Chapter 10: Alterations in Immune Functions

immune system disorders

occurs when inappropriate immune responses lead to disease

two general categories…

1. excessive immune responses

2. deficient immune responses

excessive immune responses

result from a functional increase in the activity of the immune system involving multiple interacting immune cells, includes disorders in which the immune system is overfunctuoning or hyperfuncitoning

• autoimmunity

• hypersensitivity

deficient immune responses

includes disorders in which the immune system response fails to provide protection and is ineffective b/c of disease causing genotypes or secondary / acquired dysfunction

autoimmunity

occurs when the immune system recognizes a person’s own cells as foreign and mounts an immune response that injures self tissues

• failure of self intolerance

• autoimmune reactions can be mediated through type II and III hypersensitivity mechanisms

hypersensitivity

is a normal immune response that is appropriately triggered, excessive, or produces undesirable effects on the body (immune response that causes harm)

• basic mechanism that triggers it: specific antigen - antibody reaction or specific antigen - lymphocyte (WBC) interaction

• 4 types / classes … I, II, III, IV

type I, II, and III

mediated by antibodies

antibodies are the major drivers (antigen is the target, antibody reacts / recognize / binds to it but the reaction causes harm instead of fixing / removing antigen)

type IV

cell mediated

t - cells are the main drivers

type I

(immediate hypersensitivity)

allergen (antigen) is recognized by immune system = IgE antibodies are produced = mast cells become activated (degranulation) = histamine releases

• instead of fixing it allergy symptoms occur (immediate allergy)

• anaphylaxisd

degranulation

cells release the chemicals stored inside it

anaphylaxis

type I can be expressed as life threatening allergic reaction, caused by bee stings, seafood, peanut

type II

(mediated hypersensitivity)

antibodies that attack antigens on the surface of specific cells or tissues causing cell lysis

• mechanisms occur after the binding of antibody to tissue specific antigens

• IgG and IgM are the principal antibodies

antibodies attach to the specific antigen / target on cell = cell’s function is damaged or cell dies

type III

(immune complex reaction)

antibodies combine with antigen and form immune complexes (little clumps) - usually body removes clumps but this type has too many produced clumps and they dont get removed = clumps go into tissues = activates inflammation and damage surrounding the tissue

(ie. immune complexes form = no removal = go into tissue = inflammation = tissue damage , non tissue specific)

type IV - delayed hypersensitivity reaction

memory t cells allows for persistency for months to years after initial antigen exposure

(ie. poison ivy substance = t cell recognize it = releases inflammatory signals =inflammation develops)

• slow onset and evolves gradually (begins 24 hours after exposure and lasts 2-4 weeks after exposure)

first exposure = t cells become sensitized / memory t cells created = second exposure = t cells react = cytokines released = inflammation occurs = tissue damage is result

deficient immune responses disorders

• severe combined immunodeficiency

• DiGeorge syndrome = effects t-cells

• selective immunoglobulin A deficiency (IgA) - lack of IgA antibodies that protect mucous membranes

• HIV/AIDS

etiology of type I

Strong genetic or hereditary linkage regarding IgE response to antigens (allergens)

pathogenesis of type I

Also known as immediate hypersensitivity, because the reaction is immediate (short period of time, 30-50 mins after exposure)

CM of type I

• Mild

  • Hives

  • Seasonal allergic rhinitis

  • Eczema

• More problematic symptoms

  • Throat constriction

  • Localized edema

  • Wheezing

  • Tachycardia

treatment for type I

• Antihistamines

• Beta-adrenergics

• Corticosteroids

• Anticholinergics

• Anti-IgE therapy

• Epinephrine

Antihistamines

Block the effects of histamine

Beta-adrenergics

Decrease bronchoconstriction and bronchospasm.

Corticosteroids

Decrease inflammatory response

Anticholinergics

Block parasympathetic system

Anti-IgE therapy

Inhibits binding of IgE to mast cells

Epinephrine

• Adrenergic agent given IM, subQ or IV during acute allergic reactions

• Highly allergic people can carry an EpiPen

pathogenesis of type II

Also known as tissue-specific, cytotoxic, or cytolytic hypersensitivity (Often immediate reaction, but some occur over time)

etiology of type II

Antibodies attack antigens on surface of specific cells or tissues causing lysis

Cell lysis may be mediated by

• Activated complement fragments (membrane attack complex)

type of cell lysis

transfusion reaction

transfusion reaction

(acute hemolytic blood transfusion)

• Individual receives blood from someone with a different blood

group type

• Recipient antibodies attach to the donor’s red blood cell (RBC)

antigens

pathogenesis of type III

Also known as immune complex reaction

• Not an immediate reaction - several hours

• not tissue specific

• usually ongoing

Involves antigens forming antigen-antibody complexes that precipitate out of the blood or body fluid and then deposited into tissues

• Immune complexes are not removed, which causes an inflammatory process

• Activation of the classic complement cascade causes release of C3a, C5a

• Causes tissue destruction, scarring, and further reaction

etiology of type III

Immune and phagocytic systems fail to effectively remove antigen-antibody immune complexes

• Recent history of infection or persistent low-grade infection

• An extrinsic environmental antigen from molds, plants, or animals

• Autoimmune proces

• activation complement = mediatior

mechanisms of injury for type III

• tissue injury - caused by an inflammatory reaction

• Activation of complement - mediator

• Phagocytic cells - attracted to tissue

type IV characteristics

Delayed hypersensitivity

• Tissue damage resulting from a delayed cellular reaction to an antigen

• No primary antibody involvement

• Principal mediators

  • Lymphocytes

examples of type IV

• Type IVa—Granulomatous Hypersensitivity

• Type IVa—Tuberculin-Type Hypersensitivity

• Type IVa—Allergic Contact Dermatitis

• Type IVb—Persistent Asthma

• Type IVc—Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis

• Type IVd—Pustular Psoriasis

Type IVc—Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis

deadly rash from antibiotic life threatening skin issue anti seizure medication