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MOD I Exam II > Chapter 6 Pt 2 > Flashcards

Chapter 6 Pt 2 Flashcards

1
Q

What causes type IV hypersensitivity?

A

Inflammation resulting from cytokines produced by CD4+ T cells and killing by CD8+ T cell

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2
Q

What causes type IV hypersensitivity?

A
  1. Rheumatoid arthritis
  2. Multiple Sclerosis
  3. Type I DM
  4. Inflammatory bowel disease
  5. Psoriasis
  6. Contact dermatitis
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3
Q

What is the classic example of a Delayed Type Hypersensivity?

How does this work?

A
  • Tuberculin reaction
  • Purified protein derivative (PPD; aka tuberculin), a protein-containing Ag of the tubercle bacillus is injected intracutaneously.
  • Previously sensitized pt’s will have reddening and induration of the site appear in 8-12 hrs and peaking at 24-72 hrs
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4
Q

T-cell mediated type 4 hypersensitivity can occur in what 2 processes

A
  1. CD4+ T-cells: Delayed type hypersensitivity

2. CD8+ T cell mediated cytotoxicity

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5
Q

Which T-cells usually are responsible for delayed type hypersensitivity?

A

Th1

Th17

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6
Q

If APC’s produce IL-12 which T helper cell will CD4+ T cells differentiate into?

How about if they produce IL-1, IL-6, and IL-23?

A
  • IL-12 —> TH1 —> IFN-gamma —> more TH1

- IL-1, IL-6, IL-23 —> TH17

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7
Q

Inflammation produced in psoriasis is mediated mainly by cytokines produced by?

What type of hypersensitivity is this?

A
  • TH17

- T-cell mediated (Type IV) hypersensitivity

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8
Q

Activated TH17 cells produce which cytokines and how do they contribute to the inflammatory response of typer IV hypersensitivities?

A
  • IL-17, IL-21, IL-22, and chemokines
  • Collectively, recruit neutrophils and monocytes to the rxn, thus promoting inflammation
  • IL-21 amplifies the TH17 response
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9
Q

What is the predominate infiltrate in the lungs after 2-3 weeks of a tuberculous infection?

Sustained activation causes these cells to undergo?

What then occurs?

A
  • Macrophages

transform from MO=> epitheloid cells, which will be surrounded by collar of lymphocytes, and referred to as a granuloma=> granumomatous inflammation.

Granulomatous inflammation => + Th1 cells => make IFN-y

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10
Q

Granulomatous inflammation is associated with strong _____ activation and high-level of cytokines such as _____.

A

Granulomatous inflammation is associated with strong TH1-cell activation and high-level of cytokines such as IFN-gamma

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11
Q

Contact dermatitis is tissue injury resulting from what type of reaction?

How do these substances cause a rxn?

A
  • Delayed-Type Hypersensitivity (4)

Environmental chemical (e.g. urushiol from poison ivy, nickel) binds to and structurally modifies self-proteins, which are recognized by T-cells and cause inflammation of skin (vascular dermatitis)

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12
Q

What are the 2 most important types of tissue injury seen in CD8+ T cell mediated cytotoxicity?

A
  1. Type 1 DB

2. Rejection of graft after organ transplant

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13
Q

Dysbiosis is implicated in which diseases?

A

IBD

Allergy

Autoimmune diseases

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14
Q

Autoimmune diseases affect at least _____ of the population, men or women more?

They are caused by the loss of what?

A

1-2%

Women&raquo_space;> men

loss of self tolerance; body will attack self-antigens

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15
Q

The presence of autoantibodies does or does not, mean we have an autoimmune disease?

A

Presence of autoantibodies ≠ autoimmune disease.

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16
Q

At least 3 requirements must be met before a disease can be considered autoimmune

A
  1. Rxn to a self-antigen
  2. Rxn is not secondary to tissue damage, rather, it CAUSES tissue damage
  3. Other causes are ruled out
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17
Q

How do AI diseases manifest? (3)

A
  1. organ specific: type 1 DM or MS
  2. systemic: SLE
  3. Neither: goodpasture syndrome: AB in basement membrane of lung and kidney cause lesions
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18
Q

Autoimmune diseases are formed when lymphocytes that recognize self-antigens escape both central and peripheral tolerance.

What is central tolerance; how can it prevent AI?

What is peripheral tolerance; how can it prevent AI?

A

Central tolerance: catches immature lymphocytes in BM and thymus that recognize self-antigens and:

  1. Apoptosis
  2. Become Treg cells
  3. B cells undergo receptor editing (RAG)

if they escape: another chance

Peripheral tolerance: catches mature lymphocytes in peripheral tissue and

  1. Apoptosis
  2. Inactive (anergy)
  3. Suppressed by T-reg cells
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19
Q

What are the 3 immune-privileged sites?

A

brain

eyes

testis

hard for immune reactions to antigens to occur here bc they dont communicate with blood or lymph

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20
Q

AIRE is responsible for inducing the expression of what?

.
Mutations in AIRE: cause

What normal processes would fail?

A

expressing self antigen

autoimmune polyendocrinopathy

ability to express self-antigens

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21
Q

What is CTLA?

What is the opposite of CTLA4?

A

Inhibitory receptor on T-reg that bind to CD80/86 on APC => prevent activation of the T cell to avoid immune repsonse

CD28 is a activator on T-cells that bind to CD80/86 on APC => activate the T cell => cause an immune response.

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22
Q

What has a higher affinity for CD80/86 (B7): CTLA4 or CD28?

A

CTLA4

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23
Q

PD-1 on T-cell

binds to

PD-L1 on the APC

what hpapens?

A

supresses T-cell

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24
Q

Cancer is treated with anti-CTLA4 and anti PD1 antibodies that do what

A

prevent binding of CTLA-4/CD80

and PD1-PDL1

so that we can + our immune response to cancer cells => prolonged tissue inflammation and injury

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25
Q

What is a T-reg cell

what cytokines is NECESSARY for maintance of T-cell?

A

CD4+
CD25+
FOXP3+

IL-2

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26
Q

how does anergy occur?

A
  1. Inactivates self-antigen when there is not enough co-stimulation
  2. Induces anergy by using inhibitory receptors (CTLA-4 or PD1)
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27
Q

Peripheral tolerance

  1. anergy (inactivation)
  2. T-reg do what?
  3. Apoptosis
A

Suppress to prevent reaction against self-antigens

28
Q

Generating T-reg cells requires what?

Maintaing T-cells requires what?

A

TGF-B

IL2 and FOXP3

29
Q

What are the 3 ways that T-reg cells supress immune responses against self antigens?

A
  1. Secrete IL-10 and TGF-B
  2. Express CTLA-4
  3. Protect fetal Ag inhereitas from dad
30
Q

mutations in FOXP3 cause what

A

IPEX (immune dysregulation polyendocrinopathy, enteropthy, X-linked)

=> causes systemic diseases

31
Q

How does apopotosis occur in peripheral tolerance

A

If self reactive

  1. Express Bim (+apoptosis) => intrinsic patheay
  2. FasL/Fas path
32
Q

FAS gene mutation causes what

A

Autoimmune Lymphoproliferative Syndrome (ALPS)

33
Q

TREG cells are important in maintain _____ tolerance to the developing fetus, which have _____ antigens (which is 50% foreign

A

maternal

paternal

34
Q

How do you develop AI diseases?

A
  1. Inherit a susceptibility gene
    => cause loss of tolerance and produce self-reactive lymphocytes.

However, this self-reactive lymphocyte cannot crease an AI disease: it needs to expand and activate.

Thus, to expanc and +; it needs and ENVIRONEMTNAL trigger (ex. molecular mimicry, epitope spreading)

Env trigger will active the self-reactive lymphocyte, which can

  1. Cause defective tolerance
  2. abnormal display of self-anitgens
  3. inflamm and initial innate immune response
35
Q

Once induced, autoimmune diseases tend to be ____, ____, with occasional relapses and remissions d.t the immune system ________.

A

chronic, progressive

allowing some cells to overcome infection

36
Q

what is epitope spreading?

ex?

A
  1. immune response attacks self-tissue => damages => releases more self-ag
  2. however, these new self-ag escaped tolerance and were not presented to T cells

=> cause an immine responses

=> cycle of persistant AI

ex. oral lichen planus

37
Q

Most chronic inflammatory diseases are caused by abnormal or excessive_____________ repsonses

A

Th1

Th17

38
Q

Systemic diseases tend to involve blood vessels and connective tissues.

A

BV

CT

39
Q

Ankylosing spondylitis is a heredity inflammation of the joints, particularly the spine. This leads to degeneration and fusion of the vertebra.

what inherited suscepibility gene did someone with ankylosing spondylitis inherit?

if they have it, do they have AS?
does evyerone with AS have suscpebility gene?

A

MHC Class I
HLA-B27 (05/02)

no
no

40
Q

What diseases are assx with ppl who inherited susceptibility gene

HLA- DRB?

A
  1. Rheumatoid arthritis (RA)
  2. T1DM
  3. MS
  4. SLE
41
Q

what inherited suscepibility gene did someone with celiac disease inherit?

A

HLA-DQA1

42
Q

Which gene is said to be MOST frequently implicated in autoimmunity; encodes what?

Associated with what disorders?

A
  • PTPN22; encodes a protein tyrosine phosphatase
    mutation: defective TP => cant control TK => + lymphocyte

Type I DM,
Rheumatoid arthritis
IBD

43
Q

Polymorphisms in the gene for ____ are associated with what Chrons disease?

A

NOD2

44
Q

what is the NOD2 gene?

A

NOD2 is a cytoplasmic sensor that detects microbes.

If mutated, Paneth cells in the intestinal epithlium are cannot kill commensal bacteria => increase of bacteria => BIG immune response

45
Q

Polymorphisms in gene encording for

CD25 (IL-2R) and IL-7 are assox with with?

A

MS

Type I diabetes

46
Q

What are 2 methods by which infections may induce autoimmunity?

A

1) Infections may upregulate the expression of co-stimulators on APCs; if these cells are presenting self-antigens result may be a breakdown of anergy and activation of self-reactive T cells
2) Molecular mimicry: microbe expresses Ag w/ same AA sequence as self-Ags

47
Q

What is the classic example of molecular mimicry?

Causes what?

A
  • Rheumatic heart disease; Abs against streptococcal proteins cross-react w/ myocardial proteins
  • Cause Myocarditis
48
Q

How may infections actually protect against some autoimmune diseases?

A

Promoting low levels of IL-2 production which is essential for maintaining Treg cells

49
Q

Presence of ANA (anti-nuclear AB) is used to detect the presence of ADS.

If (-), =>

. If (+), _____

A

person does not have a disease

perform a more specific test, becase ANA is a sensitive test for MULTIPLE autoimmunse desases

50
Q

What ANAs are specific for lupus, that are virtually diagnostic?

A

Anti-dsDNA

Anti-smith

51
Q

What antibodies are diagnostic for Sjogren syndrome?

A

Anti-Ro/SS-A

Anti-La/SS-B

52
Q

Autoantibody associated with diffuse systemic scleroderma?

Limited systemic scleroderma?

A

Anti-DNA topoisomerase (Scl-70)

Limited (CREST): anti-centromere AB

53
Q

SLE is a AD that involves multiple organs (skin, joints, kidneys and serosal membrane, but virtually every other organ can be affected) characterized by MANY. autoantibodies

Injury in SLE is caused by?

What type of hypersensitivity?

A
  • Deposition of immune complexes and binding of antibodies to various cells and tissues
  • Type III hypersensitivity
54
Q

Hallmark of SLE:

A

production of autoantibodies (especially ANAs)

will also have

  1. Ab directed against BCs
  2. antiphospholipid Ab
55
Q

What group of people is most common to develop SLE?

A

W

AA/hispanics

56
Q

Patients with SLE that have the presence of antiphosphlipid antibodies (30-40% have), particular lupus anticoagulant, will have increased?

These antibodies cause what kind of state?

A
  • falsely high PTT

- Hypercoagulable state (excessive clotting); leading to thrombosis

57
Q

Specific alleles of which HLA has been linked to production of anti-dsDNA, anti-Sm, and anti-phospholipid antibodies seen in SLE?

A

HLA-DQ

58
Q

What environmental factors are involved in SLE?

A
  • UV light= > increases apoptosis, cause keratinocytes to make IL-1, alter DNA
  • Gender bias: F are more likely because of estrogen and genes on X crhomosome
  • Drugs: such as hydralazine, procainamide, and D-penicillamine; once taken away, sx go away
59
Q

Congenital deficiencies in complement components (i.e. C2, C4, and C1q) may impair immune complex clearance and favor tissue deposition.

Knockout mice for ___ are prone to develop lupus-like autoimmunity

A

C4

60
Q

Most characteristic lesions of SLE affect the:

A

BV, CT, kidney, skin

61
Q

What is the morphology of the blood vessels like in patients with SLE?

How about in the chronic stages?

A
  • Acute necrotizing vasculitis involving capillaries, small arteries, and arterioles
  • Chronic stages = vessels undergo fibrous thickening with luminal narrowing
62
Q

What are the joints like in patients with SLE?

Opposite of what?

A
  • Non-erosive synovitis with little deformity

- Opposite of RA

63
Q

Kidney lesions in SLE are the result of what?

how many ppl have kidney problems?

A

immune complex deposition in the mesanguim/BM of glomerulus

50%

64
Q

What is the most common and also the most severe pattern of glomerular disease seen in SLE?

Characteristics/morphology?

A
  • Diffuse lupus nephritis (Class IV)
  • > 50% involvement of Glomeruli
    1. symptomatic; protein/hematuria
    2. Increased cellularity: Proliferation of epithelial cells —> lateral crescents that fill Bowmans space
    3. immune complexes deposit in the subendothelium => thickening of capillary wall, forming “wire loop” structures on light mircoscopy (see attached photo)
65
Q

What is the 1st pattern of glomerular dz we see in SLE?

last?

A
  1. minimal mesengial lupus nephritis first

2. sclerosing lupus nephritis; sclerosing is an end-stage process.

MOD I Exam II (16 decks)

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