Immune System Defense Mechanisms and Inflammation, B and T Lymphocytes: Functions and Hypersensitivity Types

First Line of Defense

skin and mucous; Non-specific barriers preventing foreign substance entry.

Second Line of Defense

Nonspecific inflammatory response to various problems.

Third Line of Defense

Specific immune response involving lymphocytes and antibodies.

Role of Skin

Sloughing off dead cells hinders bacterial colonization.

Mucus Function

Contains lysozymes that destroy bacterial cell walls.

Cilia Function

Moves mucus out of lungs, trapping pathogens.

Inflammatory Response

Reaction of tissues to injury, causing redness and swelling.

Inflammation Suffix

Conditions named by adding '-itis' suffix.

Goals of Inflammation

Limit infection, control process, initiate healing.

Erythrocytes

Red blood cells involved in oxygen transport.

Leukocytes

White blood cells that fight infections.

Granulocytes

White blood cells containing granules for inflammation.

Neutrophils

Most abundant granulocyte, first responders in immunity.

Monocytes

Mature into macrophages and dendritic cells when they leave the vessel

Macrophages

Phagocytize debris and initiate adaptive responses.

Dendritic Cells

present antigens to T-cells activating lymphocytes.

Natural Killer Cells

Lymphocytes that attack infected cells directly. Assist in the development of adaptiveimmune responses through the production of cytokines

Mast Cells

Release inflammatory mediators like histamine. Located in tissue.

Inflammation is signaled by

Mast cells

purpose of histamine in inflammatory response

causes fluids to collect around an injury to dilute toxins and swelling

increased temperature in inflammation can

kill temperature sensitive microbes

corticosteroid medications block

arachidonic acid

Aspirin and NSAIDS block

cyclooxygenase pathway

Inflammatory Mediators

They are located in many cells and in general cause vasodilation and increased vascular permeability

Inflammatory Mediators in Mast Cells

Histamine, Leukotrienes, Prostaglandins

Inflammatory Mediators in Platelets

Serotonin

Inflammatory Mediators in Injured Cells

Arachidonic Acid, Prostaglandins, Leukotrienes, Thromboxane

Inflammatory Mediators in Lymphocytes and Monocytes/Macrophages

Cytokines (Lymphokines, Monokines)

Mast Cell Degranulation

Release of mediators upon tissue injury.

Vascular Response

Increased blood flow to injured area.

Cellular Response

Leukocyte migration to eliminate injurious agents.

Cellular Response 3 steps

• Adhesion and Margination

• Transmigration

• Chemotaxis

Margination (pavementing)

adherence of leukocytes to endothelial cells

diapedesis (emigration)

leukocytes squeeze between endothelial cells into tissue space

Phagocytes

White blood cells that engulf and destroy invaders.

Chemotaxis

Attraction of phagocytes to damaged cells.

Cytokines

Signaling proteins that modulate immune responses.

Capillary Permeability

Increased permeability leading to edema and pain.

Signs of Inflammation

Includes redness, swelling, heat, pain, and loss of function.

Leukocyte Movement

Neutrophils migrate to injury site via cytokines.

Adhesion and Margination

Leukocytes adhere to blood vessel walls.

Transmigration

Leukocytes move through blood vessel walls.

Histamine

Increases vessel dilation and permeability.

Adaptive Immunity

Third line of defense involving lymphocytes.

Lymphocytes

Approximately 36% of total white blood cells.

T-Lymphocytes

Provide cell-mediated immunity.

B-Lymphocytes

Provide humoral immunity by producing antibodies.

Plasma Cells

Rapidly produce antibodies after B-cell activation.

Memory B-Cells

Retain memory of pathogens for quick response.

Antibodies

Bind to antigens to disable or agglutinate microbes.

Helper T-Cells

Activate other immune cells via cytokines.

Cytotoxic T-Cells

Destroy infected cells using toxic substances.

Major Histocompatibility Complex (MHC)

Distinguishes self from non-self cells.

Hypersensitivity Disorders

Exaggerated immune responses to antigens.

Type I Hypersensitivity

IgE-mediated immediate allergic reactions.

Early Phase Reaction

IgE triggers mast cell degranulation within minutes.

Late Phase Reaction

Lipid mediators cause prolonged inflammation.

Prostaglandins

Mediators involved in late phase hypersensitivity.

Leukotrienes

Cause bronchospasms during late phase reactions.

Active immunity

A form of acquired immunity in which the body produces its own antibodies against disease-causing antigens.

Passive immunity

An individual receives antibodies directly from another source, such as mother to infant through breast milk

natural active immunity

production of one's own antibodies or T cells as a result of infection or natural exposure to antigen

artificial active immunity

pathogen is introduced through vaccination

natural passive immunity

acquired by a child through placenta and breast milk

artificial passive immunity

immunity which results from the administration of antibodies from another animal or person against a dangerous pathogen.

B Lymphocytes

White blood cells that produce antibodies.

Plasma Cells

B-cells that rapidly produce antibodies.

Memory B-cells

Retain invader memory for rapid response.

Clonal Selection

Process of B-cells reproducing upon antigen binding.

Antibodies

Proteins that bind specific antigens.

Agglutination

Antibodies cause microbes to clump together.

T Lymphocytes

70% of lymphocytes, mature in thymus.

Helper T-Cells

Activate other immune cells via cytokines.

Cytotoxic T-Cells

Destroy infected cells using toxic substances.

Major Histocompatibility Complex (MHC)

Distinguishes self from non-self cells.

Cytokines

Substances released by activated Helper T-cells.

Type I Hypersensitivity

IgE-mediated immediate allergic reactions.

Anaphylaxis

Life-threatening systemic allergic reaction.

Histamine

Vasoactive agent causing allergic symptoms.

Prostaglandins

Mediators involved in late-phase allergic response.

Leukotrienes

Lipids causing bronchospasms in allergic reactions.

Type II Hypersensitivity

IgG or IgM-mediated antibody reactions.

Type III Hypersensitivity

Mediated by immune complex deposition.

IgE

Antibody involved in Type I hypersensitivity.

IgG

Antibody involved in Type II hypersensitivity.

IgM

Antibody involved in Type II hypersensitivity.

Mast Cells

Release histamine during allergic reactions.

Bronchospasm

Constriction of airways during allergic reactions.

Erythema

Redness of skin in allergic reactions.

Urticaria

Hives caused by allergic reactions.

Hypotension

Low blood pressure during anaphylaxis.

What is Systemic Lupus Erythematosus (SLE)?

Autoimmune disease characterized by multi-organ inflammation, involving type III hypersensitivity, immune complex activation, and chronic multisystem inflammatory processes.

What are some common autoantibodies in Systemic Lupus Erythematosus (SLE)?

Autoantibodies can target nucleic acids, erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, and more.

Who is more commonly affected by Systemic Lupus Erythematosus (SLE)?

SLE is more common in females than in males (9:1 ratio), with a higher prevalence in individuals aged 20-40, and more frequently affecting Black individuals compared to White individuals.

What are some clinical manifestations of Systemic Lupus Erythematosus (SLE)?

Clinical manifestations include arthralgias or arthritis (90% of individuals), vasculitis and rash (70%-80%), renal disease (40%-50%), hematologic changes (50%), and cardiovascular disease (30%-50%). Flares can be triggered by UVA light exposure.

Autoantibodies

Antibodies targeting the body's own molecules.

Malar Rash

Facial rash commonly seen in SLE patients.

Discoid Rash

Skin lesions associated with SLE, often scaly.

Photosensitivity

Skin rash triggered by sunlight exposure.

Antinuclear Antibodies (ANA)

Autoantibodies used to diagnose autoimmune diseases.