Basics of Immunity and Hypersensitivity

Innate Immune System

The body's first line of defense against pathogens.

Key Players of Innate, Physical Barriers

Skin and mucosal membranes prevent pathogen entry.

Key Players of Innate, Cellular Components

Includes phagocytes (like macrophages and neutrophils), natural killer (NK) cells, and dendritic cells that respond rapidly to invaders.

Key Players of Innate, Chemical Barriers

Secretions like mucus, sweat, and enzymes (lysozyme) kill or inhibit pathogens.

Adaptive Immune System

Provides a targeted response to specific pathogens and has memory capabilities for faster response upon re-exposure.

T-lymphocytes/ T-cells

•  Helper T-cells (CD4+) aid in activating B-cells and other immune cells.

•  Cytotoxic T-cells (CD8+) kill infected cells.

B-lymphocytes/ B-cells

Produce antibodies that specifically target antigens from pathogens.

Primary lymphatic organs

Where lymphocytes are produced and mature

What happens in the bone marrow?

Site of B-cell maturation.

What happens in the thymus?

Site of T-cell maturation

Secondary lymphatic organs

Where lymphocytes are activated and proliferate.

What is the role of lymph nodes?

Filter lymph and house immune cells

What is the role of the spleen?

Filters blood and responds to systemic infections

Interaction Between Innate and Adaptive Immunity:

The innate immune response provides the initial defense and helps to shape the adaptive response. Innate responses can instruct adaptive immunity about what specific actions to take by presenting antigens to T-cells.

Natural Killer (NK) cells

Attack and destroy infected or malignant cells.

What are the types of phagocytes

• Macrophages

• Neutrophils

• Dendritic Cells

Macrophages

Engulf and digest pathogens and debris.

Neutrophils

Rapid responders that engulf bacteria and fungi.

Dendritic cells

 Capture antigens and present them to T-cells, initiating the adaptive response

Mast cells and Basophils

Release histamines and other chemicals during allergic reactions and inflammation.

Cytokines

Signaling molecules that mediate immune responses (e.g., interleukins, interferons)

Complement System

A group of proteins that enhances (complements) the ability of antibodies to clear pathogens.

Helper T-cells

Activate B-cells and cytotoxic T-cells.

Cytotoxic T-cells

Directly kill infected or cancerous cells.

Memory Cells

 Rapid response to subsequent antigen recognition

B Lymphocytes

Produce antibodies that bind to specific antigens on pathogens, marking them for destruction. They also have memory cells

Humoral Immunity

Involves B cells and the production of antibodies

Cell-Mediated Immunity

Involves T cells that attack infected or cancerous cells directlymI

Immunoglobulin IgA

skin/mucous membranes, kind of part of first line of defense, passed to infant during breastfeeding, antiviral/antibacterial

Immunoglobulin IgD

elevated in chronic infection, important for maturation of B cells

Immunoglobulin IgE

parasites, allergic reactions, basophil and mast cell degranulation

Immunoglobulin IgG

most common, smallest (go to tissue), best for second exposure, crosses placenta, antiviral/antitoxin/antibacterial

Immunoglobulin IgM

does not go into tissue, initial responder, activates complement, blood type reactions

Type I Hypersensitivity

Immediate (IgE-mediated)

Type II Hypersensitivity

Cytotoxic

Type III Hypersensitivity

Immune Complex

Type IV Hypersensitivity

Delayed-type

Pathophysiology of Type I Hypersensitivity

IgE binds to mast cells leading to degranulation, release of histamine, and inflammatory response

Clinical features of Type I Hypersensitivity

Urticaria, bronchospasm

Examples of Type I Hypersensitivity

Hay fever, eczema, bee sting allergy, asthma, peanut allergy, anaphylaxis, drugs; NEW: pet dander, allergic conjunctivitis

Nursing Interventions for Type I Hypersensitivity

Emergency management (e.g., epinephrine). Patient education on avoiding triggers

Pathophysiology of Type II Hypersensitivity

IgG directly targets cells or tissues

Examples of Type II Hypersensitivity

Transfusion reaction, hyperacute graft reaction, hemolytic disease of the newborn, Graves disease, myasthenia gravis; NEW: Goodpasture syndrome, idiopathic thrombocytopenia purpura

Clinical features of Type II Hypersensitivity

Blood disorders

Nursing Interventions for Type II Hypersensitivity

Monitor for signs of hemolytic reactions. Patient education regarding blood type and transfusions.

Pathophysiology of Type III Hypersensitivity

Antigen/antibody complexes are deposited in tissues leading to activation of complement, tissue inflammation, and destruction

Examples of Type III Hypersensitivity

Glomerulonephritis, rheumatoid arthritis, SLE; NEW: serum sickness, hypersensitivity vasculitis, bacterial endocarditis, farmer’s lung

Nursing Interventions of Type III Hypersensitivity

Assess for systemic symptoms.

Educate patients on risk factors and management.

Clinical features of Type III Hypersensitivity

Joint pain, rashes.

Pathophysiology of Type IV Hypersensitivity

Sensitized T cells react with altered or foreign cells (mimicry)

Examples of Type IV Hypersensitivity

Contact dermatitis, skin graft reaction, TB skin test; NEW: type I diabetes, celiac disease, multiple sclerosis, Hashimoto’s thyroiditis, Guillain-Barre syndrome

Clinical features of Type IV Hypersensitivity

Rash, localized inflammation.

Nursing Interventions of Type IV

Assessment of skin reactions. Education on avoiding re-exposure to allergens.