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The Immune System

• Immunity: the body’s specific protective response to

invading foreign agent or organism
• Immunopathology: the study of diseases that result from
dysfunction of the immune system
• Immune System Disorders: Descriptions
Autoimmunity N° protective immune response
paradoxically turns against or attacks the
body, leading to tissue damage
Hypersensitivity Body produces inappropriate or
exaggerated responses to specific
Gammopathies Immunoglobulins are overproduces

Immune deficiencies
Primary Deficiency results from improper
development of immune congenital or
Secondary Deficiency results from some
interference with an already developed
Central and Peripheral Lymphoid Organs
Immune Function
• Natural immunity: nonspecific response to any foreign
White blood cell action: release cell mediators such as
histamine, bradykinin, and prostaglandins, and engulf
(phagocytize) foreign substances
Inflammatory response
Physical barriers, such as intact skin, chemical barriers,
and acidic gastric secretions or enzymes in tears and
• Acquired immunity: specific against a foreign antigen
Result of prior exposure to an antigen
Active or passive
Development of Cells of the
Immune System
• B lymphocytes mature in the bone marrow; T lymphocytes mature in
the thymus where they also differentiate into cells with various
Stages of Immune Response
Response to Invasion: Defenses

• Phagocytic immune response

- WBC (granulocytes & macrophages) to ingest foreign particles

• Humoral or antibody response

- starts with the B-lymphocytes, then transform to plasma cells (antibodies)

• Cellular immune response

- involves the T-lymphocytes, turns into cytotoxic (killer T-cells ) and

attacks the pathogen
Differences in Cellular and Humoral Immune Responses:

Humoral Responses (B-cells) Cellular Responses (T-cells)

▪ Bacterial phagocytosis and ▪ Transplant rejection

▪ Anaphylaxis ▪ Delayed hypersensitivity
▪ Allergic hay fever and asthma ▪ Graft-versus-host disease

▪ Immune complex disease ▪ Tumor surveillance or

▪ Bacterial and some viral ▪ Intracellular infections
▪ Viral, fungal, and parasitic
Stages of Immune Response
Antibody Molecule
Role of Antibodies
• Agglutination of antigens

• Opsonization

• Promote release of vasoactive substances; activation

of complement system and phagocytosis

• Act in concert with other components of the immune


• Types of immunoglobulins: IgA, IgD, IgE,IgG, and

Major Characteristics of the Immunoglobulins:

• IgG (75% of total Immunoglobulin)

▪ Appears in serum and tissues
▪ Assumes a major role in bloodborne and tissue infections
▪ Activates the complement system
▪ Enhances phagocytosis
▪ Crosses the placenta

• IgA (15% of total Immunoglobulin)

▪ Appears in body fluids
▪ Protects against respiratory, GIT, and GUT infections
▪ Prevents absorption of antigen from food
▪Passes to neonate in breast milk for protection
IgM (10% of total Immunoglobulins)
▪ Appears mostly in intravascular system
▪ Appears as the 1st immunoglobulin produced in response
to bacterial and viral infections
▪ Activates the complement system

IgD (0.2% of total Immunoglobulins)

▪ Appears in small amount in serum
▪ Possibly influences B-lymphocyte differentiation, but role
is unclear

IgE (0.004% of total Immunoglobulins)

▪ Appears in serum
▪ Takes part in allergic and some hypersensitivity
▪ Combats parasitic infections
Antigen–Antibody Binding
Cellular Immune Response
• B lymphocytes: humoral immunity
– Produce antibodies or immunoglobulins
• T lymphocytes: cellular immunity
– Attack invaders directly, secrete cytokines,
and stimulate immune system responses
– Helper T cells
– Cytotoxic T cells
– Memory cells
– Suppressor T cells (suppress immune
Non-T and Non-B Lymphocytes
Involved in Immune Response
• Null cells

– Destroy antigen coated with antibody

• Natural killer cells

– Defend against microorganisms and

some malignant cells
Complement-Mediated Immune Responses
Variables That Affect
Immune System Function
• Age and gender
• Nutrition
• Presence of conditions and disorders: cancer/neoplasm,
chronic illness, autoimmune disorders, surgery/trauma
• Allergies
• History of infection and immunization
• Genetic factors
• Lifestyle
• Medications and transfusions: see Table 50-6
• Pyschoneuroimmunologic factors
Tests to Evaluate Immune Function
• WBC count and differential
• Bone marrow biopsy
• Humoral and cellular immunity tests
• Phagocytic cell function test
• Complement component tests
• Hypersensitivty tests
• Specific antigen–antibody tests
• HIV infection tests
• See Chart 50-3
Assessing for Immune Dysfunction
Be on the alert for the following Sx and Sy
● Changes in respiratory rate ● Abnormal lung sounds
● Cough (dry or productive) ● Rhinitis
● Bronchospasm ● Hyperventilation
● Hypotension ● Vasculitis
● Tachycardia ● Anemia
● Dysrhythmia
● Hepatosplenomegaly ● Vomiting
● Colitis ● Diarrhea
Inflammation: Cellular response to an injury

– Is a defensive reaction intended to neutralize, control,

or eliminate the offending agent and to prepare the
site for repair.
– A nonspecific response meant to serve a protective
- changes in microcirculation (vasodilation, vascular
permeability, and leukocytic cellular infiltration
- cardinal signs of inflammation
● redness (rubor)
● warmth (calor)
● edema (tumor)
● pain (dolor)
● loss of function
Chemical Mediators of Inflammation:
1. Histamines
- present in many tissues
- release by mast cells
- responsible for early changes in vasodilation and vascular permeability
2. Kinins
- increase vasodilation and vascular permeability
- attracts neutrophils
3. Prostaglandins
- thought to have a role in increasing tissue permeability
Types of Inflammation:
1. Acute
- local vascular and exudative changes
- usually lasts less than 2 weeks
- “immediate and serves as a protective response”
2. Subacute
- includes elements of exudative phase of the acute response and
of repair
- “not widely used term”
3. Chronic
- injurious agent persist and the acute response is perpetuated
- symptoms lasts for many years
- debilitating and can produce long lasting effects
- cycle of cellular infiltration, necrosis, and fibrosis begins, with
repair and breakdown occur simultaneously
- scarring- permanent damage
Cellular Healing:
• Regeneration
- gradual repair of the defects occurs by proliferation of cells of the same type
as those destroyed.
-Type s of Cells:
1. labile – multiply constantly to replace cells worn out by physiologic
process (e.g., epithelial cells lining the GIT and skin)
2. permanent – the nerve cell bodies
3. stable – have latent ability to regenerate, are not shed and do not
replacement under physiologic condition
- if destroyed they are able to regenerate (kidney, liver, pancreas)
• Replacement
1. Primary intention healing – wound is clean and dry, edges are approximated (surgical
- little scar and healing takes about a week
2. Secondary intention healing – wound defect is larger and gaping, with necrotic and
dead material.
- wound fills with granulation tissue from bottom upwards
- process of repair is longer, more scar with loss of function