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Innate immunity
Natural/native defense; first and second lines of defense
First line
Physical barriers (skin, mucous membranes, cilia) and chemical barriers (lysozymes, low pH, antimicrobial secretions, normal flora)
Second line
Innate immune cellular responses (NK cells, phagocytes, fever, inflammation)
NK cells
Natural killer lymphocytes; kill infected/tumor cells without prior sensitization
Phagocytes
Engulf and digest debris and microbes (macrophages, neutrophils, monocytes)
Inflammation
First response to injury; vascular tissue reaction to harmful stimuli
Goals of inflammation
Prevent/limit damage, control response, initiate adaptive immunity, start healing
Vasodilation
Increases vascular permeability and leakage during inflammation
Margination
WBCs align along vessel walls during inflammation
Diapedesis
WBC migration through vessel wall into tissues
Chemotaxis
Directed migration of WBCs toward chemical signals at injury site
Opsonization
Coating target cells with antibodies or complement (C3b) to enhance phagocytosis
Mast cells
Tissue basophils; key activators of inflammation, release histamine and mediators
Histamine
Vasoactive amine causing vasodilation and permeability increase
Prostaglandins
Lipid mediators from arachidonic acid; induce pain; inhibited by NSAIDs
Leukotrienes
Lipid mediators similar to histamine, promote inflammation
Platelet activating factor
Increases vascular permeability + platelet activation
Endothelium
Lining of blood vessels; regulates inflammation and allows leukocyte movement
Platelets
Cell fragments from megakaryocytes; central to clotting and inflammation
Plasma protein systems
Complement, coagulation, and kinin systems
Complement system
Circulating proteins activated by antibodies, lectins, or microbes; form membrane attack complex (MAC)
Classical pathway
Complement activation via antibodies (C1 → C3, C5)
Lectin pathway
Complement activation by mannose‑binding lectin binding sugars on microbes
Alternative pathway
Complement activation directly by microbial surfaces (factors B, D, properdin)
C3a
Anaphylatoxin; triggers mast cell degranulation
C3b
Opsonin; enhances phagocytosis and activates C5
C5a
Potent chemotactic factor + anaphylatoxin
C5b
Part of MAC; directly lyses bacteria
Membrane attack complex (MAC)
C5b, C6, C7, C8, C9 proteins that lyse bacteria
Coagulation system
Forms fibrin mesh to stop bleeding, trap microbes, and provide framework for healing
Extrinsic pathway
Triggered by tissue factor and factor VII; tested with PT/INR
Intrinsic pathway
Triggered by contact (factor XII); tested with PTT
Common pathway
Both intrinsic and extrinsic converge at factor X → thrombin → fibrin
Kinin system
Produces bradykinin; roles in vasodilation, pain, permeability, smooth muscle contraction
Bradykinin
Primary kinin; causes vasodilation, pain, permeability, smooth muscle contraction, chemotaxis
Cytokines
Small proteins secreted by immune cells; primary inflammatory mediators
Chemokines
Small cytokines; guide migration of leukocytes (traffic cops of inflammation)
Interleukins
Cytokines produced by macrophages/lymphocytes in response to infection
IL‑1
Pro‑inflammatory cytokine; fever (endogenous pyrogen), neutrophil proliferation, chemotaxis
IL‑10
Anti‑inflammatory cytokine; suppresses lymphocyte and macrophage activity
Interferons
Cytokines that interfere with viral infections; produced by infected cells
IFN alpha/beta
Type I interferons; induce antiviral proteins, protect neighboring cells
IFN gamma
Type II interferon; produced by lymphocytes; activates macrophages
TNF‑alpha
Tumor necrosis factor; produced by macrophages, induces fever, apoptosis, cachexia, thrombosis
Types of inflammation
Acute (neutrophil‑dominant) vs chronic (lymphocyte/macrophage‑dominant)
Acute inflammation
Rapid onset, lasts
2 weeks, neutrophil infiltration
Chronic inflammation
Longer duration, lymphocytes/macrophages/fibroblasts; granuloma formation possible
Exudate
Fluid leakage in inflammation; types include serous, fibrinous, purulent, hemorrhagic
Serous exudate
Watery; early inflammation
Fibrinous exudate
Thick, clotted; advanced inflammation
Purulent exudate
Pus; bacterial infection
Hemorrhagic exudate
Bloody; indicates bleeding
Granuloma
Organized collection of macrophages (epithelioid + giant cells) walling off chronic infection (e.g., TB)
Langerhans giant cell
Large multinucleated macrophage in granulomas
Wound healing
Process of repair after injury; requires blood supply + connective tissue
Phases of wound healing
Inflammation (1‑2 days), proliferation (3‑4 days, angiogenesis + fibroblasts + re‑epithelialization), remodeling (weeks‑years, collagen remodeling + wound contraction)
Primary intention
Healing with minimal tissue loss (e.g., surgical wounds); clean scar
Secondary intention
Healing with large tissue loss; slower, broad scar (e.g., burns, ulcers)
Dysfunctional healing
Poor healing due to bleeding, hypovolemia, infection, poor inflammatory response
Deficient scar
Weak tissue, wound rupture, infection risk
Excessive scar
Keloid or hypertrophic scar from excess collagen
Impaired epithelialization
Poor re‑growth due to steroids, hypoxemia, malnutrition
Contractures
Excessive wound contraction → restricted joint movement
Conditions impairing wound healing
Diabetes mellitus, stress, age extremes, hypoxemia, obesity, alcoholism, poor nutrition, smoking, steroids, chemotherapy
Neonates and healing
Immature immune system, poor neutrophil chemotaxis, complement deficiency → high sepsis risk
Elderly and healing
Decreased innate immune function, chronic illnesses, polypharmacy, poor regenerative ability
Adaptive immunity
3rd line of defense; long‑term, specific, inducible
Components of adaptive immunity
Humoral (B cells, antibodies) and cellular (T cells)
Active immunity
Exposure or vaccination; long‑lasting
Passive immunity
Pre‑formed antibodies (Ig transfer); short‑term
Antigen presenting cells (APCs)
Dendritic cells, macrophages; process/present antigens to lymphocytes
Major histocompatibility complex (MHC)
Proteins presenting antigen fragments to T cells
MHC I
Presents to CD8 cytotoxic T cells
MHC II
Presents to CD4 helper T cells
B cells
Differentiate into plasma cells that produce antibodies
T helper cells (CD4)
Coordinate immune response; TH1 for cell‑mediated, TH2 for antibody‑mediated
Cytotoxic T cells (CD8)
Kill infected or cancerous cells directly
Regulatory T cells
Suppress immune response, maintain tolerance
Antibodies (immunoglobulins)
Proteins produced by plasma cells; variable Fab region binds antigens, constant Fc region mediates function
IgG
Most abundant, crosses placenta, secondary immune response
IgM
Pentamer, first produced in primary response
IgA
Found in secretions (saliva, tears, breast milk)
IgD
On B cells, initiates activation
IgE
Allergy, parasitic defense
Primary immune response
First exposure; slower, mediated by IgM
Secondary immune response
Subsequent exposure; faster, stronger; IgG dominant
Immune aging
Decreased T cell activity, antibody response, memory B cells; ↑autoantibodies and immune complexes
Primary immunodeficiency
Genetic; recurrent infections; includes B cell, T cell, combined, complement, phagocyte defects
Secondary immunodeficiency
Acquired; from illness, drugs, malnutrition, stress, trauma, viral infection (e.g., AIDS)
DiGeorge syndrome
Thymic aplasia → T cell deficiency
SCID
Severe combined immunodeficiency; defective T and B cells
Wiskott‑Aldrich syndrome
X‑linked; low IgM; recurrent infections and bleeding
C3 deficiency
Severe complement deficiency; recurrent infections
Hypersensitivity
Exaggerated immune response → host damage
Type I hypersensitivity
IgE‑mediated, immediate (allergy, anaphylaxis, asthma)
Type II hypersensitivity
Tissue‑specific; antibodies destroy cells (Grave’s disease, hemolytic anemia)
Type III hypersensitivity
Immune complex‑mediated; complexes deposit in tissues (SLE, serum sickness, post‑strep GN)
Type IV hypersensitivity
Delayed T‑cell‑mediated (TB, contact dermatitis, graft rejection)
Autoimmunity
Immune system attacks self antigens (e.g., rheumatoid arthritis, SLE)