Immunology Chapter

Question 1

Immediate (Type I) Hypersensitivity

Answer 1

Antibody Mediated (B Cells)

Anaphylactic & atopic

Free antigen cross-links IgE on presented mast cells & basophils -> triggering IMMEDIATE release of vasoactive amines that act at POST-CAPILLARY VENULES (i.e. histamine)

Reaction develops rapidly after antigen exposure because of preformed antibody (sensitization)

Delayed Response follows due to production of Arachidonic Acid metabolites (i.e. Leukotrienes)

FIRST & FAST (Type I & Immediate)

Test: skin test for specific IgE

Allergic & Atopic disorders:

rhinitis, hay fever, eczema, asthma, bee sting, food/drug allergies

Question 2

Antibody-mediated (Type II) Hypersensitivity

Answer 2

Antibody Mediated (B Cells)

Cytotoxic
IgM & IgG bind to fixed antigen on “enemy cells” leading to cellular destruction (except enemy cells are your cells)

3 Mechanisms:

1) Opsonization (tagging) leading to phagocytosis or complement activation
2) Complement-mediated lysis
3) Antibody-dependent cell-mediated cytotoxicity, usually due to NK cells or macrophages

Type II is cy-2-toxic

-antibody & complement lead to MAC (membrane activated complex)

Test: direct/indirect Coombs’ test
DIRECT: detects antibodies that HAVE adhered to pt’s RBC (i.e. Rh+ infant of an Rh- mother)
INDIRECT: detects antibodies that CAN adhere to other RBC (i.e. test an Rh- woman for Rh+ antibodies)

Autoimmune Hemolytic Anemia, Pernicious anemia, Idiopathic thrombocytopenic purpura, Erthyrobastosis fetalis, Acute Hemolytic transfusion reactions, Rheumatic Fever, Goodpasture syndrome, Bullous pemphigoid, Pemphigus Vulgaris

*Disease tends to be tissue specific/site where antigen is found

Question 3

Immune complex-mediated (Type III) Hypersensitivity

Answer 3

Antibody Mediated

Immune complex = Antigen-antibody complexes activate complement, attracting neutrophils that release lysosomal enzymes

Type 3 = 3 things stuck together: antigen+antibody+complement

SERUM SICKNESS:
- Type III where antibodies to the foreign proteins are produced (~ 5-10 days after exposure)
- Immune complexes form & are deposited in the membranes where they fix complement -> tissue damage
**more common than Arthus Reaction
**now most often caused by drugs acting as haptens, not serums
S/S: Fever, uticaria, arthralgias, proteinuria, lymphadenopathy

ARTHUS REACTION:

• Local, subacute Type III reaction
• Intradermal injection of antigens induces antibodies which from Ag-Ab complex in the skin
• Characterized by edema, necrosis, and complement activation

Test: Immunofluorescent staining

SLE, Polyarteritis nodosa, Poststreptococcal glomerulonephritis, Serum sickness, Arthus Reaction, may be associated with vasculitis & systemic manifestations

Question 4

Cell Mediated (Type IV) Hypersensitivity

Answer 4

T-Cell mediated -> delayed

Sensitized T lymphocytes encounter antigen and then release lymphokines that activate macrophages
** No antibodies are involved

4th & LAST = delayed
Non-transferable by serum
4 T's:
T lymphocytes
Transplants
TB Skin tests
Touching (contact dermatitis)

Test: Patch test or PPD

MS, Guillain-Barre syndrome, Graft vs Host disease, PPD test for TB, Contact dermatitis

Question 5

Types of Hypersensitiviity

Answer 5

ACID
A = Type I = Anaphylaxis/Allergy
C = Type II = Cytotoxic/Antibody mediated
I = Type III = Immune Complex/3 things (Ag-Ab-Complement)
D = Type IV = Delayed (T cell-mediated)