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Immune > IID block > Flashcards

IID block Flashcards

1
Q

Central thymic tolerance

A
  • Regular pos & neg selection - delete T cells that have receptors with high-binding affinity for intrathymic self-antigens
  • Deletional tolerance
  • Regulatory tolerance
  • Clonal anergy: lack of costimulation –> T cells get inactivated
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2
Q

What two kinds of T cells get to mature and leave the thymus to join the peripheral T cell pool?

A
  • Low-affinity self-reactive T cells
  • T cells with receptors specific for antigens that aren’t represented intrathymically
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3
Q

Peripheral (post-thymic) tolerance

A
  • Sequestration: antigen is hidden
    • self-reactive T cells in circulation ignore self-antigens that are sequestered in the tissue
  • Immunoprivileged site: Fas or cytokine (TGF-B, IL-10) blocks T cell response
    • Ex) eye, brain, testes
  • Deletion/anergy by CTLA4 of self-reactive T cells
  • Immune regulation via Tregs secreting IL-10 –> inhibits IFN-y secretion from Th1 –> prevents inflammation
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4
Q

When does B -cell deletion happen?

A

Occurs in the bone marrow after B cells with high-affinity Ig receptors react with self membrane-bound antigens

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5
Q

Facotrs that influence the outcome of any immune response:

A
  • Antigen structure
    • soluble antigens = good tolerangens –> no response
  • Antigen dose
    • Low induces T cell tolerance
    • High induces both B & T cell tolerance (clonal exhaustion)
    • Intermediate is actually immunogenic –> cytokines
  • Route of administration
    • Tolerogenic - oral & IV
    • SC, IM, and intraderm are more immunogenic
  • Host genetics
    • Women have more autoimmune disease
    • More HLA class II genes –> increased risk of autommune
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6
Q

Antigen-presenting cells affect immune response through

A

ability to provide or not provide costimulation to T cells

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7
Q

CD4 Tregs express and require ___ in order to differentiate.

A

Foxp3 transcription factor

Foxp3 is X-linked so males are disproportionately affected

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8
Q

Mutations or dysregulation in the Foxp3 gene can lead to ___.

What is treatment/presentation?

A

IPEX syndrome: Multiple organs, lethal if not treated early in childhood as several autoimmune responses will develop (RA, SLE, Diabetes)

Tx:immunosuppressive trx to combat self-specific T cell function

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9
Q

What are the most suppressive cytokines?

A

IL-10

TGF-B

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10
Q

While autoimmunity is common, autoimmune disease is rare.

______ persists in normal people, but autoimmune-diseased people have ____ inducing the production of autoimmune responses.

A

Autoreactive B and T cells persist in normal subjects, but in autoimmune disease, autoantigen induces the production of autoimmune responses.

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11
Q

___ inhibits Th2 secretion

____ inhibits Th1 secretion

A

IFN-y inhibits Th2 secretion

IL-10 (& IL-4) inhibits Th1 secretion

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12
Q

___ activates Th1 secretion

___ activates Th2 secretion

A

IFN-y & IL12 activates Th1

IL-4 activates Th2

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13
Q

Th1 secretes what cytokines? What do they do?

A

IFN-y

IL-2

  • Activate CD 8 cells & macrophages
  • Delayed type hypersensitivity
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14
Q

What cytokines does Th2 secrete? What do they do?

A

IL-4, IL-5, IL-6, IL-9, IL-10, IL-13

  • Antibody response
  • IL-4 & IL-5 enhances class switching
  • IL-10 is anti-inflammatory
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15
Q

Treg cells are CD_+ and CD_+

How does it do its job of suppressing immune response in the periphery (2 ways)?

A
  • CD4+, CD25+
  • Binds IL-2 receptors with its CD25+ to decrease teh IL-2 in peripheral circulation –> prevent activation of T cells
  • Secretes IL-10 to suppress autoreactivity
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16
Q

Positive & negative selection still applies to Treg cells. Describe it.

A

Positive selection: It needs to bind self MHC

Negative selection: It can’t be self-reactive (can’t bind MHC-peptide too tightly)

Or else - apoptosis

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17
Q

Immunologic tolerance

A

immunologic unresponsiveness to a specific antigen

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18
Q

3 fates of T cells in periphery

A
  • No co-stimulation -> apoptosis/anergy
  • B6 binds CD28 (costimulation)
    • IL-2 production -> effector function
    • cell proliferation & differentiation
  • B7 binds CTLA4 –> cell cycle arrest
    • Because CTLA4 from Tregs has a higher affinity for B7 that will outcompete CD28
      • –> prevent IL2, T cell development, proliferation
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19
Q

Neonatal tolerance

A

Fetal becomes tolerant of mom’s antigens (toleragens)

Later in life, baby won’t react to similar antigens because of these toleragens until maturation post-partum

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20
Q

B cell tolerance

A

Self-peptide but with no T cell help –> no self-antibodies

Exogenous peptide that T cell recognizes as foreign –> promote B cell isotype switching and hypermutation

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21
Q

In autoimmunity, there is an increase in which Th and a decrase in which one?

A

Increased Th1 –> hyperactivation of immune response & IL-2

Decreased Th2 & Tregs

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22
Q

Origins of autoimmunity

A
  • Sequestered/late-developing antigens: antigens leak from immunoprivileged site to cause response
  • Molecular mimicry: antigen looks like self, but immune still makes autoantibodies against it
  • Neoantigens: self antigen+foreign antigen
  • Anomalous antigen presentation: extremely high MHC II will overcome co-stimulation needed
  • Loss of Tregs
  • Lymphoproliferation
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23
Q

Autoimmune pathogenesis of chronic & acute inflammation

A

• Autoreactive T cells: infiltration of CD4/8 cells ⇒ increased cytokine production ⇒ chronic inflammation

• Autoantibodies: complement-mediated lysis against own self, ADCC, immune complex deposition ⇒ acute inflammation

  • ADCC: Antibody dependent cellular cytotoxicity with NK cells
    • Tolerance: NK cell + inhibitory ligand ⇒ prevention of NK activation
    • Autoimmune: NK cells will kill anything with an antibody on it.
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24
Q

Insulin-dependent diabetes is what type of autoimmune disease?

A
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25
Q

Rheumatoid arthritis is what type of autoimmune disease?

A
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26
Q

Pernicious anemia is what type of autoimmune disease

A
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27
Q

SLE is what type of autoimmune?

A
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28
Q

Delayed Type Hypersensitivity / Type IV Hypersensitivity

A
  • T cell mediated
    • Direct cell cytotoxicity: CD8+ T cells directly kill targeted cells
    • Inflammatory rxn: CD4+ T cells recognize antigens & release inflammatory cytokines
  • 4T’s:
    • T cells
    • Transplant rejections e.g. GVHD
    • TB skin test
    • Touching - Contact dermatitis from mosquitos, bed bugs, chigger
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29
Q

Process of a mosquito bite causing delayed type hypersensitivity

A
  1. Dendritic cells uptake antigens from mosquito antigens & express them on MHC II -> go to lymph nodes to present to Th2
  2. Th2 cell goes through blood to enter tissue at inflammation site, where it
    1. Interacts with macrophages
    2. Releases IL-5 to recruit eosinophils via IL-5
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30
Q

TGF-B will cause a native Th0 cell to become ___

TGF-B + IL-6 will cause a native Th0 cell to become __

A

TGF-B alone –> Treg

TGF-B + IL-6 –> Th17

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31
Q

T cells survey __ cells in the ___.

B cells survey ___ cells in the __.

A

T cells survey dendritic cells in the paracortex

B cells survey follicular dendritic cells in the cortex

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32
Q

If a B cell binds an antigen presented by a follicular dendritic cell, what happens next

A
  • It will present that antigen on an MHC II
  • It will produce IgM
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33
Q

B cell activation

A
  • Helper T cells activate B cells via antigen interaction & CD40 costimulation
  • Consequences of CD40 activation:
    • Isotype switch from IgM to other types
    • Affinity maturation: B cells with the best antigen binding sites that have the best fit will reproduce more –> higher affinity
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34
Q

Intermediate Type Hypersensitivity/ Type I Hypersensitivity

A

Anaphylaxis!!

B cell activation causes it to produce a ton of IgE, whose Fc region binds mast cells.

  • Immediate: Antigen crosslinks pre-formed IgE on presensitized mast cells –> degranulation –> histamine, tryptase, serotonin, and heparin release
  • Late: chemokines and other mediators cause inflammation & tissue damage
    • Eicosanoids - prostaglandin D2, leukotriene C4
    • Cytokines - IL4, TNF
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35
Q

Eicosanoids released in type I hypersensitivity recruit inflammatory cells.

How?

A

Prostaglandin D2 - attract eosinophils, basophils, Th2 cells

Leukotriene C4 - mediates vascular permeability and bronchoconstriction

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36
Q

What do IL-4 and TNF do in type i?

A

Il-4

  • promotes Th2 differentiation
  • promotes class switching to IgE
  • upregulate MHC-II

TNF is a pyrogen (produce heat); makes ya feel bad

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37
Q

_____ are not present in tissue because they’re very destructive, so they have to be recruited from bone in a type I hypersensitivity reaction

A

Eosinophil

Pre-formed: major basic protein, eosinophil caitonic protien, eosinophil-derived neurotoxin, eosinophil peroxidase

Newly-formed: IL-1, 2, 4, 5, 6, 8, 13, and TNF

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38
Q

Both ___ and __ have preformed granuels of histamine.

A

Mast cells & basophils

Newly formed: eicosanoids, IL-4, TNF

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39
Q

_____ has preformed elastase, cathelicidin, lactoferrin, and can phagocytose with peroxide, but no newly formed mediators.

Also makes NETs: chromatin and serine proteases

A

Neutrophils

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40
Q

Itch-scratch reflex

A
  • Mast cells release histamine & other mediators; histamine causes
    • edema at the venules
    • itch at C-fibers
      • Unmyelinated C fibers with free ends in the basal layer of skin
        • Mechanosensitive: pain; Mechanoinsensitive: itch
  • Spinal reflex modulated by input rom brain
  • Decreases the likelihood of lyme disease bc remove tick
41
Q

Desensitization vs Tolerance

A

Desensitization: Injection of small doses of allergen will wash out IgE on the surfaces of mast cells, but does not prevent plasma cels form making more IgE

Tolerance: high dose injections for years will induce long-term tolerance that persists even after stopping the injection; induce IgG4 production that outcompetes IgE

42
Q

Type 2 Hypersensitivity Reactions / Cytotoxic Reactions

A

Antibodies bind to cell-surface antigens to cause..

  • *DESTRUCTION*: opsonize the cell for death via phagocytosis, complement, or NK cells (ADCC)
  • Inflammation: activate complement system and Fc receptor-mediated inflammation
  • Dysfunction: blocks cell surface receptors to prevent downstream processes
43
Q

Injecting yourself with the blood from a patient with idiopathic thrombocytopenia results in

A

type 2 hypersensitivity reaction:

IgG bind the platelet surfaces -> complement cascade -> DESTROY platelets or promote its phagocytosis by macrophages

44
Q

Type 3 hypersensitivity rxns / Antigen-antibody complex disease

A

Immune complex: Antigen-antibody-complement –> complement attracts neutrophils

  • Antibody is usually IgG
  • SLE, poly arteritis nodosa, PSGN
  • Serum sickness:
45
Q

Serum sickness

A

Caused by repeated administration of horse antiserum to treat Diphtheria toxin

–> joint pain, fever, rash, lymph node enlargement, kidney damage

Type 3 HS

46
Q

The only example of IgA mediated hypersensitivity

A

celiac disease

IgA against tissue transglutaminase destroys intestinal villa

47
Q

Early introduction of commonly allergenic foods (aka peanuts) ____ the incidence of allergies.

A

reduces the incidence.

feed your babies pb!!!

48
Q

If the cell is being destroyed then it is

A

type 2 hypersensitivity!

49
Q

The effectiveness of a vaccine correlates with ____ to a certain antigen

A

serum IgG

50
Q

Homologous vs heterologous passive immunity

A
  • Homologous: antibodies against many antigens
    • Ex) Breast mlk has pooled human antibody, human hyperimmunoglobulin
  • Heterologous: animal-derived or synthetic antibodies
    • Risks serum sickness upon re-exposure
    • Ex) HBAT (botulism), palimizumab (RSV)
51
Q

The more similar a vaccine is to the pathogen, the better the immune response.

Live attenuated vs Inactivated vaccines

A
  • Live attenuated vaccines: weakened form of wild-type pathogen that can replicate in you
    • Ex) BCG vaccine, measles, mumps, rubella, etc
  • Inactivated vaccine: organism can’t cause disease, but still stimulates an immune response
    • May be the whole thing or just a protein or polysaccharide of it
      • Protein-based: toxoid (inactivated toxin) or a subunit
      • Polysaccharide based: pure or conjugate
52
Q

Inactivated > part of an organism > polysaccharide > conjugated

What are conjugated vaccines?

A

A polysaccharide antigen fused to a carrier protein

Induces T- cell dependent response & memory cell development

53
Q

___ vaccines induce a T-cell independent response, which does not work well in children <2 years because low immunogenicity.

A

Pure polysaccharide vaccines

54
Q

Name tow protein-based toxoid vaccines

A

Diphtheria & Tetanus

55
Q

Difference in antibody resposne upon the first exposure vs the second exposure of the vaccine

A

First time: mostly IgM, low affinity

Next time: mostly IgG, higher affinity

56
Q

Adjuvants

A

Natural or synthetic substances that enhance immune response to co-administered antigens

Replaces immunological characteristic(s) lost during the conversion of the pathogen to a vaccine

57
Q

Vaccines induce what 3 mediators?

A
  • Bcells make antibodies to the pathogen/toxin
  • CD8 cells recognize & kill infected cells via cytokines
  • CD4 cells produce cytokines and support B and CD8 T cell response
58
Q

Issues with vaccine development

A

Complex pathogens

Insufficient supply, price of production, accessibility

Refusal, lack of knowledge, misinformation

59
Q

Vaccinating “at-risk” groups

A

Elderly, neonates, and immunocompromised individuals

  • Increased susceptibility to disease
  • Different treatment and infection control
  • Different formulations are required to make an effective vaccine
60
Q

Eradication vs Elimination

A

Eradication refers to the complete and permanent worldwide reduction to zero cases of the disease throughout deliberate efforts

Elimination refers to the reduction to zero of new cases in a defined geographical area

61
Q
  • Recurrent bacterial & enteroviral infections in 4-6mo. babies
  • No B cells
  • No Ig’s of any class
    • Absent/scanty lymph nodes and tonsils
  • No primary follicles or germinal centers
  • Normal WBC count & lymphocyte levels

What is the disease and its cause?

A

X linked Brton agammaglobulinemia

Defect in BTK–> no B cell maturation (stuck as pre-B cells) –> can’t make antibodies

62
Q

Treatment for X-linked Bruton agammaglobulinemia?

A

Pre-B cells aren’t maturing due to BTK defect–> no Igs, so tx: gamma globulin (IV or subcutaneously)

63
Q
  • Bacterial infections, e.g. pneumocystitis pneumonia
    • Mouth ulcers
    • Always on antibiotics
  • Decreased IgG, A, and E
  • High IgM
  • No germinal centers

What is the disease and the cause?

A
  • Defective CD40L on Th cells
    • –> terminal B cell can’t differentiate –> no isotype switching
    • –> Can’t activate macrophages to release GM-CSF, so decreased phagocytosis & low neutrophils
64
Q

Wha tis TX of hyper-IgM syndrome?

A

Defective CD40L on Th cells –> infections due to inability to class switch & decrased phagocytosis –> Tx: IVIG (intravenous immunoglobulin) replacement for infections

65
Q
  • Frequent bacterial infections (staph, serratia, nocardia)
    • ​Cold staph abscesses
  • Pneumonia
  • Fungal infections (esp aspergillus)
  • *Catalase positive organisms*
  • Males

Disease? Cause? Test? Tx?

A

Chronic granulomatomatous disease

  • Defective NADPH oxidase –> can’t perform respiratory burst in neutrophils to kill catalase + organisms
  • Test:
    • Nitroblue Tetrazolium (NBT) dye test can’t turn blue
    • Abnormal flow cytometry (can’t turn green)
  • Tx: bone marrow transplant, bacterial & antifungal prophylaxis, IFN-gamma to upregulate neutrophils
66
Q
  • Failure to thrive / Diarrhea / Thrush / Otitis media
  • Recurrent infections of ALL KINDS
  • No thymic shadow on CXR
  • No/low TRECs
  • No germinal centers
  • No T cells on flow cytometry
  • Low Ig

Disease & cause?

A

SCID

  • Cause:
    • ADA or PNP deficiency (aut recessive) –> lymphocytes can’t clear purine metabolism byproducts so T & B cells don’t survive
    • Gamma chain deficiency (X-linked) –> no receptors for T cells so they can’t develop; B cells don’t work
67
Q

Best way to screen for and diagnose SCID?

A

Examine T cells, B cells, then NK cells

PCR to measure TRECs (DNA molecules that are byproducts of excessional rearrangements of T cell receptor genes, which in SCID, aren’t working)

Tx: gene therapy, bone marrow transplant

68
Q

What is the catch 22 of digeorge syndrome? What else presents with it?

A

Cleft palate

Abnormal facies

Thymic aplasia, so absent thymic shadow! –> lack of T cells

Conotruncal abnormalities: Congenital heart disease

Hypocalcemia due to lack of parathyroids –> tetany

Presents with: seizures, murmur

Tx: thymic transplant

69
Q

Cause of digeorge?

A

22q11 deletion TBX gene due to defect in embryogenesis, 3rd and 4th pharyngeal pouches

–> Lack of development of the thymus and parathyroid

–> No functional T cells and depressed T cell immunity –> thymic, parathyroid, and cardiac defects

70
Q
  • Low T cells
  • Low PTH & Ca2+
  • Thymic shadow absent on CXR
A

Digeorge syndrome - absent thymus & parathyroids

Will also see CATCH22!

71
Q

What is the cause of autosomal scid?

A

RAG defects prevent VDJ recombination

–> no T or B cell development

72
Q

What two diseases cause problems that present at any age (including later in life)?

A

AIDS & CVID

73
Q

HIV/AIDs

Cause? Presentation?

A

Loss of CD4+ cells after infection with retrovirus HIV

Presentation: opportunistic infections

74
Q
  • 20 or 30 year old
  • Sinopulmonary infections (usu bacterial)
  • *Bronchiectasis*
  • Gastrointestinal, endocrine, hematological disorders
  • Low IgG, IgA, and/or IgM
  • Low plasma levels

Disease? cause?

A
  • CVID
  • Defect in B cell dfiferentiation after age 2
75
Q

90% is the target vaccinated/otherwise immune population for herd immunity.

Boosters are required for ___ of lymphocytes and ___ of antibodies.

A

Clonal expansion of lymphocytes

Affinity maturation of antibodies

76
Q

MMR, Varicella, and the Rotavirus vaccine are ___ vaccines that stimulate what kind of response?

A

Live, attenuated vaccines that stimulate cell-mediated and humoral responses

77
Q

Killed/inactivated vaccines (e.g. pertussis, polio) often have to use a ___ to get an adequate cell-mediated & humoral immune response.

What is the most common type?

How do they do what they do?

A

Adjuvants ; Aluminum

Delays clearance of antigen from the site of injection to increase contact with the APC

78
Q

Subunit vaccines?

Name two toxoids

A

Conjugation of weak antigen + strong antigen

Two toxoids: Diphteria & tetanus

79
Q

Immunosuppression of allergies/IgE - name the mechanisms of

  • Antihistamines
  • Leukotriene modifiers
  • NSAIDs
A

Antihistamine: block H1 receptors to prevent histamine degranulation

Leukotriene modifiers: block late mediators of allergic response

NSAIDs: inhibit COX to block prostaglandin synthesis

80
Q

Corticosteroids

Anti-proliferative drugs

Inhibitors of T cell activation

are all _____ drugs

A

globally immunosuppressive

81
Q

The efficacy of a vaccine is dependent on the __ and ___.

Why do we have a vaccine to some microbes and not others? (low yield)

A

Depends on microbe and its pathogenesis.

Microbes that have to replicate/spread extensively to cause disease OR are only pathogenic because they secrete a toxin are easy to make a vaccine to because you just have to stimulate an immune response

Microbes that are antigenic and ALREADY cause a potent immune response but still can’t be cleared are harder. Our vaccine can make a potent immune response, but may still not prevent disease.

82
Q

In targeted immunomodulation, we want to strike a balance between anti-inflammatory and pro-inflammatory mediators. What are the two big targets

A

TNF-a & IL-6

83
Q

We want monoclonal antibodies (“-mab”) to be as close to human as possible (minimize mouse component).

“muro-“

“-xi-“

“-zu-“ or “-iz-“

“umab”

A

“muro”: murine

“xi”: chimeric

“zu”: humanized

“-umab”: fully human

84
Q

Which cytokines are targeted in asthma/allergy therapy and why?

A
  • IgE production depends on Th2 cells producing IL4 and IL-13.
    • Targeted in asthma and atopic dermatitis
  • Inflammation results from eosinophils’ presence, mediated by IL-5
85
Q

In rheumatoid arthritis, which cytookines are upregulated? Which Th cell is upregulated?

A

IL-1, IL-6, IL-15, IL-18, TNF, and chemokines.

Th1 T cells are upregulated –> increased IFN-y production,

B cells produce abnormal antibodies (ANA, RF)

86
Q

Steroids, methotrexate, and NSAIDs were standard therapy for rheumatoid arthritis.

“Salmon-colored” fleeting, migratory rash on the trunk & extremities that synchronizes with fever spikes is associated with what arthritis?

A

systemic juvenile arthritis

Will see high IL-6, and in older children, high IL-1

87
Q

Whats the big concern with anti-TNF therapies for rheumatoid arthritis?

A

reactivating TB & increasing lymphoma risk

88
Q

Probiotics & helminthic therapy (triggers Th2 response to depress Th1) are therapies for what disease?

A

Crohn’s

89
Q

Plasmophoresis

IVIG

Cancer treatment: anti-HER2 & CAR & TCR

A

Plasmophoresis: filter out bad antibodies; maybe exchange for healthy Abs

IVIG:

low dose to replace missing IgG

high dose as immunomodulatory agent

Cancer treatment:

  • anti-HER2 inhibits tumor growth factors and tags cancerous cells for immune respons
  • CAR and TCR-modified T cells for cancer
90
Q

Define:

Auto-

Iso-

Allo-

Xeno-

A

Autograft: transplant from the same individual

Isograft: genetically identical, but different individual

Allograft: two different members of the same species; differ by one or more MHC alleles

Xenograft: totally foreign

91
Q

Alloantigens

A

Antigen on the graft that isn’t present in the recipient.

Ex) Blood group antigens and HLA antigens

92
Q

Host-vs-graft reaction

vs

Graft-vs-host reaction:

A

Host-versus-graft reaction: The recipient’s immune response to the grafted organ or tissue.

Graft-versus-host reaction: The graft’s immune response (donor T cells in the graft) to the recipient following bone marrow transplantation

93
Q

Hyperacute rejection

A
  • Preformed antibody-mediated
  • Type II HS
  • Rapid (min-hrs)
94
Q

Acute rejection

A
  • Cell-mediated: CD8 T cells recognize HLA antigens on the graft –> recognizez HLA incomptability
  • Type 4 HS
    • ​Delayed: takes 10-20 days after transplant to built up significant T cell mediated response
  • Likely occurs due to direct allorecognition
95
Q

Secondary rejection reaction

A

Even more rapid rejection of a second transplant due to immunological memory

96
Q

Chronic rejection

A
  • Mediated by both antibodies & T cells
  • Type 2 and 4 hypersensitivty reaction
  • months-years due to lesser degree of MHC polymorphism
  • Interstitial fibrosis (collagen)
97
Q

Two ways T cells are activated against a donor MHC

A
  • Direct allorecognition: Donor dendritic cells present w/ foreign MHC/HLA to recipient CD4 & 8 T cells –> T cell recognizes foreign donor HLA and activates
    • Exposed him damn self
  • Indirect allorecognition: donor MHC is degraded and taken up by recipient dendritic cells and presented as a foreign antigen on a self-MHC II
    • Ratted out by recipient APC
98
Q

What happens in graft vs host disease?

A

Donor T cells in the graft react with host antigens

  • 70% mortality
  • Severity correlates with MHC disparity
  • CD4/CD8-mediated, but mostly cd8
99
Q

Antigen cross presentation

A

Dendritic cells can take things form the outside and present them on MHC 1 as well as MHC 2 to activate CD8 T cells

Allows activation of both CD4 and CD8 T cells in GVHD

Immune (4 decks)

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