Immunity to Infection: Forms of Immunity and Hypersensitivity Flashcards
Dr. Idowu
Briefly discuss the two forms of adaptive immunity.
i. Active immunity: This is conferred when an individual actively produces antibodies in response to a foreign antigen (infectious agent). This immunity can occur due to infection, immunisation, exposure to toxins, or tissue transplant. The antibody produced during active immunity is long lasting. However, protection is delayed until antibody production reaches an effective level.
ii. Passive immunity: Passive immunity is generated by the administration of preformed antibodies. The main advantage of passive immunisation is that the recipient receives a large concentration of antibody immediately. This does not confer long-term protection but is useful when the patient has no time to produce an antibody response.
*In passive immunity it is possible to initiate hypersensitivity reactions if the antibody is from another species. However, in active immunity, the binding of antibodies to the antigen leads to the formation of circulating immune complexes. The deposition of these complexes may be an important feature in the development of organ dysfunction.
What is hypersensitivity?
It is a condition in which an exaggerated or augmented immune response occurs that is harmful to the host.
List the classes of hypersensitivity reactions.
-Type I: Immediate hypersensitivity (Allergy)
-Type II: IgG-mediated hypersensitivity (Complement)
-Type III: Immune-complex hypersensitivity
-Type IV: Cell-mediated hypersensitivity
Briefly discuss Type I hypersensitivity.
This occurs within seconds after exposure to the antigen.
On initial exposure, the antigen induces the formation of IgE, which binds to the Fc portion of IgE receptors on mast cells, basophils and eosinophils. When the individual experiences a second exposure to the same antigen, the cell-bound IgE molecules cross-link and release hypersensitivity mediators.
symptoms may manifest as a systemic anaphylaxis (e.g. after IV administration of heterologous proteins) or as a local reaction (e.g. an atopic allergy involving rhinitis like in hay fever).
Mention two hypersensitivity mediators in Type I hypersensitivity.
- Histamine: exists in a preformed state in platelets and in granules of mast cells, basophils, and eosinophils. The release of histamine causes vasodilation, increased capillary permeability, and smooth muscle contraction
- Prostaglandins and leukotrienes: they are newly formed mediators derived from arachidonic acid via the COX pathway. Prostaglandins induce edema and bronchoconstriction.
What is atopy?
It is a genetic hypersensistivity disorder associated with elevated IgE levels.
The antigens could be environmental e.g. pollen, dander, dust, or food e.g. seafood.
Clinical manifestations include: asthma, eczema, hives, hay fever.
What is the aim of treatment of anaphylactic reactions?
Maintaining the airway and supporting cardiac function.
Mention 3 drugs used in the treatment of anaphylactic reactions?
- Epinephrine
- Antihistamines
- Corticosteroids
Briefly discuss Type II hypersensitivity.
IgG antibodies bind to the cell-surface antigens or extracellular matrix molecules, and activate the complement system, resulting in complement-mediated cell lysis, as seen in haemolytic anemia, ABO transfusion reactions.
E.g. Drugs such as penicillin bind to surface proteins on RBCs and induce antibody formation. These antibodies then initiate haemolysis.
E.g. Goodpasture syndrome, where antibodies are generated in the basement membranes of the kidney and lungs, activating the complement system and causing memebrane damage.
E.g. Graves disease
Briefly discuss Type III hypersensitivity.
Antibodies bind with antigens to form immune complexes, which persist and are deposited in tissues, resulting in tissue and organ dysfunction.
Briefly discuss Type IV hypersensitivity.
The interaction of an antigen with a specifically sensitised T-cell results in T-cell proliferation and the release of potent inflammatory cytokines—e.g. gamma-interferon and interleukin 2— and the activation of macrophages.
This begins 2-3 days after contact with the antigen and lasts several days. It is a delayed-type reaction.
E.g. Contact hypersensitivity, Tuberculin-type hypersensitivity.
Describe contact hypersensitivity.
This occurs after sensitisation with simple chemicals (e.g., nickel, formaldehyde), plant materials (e.g., poison ivy, poison oak), topical medications (eg, sulfonamides, neomycin), cosmetics, soaps, and other substances.
Small molecules enter the skin and then, acting as haptens, attach to body proteins to serve as complete antigens to induce cell-mediated hypersensitivity, particularly in the skin.
When the skin again comes in contact with the offending agent again, the sensitised person develops erythema, itching, vesication, eczema, or necrosis of the skin within 12–48 hours.
Describe tuberculin-type hypersensitivity.
This is a delayed-type hypersensitivity.
When a small amount of tuberculin is injected into the epidermis of a patient previously exposed to Mycobacterium tuberculosis, there is little immediate reaction. Gradually, however, induration and redness develop and reach a peak in 24–72 hours as mononuclear cells, especially CD4 Th1 cells, accumulate in the subcutaneous tissue.
A positive skin test indicates that the person has been infected with the microorganism but does not imply the presence of a current disease. However, a recent change of skin test response from negative to positive suggests recent infection
