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Immunology Exam 2 > Lecture 18-19 - T4-HS & Autoimmunity > Flashcards

Lecture 18-19 - T4-HS & Autoimmunity Flashcards

1
Q

T4HS mediators (immune reactants)

A

TH1, TH2, and CTL

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2
Q

T4HS Antigens are ____ and ____

(Which go with which?)

A

Soluble and Insoluble

(cell-associated antigen –> CTL)
(Soluble –> Th1 and Th2)

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3
Q

Three syndrome-types caused by T4HS

A

Delayed type HS (PROTEINS)

Contact Type HS (HAPTENS)

GIT Disease (Gliadin)

**all involve T cells

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4
Q

Causative agent for Poison ivy

A

pentadecacatechol

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5
Q

First encounter causes ____

A

sensitization

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6
Q

Steps of a “first encounter” sensitizing process

A
  1. skin penetration
  2. modification of self proteins
  3. Ag captured by APC, presented in LN
  4. (in LN) Activate T cells and generate specific T cells)
  5. –> leads to asymptomatic response
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7
Q

Later encounter of Ag results in ________

A

hypersensitivity reaction

  1. Same first steps as first response (skin, mod’ self proteins)
  2. Presented in LN and in skin
  3. Memory Tcells are activated
  4. Activation of downstream effectors and phagocyte recruitment
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8
Q
  • DC’s in epidermis
  • DC’s in afferent lymphatic
  • DC’s in LN
A
  • Langerhans
  • Veiled cell
  • Interdigitating DC
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9
Q

Lymphocytes found in skin express what three things

A
  • CLA (cutaneous LC antigen)
  • P/E selectin ligands
  • chemokine receptors (CCR4/8, CCR10)
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10
Q

Skin DTH reaction steps

A
  1. penetrates skin
  2. taken up by langerhans
  3. present self peptides (haptenated with the agent) to Th1 cells (secrete IFN)
  4. keratinocytes secrete cytokines and chemokines (secrete IL1, TNFa, etc)
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11
Q

In skin DTH reaction, naive T cells are matured to Th1 cells in…

A

Lymph node

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12
Q

Th1 cells secretions and their effects

A
  1. Chemokines = MQ recruitment
  2. IFNgamma = Activates MQ
  3. TNFa and LT = Local tissue destruction
  4. IL3 & GM-CSF = Monocyte productions by stem cells in BM
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13
Q

Tx for Contact HS

A

Corticosteroids

(suppress inflammator genes, induce synthesis of anti-inflamm proteins)

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14
Q

Examples of DTH

A

Tuberculin skin test

Poison ivy

celiac

chromic asthma (Th2)

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15
Q

How to we get immune tolerance to self (B cells?)

A

B cells anergized or deleted in bone marrow, periphery, germinal centers

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16
Q

How do we get immune tolerance to self (T cells)?

A
  • Autoreactive T cells are deleted in the thymus
  • Autoreactive T cells are anergized or deleted in the periphery
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17
Q

5 ways to gain immune tolerance to prevent autoimmunity

A
  1. Delete or anergize B cells in BM, periphery, or GC’s
  2. Delete T cells in thymus…..Anergize or delete T cells in periphery
  3. Supress Treg (CD4+CD25+)
  4. Physically separate tissue Ag from immune cells
  5. Limit MHC2 and B7 expression (reduces activation)
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18
Q

Susceptability factors in AI diseaes

A
  1. HLA genotype
  2. Microbial infection
  3. injury
  4. environmental factors and behavior
  5. gender/sex hormones
19
Q

Three ways microbial infection increases AI risk

A
  1. Adjuvant effect: recruitment and activation of immune cells
  2. Induction of MHC molecules and B7
  3. Molecular mimicry
20
Q

Sympathetic Ophthalmia

A

Physical trauma in one eye initiates AI in both

  1. eye anterior is IMMUNE PRIVILEDGED SITE
  2. Injury in one eye drains to LN
  3. Immune response of effector T cells
  4. return to BOTH eyes to react and cause damage/blindness
21
Q

Most AI diseases affect ___

Which ones dont?

A

Females

  • Psoriasis, UC, AI uvitis, Bechets* hit both equally
  • (Ankylosing spondylitis* = males)
22
Q

What is APECED? What is deficient? What diseases result?

A

AI polyendocrynology candidiasis ectodermal dystrophy

Mutations in AIRE (AI regulator) gene = Defective Thymic deletion because inability to express peripheral antigens in thymus

Endocrine = Hypoparathyroidism, adrenal failure, ovarian fail

Other = Candidiasis (100%!), Dental enamel hypoplasia, nail dystrophy

23
Q

IPEX is a _____mutation

A

FOXP3

(essential for generation of Tregs –> inflamed small intestine)

“immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome”

24
Q

Celiac CD4 T cells specific for…

How does this happen?

What ends up being made?

A

gluten peptide

DQ2 and DQ8 present the peptide to CD4 T cells

Anti-transglutaminase autoantibodies = destruction of villi

25
Q

Molecular mimicry main cause (molecularly)

A

Same MHC moleucle presents both a pathogen peptide and a self peptide that mimics it

Effector TH1 cell responds in the same way it would to the pathogen, activating MQ

26
Q

Infection induces ____ production, which increased _____ expression on tissue cells

A

IFN gamma

MHC class 2

**results in T cell activation and AI

27
Q

AI hemolytic anemia (Type 2) initiation, steps, and treatment

A

RBC’s bind to antiRBC autoAB’s

  • FcR cells in spleen –> phagoc.
  • complement activation and CR1 cells in spleen –> phagoc.
  • complement activation and Intravascular hemolysis = Lysis

Splenectomy reduces RBC loss

28
Q

Immune Thrombocytopenic Purpura (ITP)

What do antibodies attach to?

Half-ish cases are classified as _____

A

antobodies attach to blood platelet for destruction

half are idiopathic

29
Q

Goodpastures syndrome is IgG against…

A

Alpha-3 chain of Type 4 Collagen

(present in basement membranes of lung, kidney, etc) = infiltration with PMN and MNC

Tx = plasma exchange + immunosuppressants

30
Q

Graves disease antibodies effect?

Sx?

Tx?

A

autoantibodies are STIMULATORY to the TSH receptor

leads to increased thyroid hormone = hyperthyroid diseases (heat intolerance, nervousness, weight lost, thyroid enlargement)

Tx = thyroidectomy or radioactive destruction with 131Iodine

31
Q

Vertical transmission of antibodies in Graves disease (with treament)?

A
  1. Mom makes anti TSH receptor AB’s
  2. Crosses placenta
  3. Newborn has disease
  4. Plasmapheresis removes moms AB’s and cures
32
Q

Hashimoto’s pathology?

Tx?

A

ABs and effector T cells against thyroid

(TH1 mediated)

Tx = oral administration of thyroid hormone

33
Q

IDDM autoantibodies attack

A

Islet cells in Pancreas = no insulin

34
Q

SLE involves AB’s to ____

What causes the symptoms (rash, etc..)

A

DNA and histones

Immune complexes form and get deposited in BV, kidney, joints etc

35
Q

Rheumatoid factor =

Produced by ______

A

IgM, IgG, or IgA against the Fc region of IgG

Produced by Plasma B cells

36
Q

Pathology behind RA

Tx?

A
  • Leukocytes infiltrate the joint synovium (CD4/8 and B cells, PMN, MQ)
  • Inflammatory cells make PG’s, LT’s, enzymes and collagenases

Tx = anti-inflammatories, immunosuppressive drugs

(like anti-TNFa)

37
Q

What effect does smoking have on RA

A
  • generates CITRULLINE residues = CD4 activation
  • increases peptidylarginine deiminase 2 expression

*causes peptides with citrulline residues to be presented to CD4 Tcells (by HLA class 2)

38
Q

Tx for RA

A

Anti-CD20

reduces the interaction of CD20 on B cells with FcgRIII receptor on NK cells (stops killing)

39
Q

GBS tx

A

plasmapheresis and high dose IVIG

40
Q

MS is a response against _____

_____ cells are implicated. What is their effect?

Treatment = ?

A

against myelin

Activated T cells (Th17 or Th1) = induce expression of chemokines/cytokines that recruit the demyelinating inflammatory cells

Tx = IFN-beta injections (suppress Th17), immunosuppressants, Natalizumab

41
Q

Natalizumab is anti ______ treatment for _______

A

anti-VLA4/integrin

Tx for MS

42
Q

What is the role of CNS inflammation in demyelination

A

Generation and migration of CNS specific T cells causes IL17 and IFN gamma to be released

Astrocytes and microglial cells are activated by leukocytes

43
Q

MS drugs and targets

A

Daclizumab = IL2Ra and T cell activation

Natalizumab = a4 integrin and T cell migration

Fingolimod = T cell migration

Azathioprine = T cell proliferation

Methotrexate

Rapamycin = mTOR

44
Q

Myasthenia Gravis Tx

A

Pyridostigmine (cholinesterase inhibitor)

Azathioprine (blocks T cell proliferation = immunosuppressant)

Thymectomy

Immunology Exam 2 (11 decks)

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