Immunology: Innate and Adaptive Defense Mechanisms, Cells, and Hypersensitivities
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53 Terms
Innate Immunity
Immediate, non-specific defense using physical barriers, phagocytes, and protein systems
Adaptive Immunity
Targeted defense using T and B cells that develops memory for faster future responses
Neutrophils
Most common WBCs that phagocytize bacteria and fungi
Eosinophils
WBCs that destroy parasites and large pathogens
Basophils
Rare WBCs (
Monocytes
Blood precursors that differentiate into macrophages and dendritic cells
Macrophages
Large phagocytes that ingest pathogens, clean up cell debris, and release cytokines
Dendritic Cells
Antigen-presenting cells (APCs) that capture antigens and activate T cells in lymph nodes
Mast Cells
Tissue granulocytes coated in IgE that release histamine during allergic responses
Complement System
Innate protein cascade that opsonizes pathogens, forms MAC perforations, and summons phagocytes
Clotting System
Protein cascade that walls off injury sites, traps antigens, and stops bleeding
Kinin System
System producing bradykinin to cause vasodilation, permeability, and pain
IgG
Most abundant antibody (80%) and the only one that crosses the placenta
IgM
First antibody produced during an acute infection; agglutinates pathogens
IgE
Antibody responsible for Type I allergic reactions and parasite defense
IgD
Early-phase antibody that signals B cells to release IgM
Rubor (Redness)
Cardinal sign of inflammation caused by increased blood flow from histamine.
Tumor (Swelling)
Cardinal sign caused by fluid leaking through permeable capillaries into tissue.
Dolor (Pain)
Cardinal sign caused by tissue injury and irritation of nerves by bradykinin and prostaglandins.
Type I Hypersensitivity
IgE-mediated allergic response causing rapid mast cell histamine release (e.g., anaphylaxis).
Type II Hypersensitivity
Antibody-mediated (IgG/IgM) direct attack causing cell lysis (e.g., blood transfusion reaction).
Type III Hypersensitivity
Immune complex-mediated reaction where circulating antibody-antigen clusters lodge in tissues.
Type IV Hypersensitivity
T-cell mediated delayed reaction taking 12-72 hours (e.g., poison ivy rash, PPD test).
CD4 T-Helper Cells
Central coordinators that activate B cells to make antibodies and CD8 cells to become killer T cells.
CD8 Cytotoxic T Cells
T cells that directly kill infected cells via membrane lysis or apoptosis.
HIV Primary Target
CD4 T-helper lymphocytes, leading to eventual collapse of the adaptive immune system.Innate Immunity Immediate, non-specific defense using physical barriers, phagocytes, and protein systems.
Adaptive Immunity
Targeted defense using T and B cells that develops memory for faster future responses.
Neutrophils
Most common WBCs that phagocytize bacteria and fungi.
Eosinophils
WBCs that destroy parasites and large pathogens.
Basophils
Rare WBCs (
Monocytes
Blood precursors that differentiate into macrophages and dendritic cells.
Macrophages
Large phagocytes that ingest pathogens, clean up cell debris, and release cytokines.
Dendritic Cells
Antigen-presenting cells (APCs) that capture antigens and activate T cells in lymph nodes.
Mast Cells
Tissue granulocytes coated in IgE that release histamine during allergic responses.
Complement System
Innate protein cascade that opsonizes pathogens, forms MAC perforations, and summons phagocytes.
Clotting System
Protein cascade that walls off injury sites, traps antigens, and stops bleeding.
Kinin System
System producing bradykinin to cause vasodilation, permeability, and pain.
IgG
Most abundant antibody (80%) and the only one that crosses the placenta.
IgA
Antibody found in mucosal secretions, saliva, tears, and breast milk.
IgM
First antibody produced during an acute infection; agglutinates pathogens.
IgE
Antibody responsible for Type I allergic reactions and parasite defense.
IgD
Early-phase antibody that signals B cells to release IgM.
Calor (Heat)
Cardinal sign of inflammation caused by capillary dilation and increased blood flow.
Rubor (Redness)
Cardinal sign of inflammation caused by increased blood flow from histamine.
Tumor (Swelling)
Cardinal sign caused by fluid leaking through permeable capillaries into tissue.
Dolor (Pain)
Cardinal sign caused by tissue injury and irritation of nerves by bradykinin and prostaglandins.
Type I Hypersensitivity
IgE-mediated allergic response causing rapid mast cell histamine release (e.g., anaphylaxis).
Type II Hypersensitivity
Antibody-mediated (IgG/IgM) direct attack causing cell lysis (e.g., blood transfusion reaction).
Type III Hypersensitivity
Immune complex-mediated reaction where circulating antibody-antigen clusters lodge in tissues.
Type IV Hypersensitivity
T-cell mediated delayed reaction taking 12-72 hours (e.g., poison ivy rash, PPD test).
CD4 T-Helper Cells
Central coordinators that activate B cells to make antibodies and CD8 cells to become killer T cells.
CD8 Cytotoxic T Cells
T cells that directly kill infected cells via membrane lysis or apoptosis.
HIV Primary Target
CD4 T-helper lymphocytes, leading to eventual collapse of the adaptive immune system.