
Q

What drugs can strongly prevent inflammation?

A

corticosteroids

132
Q

What is an example of a tolerance-inducing therapy?

A

induce Tregs with low dose IL-2

133
Q

Which type of hypersensitivity does anti-cytokine therapy primarily target?

A

type IV

134
Q

Which type of hypersensitivity does antibody depletion therapy most likely target?

A

type II and III

135
Q

How might low-dose IL-2 induce tolerance to treat autoimmune disorders?

A

promoting activation and proliferation of Tregs

136
Q

What kind of antibodies are part of an IVIG treatment?

A

all immunoglobulins isolated from the blood plasma of donors

137
Q

What is the main mechanism of corticosteroids to suppress inflammatory signals?

A

reduce cytokine release

138
Q

What is the difference between immediate allergic reactions and late-phase reactions?

A
139
Q

How is Th2 cells involved in

A
140
Q

How are mast cells involved in allergy?

A
141
Q

What does granulation do in early allergy?

A
142
Q

What does granulation do in late allergy?

A
143
Q

Allergy is also known as

A

Type I hypersensitivity

144
Q

What is an allergen?

A

an antigen that causes a response in an inappropriate way?

145
Q

What happens during first exposure to antigen (none of which are noticeable)?

A

T-cell dependent production of IgE, Th2 cells stimulate class switching in B cells, plasma cells secrete IgE, and IgE binds to high affinity IgE receptors on Mast cells

146
Q

FcεR1 represents what?

A

constant region of IgE

147
Q

IgE comes from what?

A

B cells that are activated by T cells

148
Q

Eosinophils are identified based on what?

A

granules contain basic proteins that bind acidic dyes

149
Q

Polyvalent means what?

A

multiple epitopes that bind to the same antigen

150
Q

What happens upon second exposure to allergen?

A

antigen binds to mast cell, cross-links the antibody, and releases all the granules inside

151
Q

Vascular and smooth muscle response causes what (histamine and other mediators)?

A

immediate reaction

152
Q

True or False: Mast cells respond only to cross-links

A

False, mast cells do not respond only to cross-links

153
Q

Cytokine has to be expressed from the _____

A

genes

154
Q

What are the two outcomes of the signaling pathway of granule exocytosis?

A

vascular dilation, smooth muscle contraction and tissue damage

155
Q

What are the two outcomes of the signaling pathway of enzymatic modification of arachidonic acid?

A

vascular dilation and smooth muscle contraction

156
Q

What is the outcome of the signaling pathway of transcriptional activation of cytokine genes?

A

inflammation (leukocyte recruitment)

157
Q

After second exposure, there is an _______ reaction and a ___ ____ reaction

A

immediate; late phase

158
Q

Late phase is driven by _________

A

cytokines (causing inflammation)

159
Q

Immediate phase is driven by __________

A

histamines

160
Q

Upon first exposure to an allergic antigen, what key cell types are activated?

A

Th2 and B cells

161
Q

Upon second exposure to an allergic antigen, what cells are activated?

A

eosinophils, basophils, and mast cells

162
Q

What antibody isotype is associated with allergic responses?

A

IgE

163
Q

What mechanisms lead to the immediate allergic reaction?

A

mast cells degranulate vasoactive amines and lipid mediators

164
Q

What mechanisms lead to the late-phase allergic reaction?

A

cytokines produced by mast cells recruit leukocytes

165
Q

What are the differences and similarities between primary (congenital) and secondary (acquired) immunodeficiency?

A

In primary immunodeficiency, genetic defect results in an increased susceptibility to infection that is frequently. In secondary

166
Q

What are the general principles behind innate cell deficiencies?

A
167
Q

What are the general principles behind

A
168
Q

Serum Ig levels test whether or not you can make what?

A

antibodies

169
Q

What is T cell receptor excision circles?

A

during VDJ, VDJ recombinase brings two combinases and forms a loop and then cuts off that loop

170
Q

______ and ______ are your first line of defense

A

phagocytes; complement system

171
Q

Complement is responsible for what three purposes?

A
172
Q

Chronic Granulomatous Disease is caused by what?

A

mutations in components of the phagocyte oxidase (phox) enzyme complex

173
Q

Another example of immunodeficiency is

A

leukocyte adhesion deficiencies

174
Q

What is leukocyte adhesion deficiency?

A

inflammation doesn’t work the way it’s supposed to

175
Q

APCs are triggered by ___

A

toll-like receptor signaling

176
Q

What is severe combined immunodeficiency (SCID)?

A

any immunodeficiency that affects both B cells and T cells

177
Q

What types of cells lead to SCID?

A

T cells

178
Q

Genetic defects that cause SCIDs are _________ ________ or ________

A

autosomal recessive; X-linked

179
Q

RAG1, RAG2, and artemis are involved in what process?

A

VDJ

180
Q

MHC class II is involved in what process?

A

positive or negative selection of the thymus

181
Q

What is the consequence of RAG1 and RAG2 being knocked out in a patient?

A

no mature B cells or T cells

182
Q

________ __________ can be a major part of causing immunodeficiency

A

cytokine signaling

183
Q

A severe type of SCID is

A

no VDJ recombination

184
Q

No signaling from TCR stage, then what happens to the T cell?

A

the T cell will not continue

185
Q

MHC class II deficiency, or Bare lymphocyte syndrome, results in what?

A

no CD4+ T cells (and also no B cells)

186
Q

SCID can be caused by what type of defective cell activation?

A

defective T cell activation

187
Q

What are selective immunoglobulin isotype deficiencies caused by?

A

a problem of the signaling of certain cytokines in B cells

188
Q

How does early phase response differ from late phase response?

A
189
Q

Why do people get allergies?

A
190
Q

How do different modes of entry alter the immune response to allergens?

A
191
Q

How do antihistamines work?

A
192
Q

What is anaphylaxis and how is it treated?

A
193
Q

What is bronchial asthma and how is it treated?

A
194
Q

What is sensitization/desensitization?

A
195
Q

Immediate phase is driven by what?

A

histamines

196
Q

Late phase is characterized by what?

A

inflammation, primarily by eosinophils

197
Q

Immediate reaction is the [first or second] exposure to antigen?

A

second

198
Q

Immediate reaction is also known as what?

A

Wheal and Flare Response

199
Q

Why do individuals develop allergies?

A

genetics, microbiota, and exposure to environment

200
Q

People are more likely to have allergies when they develop strong ___ responses

A

Tₕ2

201
Q

Responses to the [same or different] allergen may have the [same or different] manifestations depending on the tissue targeted

A

same; different

202
Q

Histamine acts primarily on what receptor?

A

H1 receptor

203
Q

In chronic allergic inflammation, histamine effects on inflammatory cells cause what?

A

cellular activation and release of proinflammatory mediators

204
Q

What is anaphylaxis?

A

a systemic reaction in which a patients come into contact with something they’re allergic to

205
Q

Anaphylaxis is driven by what?

A

histamines and other amines

206
Q

What is a treatment for anaphylaxis?

A

epinephrine

207
Q

What are the two ways epinephrine treats anaphylaxis?

A

causes peripheral vasoconstriction and relaxes smooth muscles for bronchodilation

208
Q

What are the two major targets for asthma?

A

prevention and reversal of inflammation

209
Q

What can reduce bronchial constriction?

A

leukotriene antagonists and muscle relaxants

210
Q

Antihistamines [are or are not] effective treatments for asthma?

A

are not

211
Q

What can be used to treat atopic dermatitis?

A

corticosteroids

212
Q

Desensitization uses the ___ to regulate the environment and prevent inflammation from occuring

A

gut

213
Q

How does desensitization occur?

A

by inducing small doses of allergen over time

214
Q

What is the early phase of an allergic response in the skin?

A

Wheel and flare

215
Q

True or False: There is a strong genetic component to a person’s susceptibility to developing an allergic response

A

True, there is a strong genetic component to a person’s susceptibility to developing an allergic response

216
Q

For what type of hypersensitivity are antihistamines the most effective and why?

A

Type I, because antihistamines counter the effects of degranulation of granulocytes

217
Q

Eczema is an allergic response, but where do allergens (most commonly) come from?

A

exposure to airborne allergens

218
Q

What allergic response is NOT helped with treatment using antihistamines?

A

asthma

219
Q

What are some of the causes and mechanisms of acquired immunodeficiency?

A
220
Q

What is the viral lifecycle of HIV?

A
221
Q

and how it infects cells and causes diseases at the cellular level?

A
222
Q

What is secondary (acquired) immunodeficiencies?

A

immunodeficiency due to something that was acquired during life

223
Q

Malnutrition and immunodeficiency is associated with what?

A

impaired cellular and humoral immunity to microorganisms

224
Q

All the immune cells come from where?

A

the bone marrow

225
Q

What are some ways immunodeficiency can cause cancer?

A
226
Q

What are the two ways to suppress the immune system?

A

functionally inactivate lymphocytes and inactivate cytokines

227
Q

HTLV-1 infects and transforms what types of cells?

A

CD4+ T cells, reducing the number of T cells that can fight infection

228
Q

Why would we need the immune system to fight viral tumors?

A

immune system is responsible for fighting tumors

229
Q

What work to shut down viral production?

A

restriction factors

230
Q

HIV enters immune cells via what method?

A

chemokine receptors

231
Q

CD8 T cells responds at what point during the immune response to HIV?

A

Day 20

232
Q

What types of receptors detect virally infected cells?

A

TLRs and RIG-I

233
Q

The initial adaptive immune response to HIV infection is characterized what?

A

expansion of CD8+ T cells specific for HIV peptides

234
Q

What are the two mechanisms of immune evasion by HIV?

A

HIV has a high mutation rate and down-regulate class I MHC

235
Q

What are the 3 mechanisms that contribute to the loss of CD4+ cells in HIV?

A

cytopathic effects of viral infection, killing by antigen-specific CTLs, and activation of inflammosome and elimination of infected cells by pyroptosis

236
Q

The most prominent defects caused by HIV are in [humoral or cell-mediated] immunity with results from the destruction of [CD4+ or CD8+] T cells

A

cell-mediated; CD4+

237
Q

What is the primary form of treatment for HIV?

A

target replication of the virus (antiretroviral therapy)

238
Q

How do anti-HIV treatments target the virus?

A

inhibit enzymes and proteins required for viral infection

239
Q

How does HIV lead to immunodeficiency?

A

it targets and infects CD4 T cells

240
Q

How does HIV evade the immune system?

A

it has an extremely high mutation rate, preventing detection by antigen-specific T cells & antibodies

241
Q

What about HIV makes it especially challenging to design a vaccine for?

A

the high rates of mutations makes the target antigen a moving target

242
Q

What is NOT something that leads to acquired immunodeficiency?

A

genetics

243
Q

No detectable vascular reactions from an immediate reaction happen in what disease?

A

bronchial asthma