Unit 4 Lec 4

Question 0

What type of hypersensitivity reaction is T cell mediated?

Answer 0

Type IV

Question 1

What type of hypersensitivity reactions are antibody mediated?

Answer 1

I, II, III

Question 2

What type of immune response causes tissue injury and disease?

Answer 2

Hypersensitivity reactions

Question 3

What are three mechanisms in which the immune response can cause tissue injury?

Answer 3

Reactions against microbes

Reactions against environmental antigens

Autoimmunity (reactions against self-antigens)

Question 4

In what way can immune reactions against microbes cause hypersensitivity?

Answer 4

Immune response is excessive (usually if microbe is persistanct
- TB persistance– Ongoing T cell response– Granuloma formation

Antibodies produce antibodies that bind to antigen and form IMMUNE COMPLEXES that deposit in tissues lead to INFLAMMATION
- Post streptococcal glomerulonephritis

Antibodies or T cells against a mircrobe can cross react with normal tissue cells
- Rheumatic heart disease

Question 5

How much of the population has an immune reaction against environmental antigens?

Answer 5

20 percent have abnormal responses to one or more of these substances
- Allergies to pollen, animal dander, and dust mites

Question 6

What consitutes autoimmunity?

Answer 6

Failure of normal mechanism of self tolerance– immune reactions against self antigens

• 5 percent general population, common in age groups 20-40
• Varied in severity

Question 7

What are the mechanisms of tissue injury in the mechanisms and classifications of hypersensitivity reactions?

Answer 7

Tissue injury is caused by the same mechanisms that are used to eliminate infections
- Reponse is triggered but maintained inappropriately

Question 8

What is the mechanisms of Type I hypersensitivity?

Answer 8

Pathologic mech IgE

Tissue injury mech: Mast Cells and Mediators (vasoactive amines, lipid mediators, cytokines)

Question 9

What is type Ii hypersensitivity?

Answer 9

Antibody mediated (IgM, IgG against cell surface or extracellular matrix antigens)

• Opsonizaiton and phagocytosis of cells is mechanism for tissue injury
• Complememtn and Fc receptor mediated recruitment and activation of leukocytes

Question 10

What is type IV hypersensitivity?

Answer 10

Type IV T cell mediated
CD4 (cytokine mediated)
CD8 CTL (T cell mediated cytolysis)

• Recruitment and activation of leukocytes
  Direct targeting cell killing cytokine mediated inflammation

Question 11

What is seen in goodpastures syndrome?

Answer 11

Glomerulonephritis induced by antibody against the glomerular basement membrane
- Glomerular inflammation and severe damage
SMOOTH LINEAR DEPOSITS OF ANTIBODY ALONG THE BM

Question 12

What is systemic lupus erythematosus?

Answer 12

Type III hypersensitivy where immune complexes deposit on glomerular basement membrane showing neutrophilic inflammation

• COARSE GRANULAR DEPOSITS OF ANTIGEN ANTIBODY COMPLEXES

Question 13

What is seen in autoimmune hemolytic anemia?

Answer 13

IgG against protein antigens on surface of RBCs
- Idiopathic (associated with lymphoma or leukemia)

Treatment

• Immunosuppression (glucocorticoids)
• Others including anti-CD20 (B cell) rituximab
• May need splenectomy

Question 14

What are the effector mechanisms of type II?

Answer 14

Opsonization
Antibody deposition in tissues
Antibody binding to cellular receptors or proteins

• Usually affect the cells tissues where the antigen is present rather than systemic

Question 15

How does opsonizaiton work in hypersensitivy reactions?

Answer 15

Directly or indirectly through complement activation (phagocytosis (receptors for Fc portion of IgG and complement proteins)

• Autoimmune hemolytic anemai
• Autoimmune thrombocytopenic purpura
• Hemolysis in transfusion reaction

Question 16

What happens in Antibody deposition of tissues in hypersensitivity reactions?

Answer 16

Recruitment of neutrophils/macrophages— mediator release (lysozyme, reactive oxidative species)

• Inflammation and tissue injury (Glomerulonephritis, Goodpastures syndrome, Acute rhemuatic fever)
• Complememtn by products C3a C5a activate neutrophil

Question 17

What happens in abnormal physiologic responses without cell tissue injury?

Answer 17

Antibody stimulates receptor without ligand or antibody inhibits binding of ligand to receptor

• Myasthenia gravis and Graves’ disease are examples

Question 18

What is the most common cause of acquired valvular heart disease?

Answer 18

Rheumatic heart disease
Occurs as antibodies againsT GAS antigens cross react with host antigens (molecular mimicry)
- Strep M protein and Myosin share similar epitopes

Question 19

What is the most common cause of poststreptococcal glomerulonephritis?

Answer 19

Most common cause of acute nephritis worldwide

• Patients have low serum c3
• Occurs after skin or throat infection with certain strains of group a streptococc
• CLinical presentation ranges from asymptomatic microscopic hematuria

Question 20

What are particulary susceptible locations for Type III hypersensitivity?

Answer 20

Vasculitis, nephritis, vasculitis

- Due to that plasma is ultrafiltrate in glomeruli and synovia of joints

Question 21

What is the arthus reaction?

Answer 21

Localized form of immune complex mediated vasculitis

• Antigen injected subcutaneously into previoulsy immunized animal
• Immune complexes deposit in the walls of small arteries at the injection site
• Local cutaneous vasculitis with tissue necrosis

Question 22

What happens in serum sickness?

Answer 22

Systmeic immune-complex mediated reaction
Named after reactions to administration of horse anti-serum to treat pneumococcal infections
- Starts 7-10 days after exposure (time needed for IgG response)
- Symptoms are fevers chills rash arthritis glumerulonephritis

Question 23

What is serum sickness an example of?

Answer 23

Transient immune complex mediated syndrome

Question 24

What is systemic lupus erythematous?

Answer 24

Type III hypersensitivity
DNA Nucleoproteins
Nephritis, arthritis, vasculitis

Question 25

What is polyarteritis nodosa?

Answer 25

Hep B virus surface antigen

Vasculitis

Question 26

What is poststreptococcal glomerulonephritis?

Answer 26

Strep Cell wall antignes

Nephritis

Question 27

What is serum sickness?

Answer 27

Various proteins are antigens involved

Arthritis, vascuilitis, nephritis

Question 28

What happens in cytokine mediated inflammatory reaction?

Answer 28

CD4 T cells respond to tissue antigens by secreting cytokins that stimulate inflammation and activate phagocytes leading to tissue injury

Question 29

What happens in CD8 CTL hypersensitivity?

Answer 29

The CD8 cell kills cells directly can be a response to viral infection that leads to tissue injury by killing infected cells even if virus has no cytopathic effects

Question 30

What is delayed hypersensitivity reaction (DTH)?

Answer 30

Develop 24-48 hours after exposure

• PPD test, Contact dermatitis
• 4 hours after injection neutrophils are recruited around post capillary venules
• 12 hours T cells enter around venules

Question 31

What is induration?

Answer 31

As endothelial cells become plump and leaky the fibrinogen that is leaked into surrounding tissues is converted to fibrin and causes accumulation in the tissue to swell and become firm

Question 32

What is a granuloma?

Answer 32

A type of chronic DTH
Th1 reponse to infectino activates macrophages but fails to eliminated phagocytosed bacteria
leads to NODULES OF INFLAMMATORY TISSUE

Macrophages may fuse to become multinucleated giant cells

Question 33

What occurs in fibrosis?

Answer 33

Prolonged cytokine signal leads to cycle of tissue injury and chronic inflammation followed by replacement with CT

Question 34

What is a characteristic response to persistant microbes such as myobacterium tuberculosis and some fungi?

Answer 34

Much of respiratory is difficult because lung tissue has been replaced with fibrotic tissue