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065. My HDM Exam 2 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Immune responses that cause tissue injury are called hypersensistivity reactions. The diseases associated with these reactions are called hypersensitivity or immune mediated inflammatory diseases. The arise from uncontrolled or abnormal responses to foreign antigens or autoimmune responses against self antigens. What are the different types?

A

Type I (Immediate)
Type II
Type III
Type IV (delayed)

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2
Q

Type I hypersensistivity is mediated by IgE and results from actions of mediators secreted by mast cells. Type II hypersensitivity is mediated by Abs that bind and cause what?

A

Abs that bind tissue Ags and cause complement-dependent tissue injury and disease

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3
Q

Type III hyperS is mediated by Abs that bind to circulating Ags to form immune complexes which deposit in vessels and cause complement dependent injury in the vessel wall (vasculitis). What is type IV?

A

mediated by T cell diseases and results from inflammation caused by cytokines produce by CD4+Th1 and Th17 cells or killing of host cells by CD8+CTL

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4
Q

Type I is immediate caused by environmental Ags which activate mast cells in an IgE dependent manner. Atopy refers to the genetic tendency to?

A

to develop allergic diseases. So people with a strong propensity to develop allergic reactions are said to be atopic

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5
Q

Mast cell mediators are responsible for acute reactions and inflammation (Type I). Histamine is the MAJOR amine that causes dilation of small blood vessels and increases vascular permeability. What do mediators vasoactive amines, proteases, prostaglandins (PGs),leukotrienes (LTs) and cytokines do?

A

Vasoreactive amines: HISTAMINE: vascular dialation and smooth muscle contraction
Proteases cause tissue damage
PGs cause vascular dialation
LTs cause prolonged smooth muscle contraction
Cytokines induce local inflammation (late phase reaction)

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6
Q

When an allergen is inhaled, ingested, injected or touched, your adaptive immune response by B cells that mature into plasma cells which make what and does what?

A

Makes IgE which enters circulation and is bound by FcRE (high affinity) on mast cells in the tissues

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7
Q

Once IgE binds the to the CD23 receptor or FcRE on mast cells, crosslinking occurs and the mast cell degranulates and releases?

A

Histamine, proteases, prostaglandins, leukotrienes, and cytokines

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8
Q

Overview of Type I:

  1. PRIMARY exposure to allergen
  2. Ag activates Th2 which mature
  3. Plasma secreting IgE cells secrete and bind to FcRE on mast cells
  4. ?
A
  1. AFTER secondary exposure to same allergen antigen on IgE and crosslinking of IgE on bound on mast cells, mast cells degranulate.
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9
Q

What substances from the mast cell causes immediate hypersensitivity reaction, minutes after repeat exposure?

What causes the late-phase reaction 6-24 hours after repeat exposure to the allergen?

A

Immediate: vasoactive amines, lipid mediators

Laterphase: cytokines

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10
Q

Immediate reaction is characterized by vasodilation, congestion and edema while late phase reaction is characterized by?

A

an inflammatory infiltrate rich in eosinophils. neutrophils, and T cells

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11
Q

Asthma is a reversible airway obstruction casued by inflammatory mediators from mast cells once encountered by allergens. The mediators cause loosening of tight junctions in the BRONCHIOLE epithelium, increased capillary permeability and spasmatic contraction of smooth muscle, resulting in?

A

Decreases the size of the bronchial lumen, resulting in shortness of breath

Bronchospasms

Lumen of bronchi also contains goblet cells which secrete mucus

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12
Q

Anaphylaxis is characterized by blood pressure decreasing leading to vascular shock and difficulty breathing. What makes this happen?

A

Allergens cause releases of vasoactive amines from mast/basophils resulting in contraction of smooth muscle in vasculature and vasodilation of capillary endothelium. Hard breathing is due to same as asthma, contraction of smooth muscle in the bronchi and bronchioles

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13
Q

What is a positivie reaction for allergen testing on the ventral side of the arm?

A

Positive reactions are indicated as redness and swelling within 20-30 minutes after exposure

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14
Q

Allergen-specific immunotherapy (Allergen-SIT) is the single curative approach to allergic diseases. The aim of Allergen-SIT is to induce? (3)

A
  1. peripheral T cell tolerance
  2. modulate the thresholds for mast/basophil activation
  3. Decreases IgE mediated histamine release
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15
Q

The reason why induction of peripheral T cell tolerance and formation of regulatory T cells are important is becuase they (FOXP3+CD4+CD25+Treg) play a key role in?

A

successful allergen-SIT and helathy immune response to allergens

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16
Q

What is the general cause of Type II and III hypersensitivities?

A

Abs and Ag-ab complexes

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17
Q

Abs and tissue antigens can deposit in tissues can cause injury by inflammation. IgM/IgG activate complement pathway which makes byproducts (C3b/C4b) that recruit?

A

leukocytes and induce inflammation

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18
Q

IgG abs bind to neutrophil and macrophage Fc receptors (FcRs) and activate them, resulting in inflamation reponse. ROS and lysosomal enzymes that are released do what?

A

damage the adjacent tissues

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19
Q

What are important diseases that are associated with Type II hypersensistivity?

A 
Hemolytic anemia
Graves disease (hyperthyroidism-TSH receptor)
Myasthenia gravis (Ach receptor)
Pemphigus vulgaris
Pernicious anemia
Rheumatic fever
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20
Q
  1. Abs opsonize cells and may activate complement and lead to phagocytosis of the cells througg phagocyte FcR (FcRI) or CR1 for C3b.
  2. Complement byproducts C3a and C5a are chemotactic for leukocytes and recruit leukocytes which causes?
A

inflammation and tissue injury

21
Q

Some Abs are specific for cell receptors for hormones or neutransmitters:

  1. may stimulate activity of TSH receptors even in absense of the hormone, causing hyperthyroidism (GRAVES0
  2. Abs may inhibit binding of acetylcholine neutrotransmitter to Ach receptor (since Ab is bound to receptor) causing?
A

Myasthenia gravis

22
Q

Type III: immune-complex mediated diseases: immune complexes of circulation antigens and IgM or IgG antibodies deposited in vascular basement membrane resulting in?

A

Complement and Fc receptor mediated recruitment and activation of leukocytes

23
Q

Type II: antibody-mediated diseases: IgM IgG antibodies against cell surface or extracellular matrix antigens resulting in?

A

Complement and Fc receptor mediated recruitment and activation of leukocytes, Opsonization and phagocytosis of cells, Abnormalities in cellular funciton

24
Q

Ab-ag complexes deposit in blood vessels inducing vascular inflammation and ischemic damage to the tissues. What is the major mechanism of triggering tissue damage in Type III?

A

classical activation of complement and recruitment of leukocytes

25
Q

How is injury caused in all Type III hypersenssitivities?

A

caused by complement-mediated and Fc receptor-mediated inflammation

26
Q
  1. Lupus: Abs to DNA, nucleoproteins: Clincal Manes(CM)?
  2. Polyarteritis: abs to microbial antigens CM?
  3. Post streptococcal gomerulonephritis: ab specific to streptococcal wall ags, CM?
  4. Serum sickness: Abs to many proteins/ CM?
  5. Arthus reaction: Abs to many proteins/
A
  1. Nephritis, arthritis, vasculitis
  2. Vasculitis
  3. Nephritis
  4. Systemic vasculitis, nephritis, arthritis
  5. Cutaneous vasculitis
27
Q

Systemic reactions of Type III: Fc receptors on endothelim of blood vessels bind antitoxin abs that have bound to toxoids. Many more bind forming a complex in the BV on the endothelium. The classical complement pathway is activated and what occurs?

A

C5aC4aC3a are released attracting macrophages and neutrohpils to the blood vessel, causing damage

28
Q

Local reaction/arthus Type III: Abs are transported to site of Ag deposition, and classical activation occurs and what happens?

A

Anaphylatoxins attract macrophages and neutrophils to cause tissue damage

29
Q

Type IV: T cell mediated diseases: 1. CD4Tcells (cytokine mediate inflammation) 2. CD8Tcells (Tcell mediated cytolysis) resulting in

A
  1. macrophage activation, inflam by cytokine

2. direct target cell lysis, inflam by cytokine

30
Q

What are the major triggers of type IV hypersensistivity reactions?

A

autoimmunity, exaggerated responses to environmental Ags and some microbial Ags
Injury by cytokines produced by Th1,Th17 or CTLs

31
Q

Autoimmune diseases mediate by type IV hypersensitivity include?

A

MS, rheumatoid arthritis and type 1 diabetes d/t T cells being specific to myelin proteins, unknown joint antigens and pancreatic islet antigens

32
Q

What disease has both autoimmunity component and is likely caused by the aberrant reactions to intestine microflora?

A

Chron’s disease

33
Q

T cell mediated inflammatory reaction is delayed type hypersen (DTH) or Type IV. during inflammation, Th1 and Th17 cells secrete cytokines that recruit and activate leukocytes. Tissue damage results from products of the recruited neutrophils and macrophages, such as?

A

Lysosomal enzymes, ROS, NO, and proinflammatory cytokines

34
Q

T cell mediated inflammation is considered chronic, many autoimmune diseases are cuased by interaction of autoreactive T cells with self ags leading to?

A

cytokine release and inflammation

35
Q

T cell reactions specific for microbes (M tuberculosis) and other foreign Ags may also lead to inflammation and?

A

tissue injury

36
Q

DTH occurs 24-48 hours after Ag challenge. Humans can be sensitized for DTH reaction by TB, poison ivy or immunizations(Tet/Dipth). Purified protein derivative (PPD) a protein antigen of mycobacterium tuberculosis elicits?

A

Elicits a DTH reaction called the tuberculin reaction

37
Q

Allergic contact dermatitis (ACD) is caused by environmental exposure to external agents that in contact with the skin trigger an inflammatory reaction. ACD resilts from ?

A

A DTH reaction (Type IV hypersensitivity)

38
Q

Poison Ivy releases pentadecacatechol molecules which come in contact with the skin protein and combine. During primary contact (T cell sensitization) and T memory cells are made **no dermatitis. During secondary contact what occurs?

A

T memory cells respond to the pentdecacatechol and activate many T cells leading to dermatitis

39
Q

Metals are the most common contact allergens. Sensitization occurs at any age, costume jewelery is linked to increased sensitation to Nickel and Cobalt. Whats the most common source of sensitization to chromium?

A

Leather

40
Q

In a TB granuloma, it contains activated Mø, multinucleate giant cells, and lymphocytes (primarily T cells). Some granulomas may be the central area of necrosis. CD4Th1 cells release TNF and IFNy which does?

A

recruits mø and leukocytes, prolonged reactions of this type lead to formation of granulomas

41
Q

A mature granuloma formation
1. within hours to days after Ag exposure, activated Th1 cells home to the tissue. If Ag source is not eliminated, inflammation will persist
2. Th1 CD4 T release IFNy which activates Mø, leading to production of TNF
3?

A
  1. IFNy and TNF further stimulate Mø, forming a mature granuloma in days to weeks
42
Q

Systemic Lupus erythematosus (SLE) is prototypic immune complex mediated disease: Type III hypersensitivity. Manifests as rashes, arthritis and gomerulonephritis. Mainly consist of anti-DNA abs (auto-abs). Immune complexes formed from these auto-abs and specific Ags are responsible for the side affects. What is the principle diagnostic test?

A

To test for the presence of anti-nuclear IgG abs (DNA)

43
Q

RA is an inflammatory disease involving small and large joints. Inflammation here is associated with destruction of the joint cartilage and bone. Mediated by Type II/III hypersensistivities. Cells involved?

A

Th1, Th17, Activated B cells and plasma cells and Mø

44
Q

Patients frequently have circulating IgM or IgG that react with the Fc of THEIR own IgG molecules. These auto-abs are called?

A

Called rheumatoid factors and their presence is used as a diagnostic test for RA

45
Q

MS pathogenisis- TYPE IV

  1. Activated T cell by APC is released into blood, uses rolling adhession to move into brain tissue.
  2. T cell reactivated by APC-microglialcell/astrocyte
  3. T cell activates mø in brain tissue by releasing IFNy/IL2, Mø releases IL1/IL12 and chemokines to attract more T cells to the site
  4. Mø releases TNFA/ROS/NO which degrades axon
  5. B cells come to the brain tissue and do what???
A
  1. B cells make autoantibodies to complmenet on axons and degrade the axons
46
Q

In type I diabetes TYPEIV, the C peptides which are needed to make insulin are attacked in the islets and killed. What are some treatments that help with C peptide levels?
1. CTLA4 Ig treatment had + effect on C peptide levels
2. CD3 specific Abs decreased decline of C/ ATG with prednisone/BM transplant
3-4?

A
  1. CD20-specific antibodies delayed the decline in C peptide for about 1 year
  2. Elmination of cows milk from diet decreases production of autoantibodies
47
Q

IBD : Type IV: APC in epithelial barrier presents bacteria to Th1, which releases IFNy to macrophage, mø releases macrophage migration inhibitor factor, IL 12/18 to T cell as well as __________ to epithelial barrier?

A

Tumor necrosis factor
IL1
IL6

48
Q 
TNF is produced by Mø, DC, T cell, Adipocytes and Fibroblasts and have target cells of
1.endothelial cells
2. mø
3. paneth/IEC cells
4. myofibroblast
5. Effector T cells
which produce a consequence of?
A
  1. Angiogenisis and hypervascularization
  2. Activation/proinlfmamatory production/suppression of regulatory mø
  3. IEC:cell death/impaired barrier paneth: necroptosis
  4. MMP-induces tissue destrcution and impaired migration
  5. Apopstosis resistance, cell survival and IL6 syn
49
Q

Immunotherapy:
CTLA4-iG blocks costimulation
Anti-TNF, Anti-IL1,Anti-IL6R Anti-IL17: block inflammation
Anti-integrins (Anti CD40L) block adhesion
Antip40=?

A

Antip40 blocks Th1 Th17 response by inhibiting IL12/IL23

065. My HDM Exam 2 (7 decks)

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