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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.
