Immunology – Innate & Adaptive Responses, Inflammation and Complement

A comprehensive set of vocabulary flashcards covering key cells, molecules, pathways and processes involved in innate and adaptive immunity, inflammation, complement activation, cytokine signaling and lymphocyte biology.

Innate Immunity

Rapid, first-line defense composed of physical barriers, phagocytes, NK cells, complement, cytokines and other pre-existing mechanisms.

Adaptive Immunity

Slower, highly specific immune response mediated by B and T lymphocytes that generates immunological memory.

Epithelial Barriers

Skin and mucosal surfaces that provide mechanical, chemical and microbiologic protection against pathogens.

Phagocyte

Cell (e.g., neutrophil, macrophage) that ingests and destroys microbes and debris.

Neutrophil

Most abundant circulating leukocyte; first cell to reach sites of acute inflammation and principal component of pus.

Monocyte/Macrophage

Blood phagocyte that becomes a tissue macrophage; key effector in inflammation and tissue repair.

Dendritic Cell

Professional antigen-presenting cell that links innate and adaptive immunity by activating naïve T cells.

Mast Cell

Granulocyte that releases histamine and other mediators; central to allergic and acute inflammatory reactions.

Innate Lymphoid Cell (ILC)

Innate lymphocytes lacking antigen-specific receptors; produce cytokines that shape early immune responses.

Natural Killer (NK) Cell

Cytotoxic lymphocyte that kills virus-infected and tumor cells without prior sensitization; produces IFN-γ.

Complement System

Cascade of plasma proteins that opsonize microbes, lyse cells (MAC) and promote inflammation.

Cytokine

Soluble mediator produced by many cells that regulates immunity, inflammation and hematopoiesis.

Toll-like Receptor (TLR)

Pattern-recognition receptor on cell surfaces/endosomes that detects microbial molecules and activates innate immunity.

Membrane Attack Complex (MAC)

Terminal complement assembly (C5b-9) that inserts into microbial membranes and causes lysis.

Opsonization

Coating of microbes with molecules (e.g., antibodies, C3b) that enhances phagocytosis.

C3b

Key complement fragment that opsonizes pathogens and participates in C5 convertase formation.

Chemotaxis

Directed leukocyte migration along a chemical gradient toward sites of infection or injury.

Acute Inflammation

Fast, short-lived response featuring vasodilation, increased vascular permeability and neutrophil influx.

Chronic Inflammation

Prolonged inflammation characterized by macrophages, lymphocytes, tissue destruction and fibrosis.

Margination

Peripheral displacement of leukocytes along vessel walls during slowed blood flow (stasis).

Rolling

Transient, weak leukocyte binding to endothelium mediated by selectins during recruitment.

Selectin

Adhesion molecule (L, E, P types) responsible for leukocyte rolling on vascular endothelium.

L-Selectin

Leukocyte selectin that binds endothelial ligands and initiates rolling.

E-Selectin

Endothelial selectin induced by TNF/IL-1 that binds leukocyte ligands during inflammation.

P-Selectin

Preformed endothelial/platelet selectin rapidly expressed on the surface after histamine or thrombin stimulation.

Adhesion (Firm)

Stable leukocyte attachment to endothelium via high-affinity integrins and ICAM/VCAM ligands.

Integrin

Heterodimeric leukocyte receptor that mediates firm adhesion and signaling (e.g., LFA-1, VLA-4).

ICAM-1

Intercellular adhesion molecule-1; endothelial ligand for β2 integrins (LFA-1) enabling firm adhesion.

VCAM-1

Vascular cell adhesion molecule-1; endothelial ligand for VLA-4 integrin.

Diapedesis (Transmigration)

Leukocyte passage through the endothelial junctions into tissues, guided by PECAM-1.

PECAM-1 (CD31)

Platelet–endothelial cell adhesion molecule mediating leukocyte diapedesis.

Exudate

Protein-rich, often cellular fluid that escapes vessels due to increased permeability in inflammation.

Transudate

Low-protein fluid resulting from hydrostatic or osmotic imbalance, not primarily inflammatory.

Edema

Excess fluid accumulation in interstitial tissue or serous cavities; may be exudate or transudate.

Serous Inflammation

Accumulation of cell-poor, protein-rich fluid (serous exudate) in body cavities or skin blisters.

Fibrinous Inflammation

Exudate with fibrin deposition due to high vascular permeability; may organize into scar.

Suppurative (Purulent) Inflammation

Pus-forming response rich in neutrophils and necrotic debris; characteristic of pyogenic bacteria.

Abscess

Localized collection of purulent exudate with central necrosis and peripheral leukocytes.

Ulcer

Local surface defect resulting from shedding of inflamed necrotic tissue, often with granulation base.

Fibrosis (Scarring)

Connective tissue replacement of normal tissue after significant injury or chronic inflammation.

Caseating Granuloma

Granulomatous inflammation with central necrosis (e.g., tuberculosis).

Non-caseating Granuloma

Granuloma lacking central necrosis (e.g., sarcoidosis).

Classical Complement Pathway

Antibody-triggered complement activation involving C1q, C1r, C1s leading to C3 convertase (C4b2a).

Alternative Complement Pathway

Antibody-independent pathway initiated by microbial surfaces generating C3 convertase (C3bBb).

Lectin Complement Pathway

Pathway activated by mannose-binding lectin binding microbial carbohydrates; forms C4b2a convertase.

C3 Convertase

Central enzyme complex that cleaves C3 into C3a and C3b during complement activation.

C5a

Potent complement anaphylatoxin and chemoattractant for neutrophils.

C3a

Complement fragment that triggers mast-cell histamine release and vascular permeability.

C5b-9

Terminal complement components forming the membrane attack complex (MAC).

Natural Killer T (NKT) Cell

T cell subset recognizing lipid antigens on CD1d molecules; rapidly produces cytokines.

γδ T Cell

T-cell subset with γδ TCR, limited diversity, often found in epithelial tissues providing innate-like defense.

Cytokine Storm

Pathologic, excessive cytokine release leading to systemic inflammation and tissue damage.

ELISA

Enzyme-linked immunosorbent assay used to quantitatively detect soluble proteins such as cytokines.

JAK-STAT Pathway

Signal transduction cascade activated by cytokine receptors leading to transcriptional responses.

MHC Class I

Molecule presenting endogenous peptides to CD8+ T cells; expressed on all nucleated cells.

MHC Class II

Molecule presenting exogenous peptides to CD4+ T cells; expressed on professional APCs.

Costimulation (CD28/B7)

Second signal for T-cell activation provided by CD28 on T cells binding B7-1/2 on APCs.

Opsonin

Any molecule (e.g., IgG, C3b) that enhances phagocyte binding to and ingestion of targets.

IL-2

T-cell growth factor produced by activated T cells; drives clonal expansion.

IL-12

Cytokine from dendritic cells/macrophages that promotes Th1 differentiation and activates NK cells.

IFN-γ

Key Th1 and NK cytokine that activates macrophages and enhances antigen presentation.

TNF

Pro-inflammatory cytokine causing fever, endothelial activation and cachexia at high levels.

IL-1

Fever-inducing cytokine that activates endothelium and leukocytes.

IL-6

Cytokine inducing acute-phase proteins and promoting B-cell differentiation.

Th1 Cell

Helper T subset producing IFN-γ to activate macrophages and defend against intracellular microbes.

Th2 Cell

Helper T subset producing IL-4, IL-5, IL-13 that mediates eosinophil activation and defense against helminths.

Th17 Cell

Helper T subset producing IL-17 that recruits neutrophils against extracellular bacteria and fungi.

T Follicular Helper (Tfh) Cell

CD4+ subset residing in germinal centers aiding B cells in affinity maturation and isotype switching.

Neutrophil Extracellular Trap (NET)

Web-like chromatin structure expelled by neutrophils to capture and kill microbes.

Positive Selection

Thymic process selecting T cells with TCRs that weakly recognize self-MHC, ensuring MHC restriction.

Negative Selection

Deletion of strongly self-reactive lymphocytes in thymus or bone marrow to maintain tolerance.

Naive Lymphocyte

Mature B or T cell that has not yet encountered its specific antigen.

Effector Lymphocyte

Activated lymphocyte capable of immediate functions such as cytokine secretion or cytotoxicity.

Memory Lymphocyte

Long-lived antigen-experienced cell that mounts rapid, robust responses upon re-exposure.

Immunoglobulin Variable Region

Antibody domain responsible for antigen recognition; exhibits high diversity.

Immunoglobulin Constant Region

Antibody domain mediating effector functions such as complement activation and Fc receptor binding.

Hinge Region

Flexible segment of IgG, IgA, IgD that allows Fab arms to assume different angles for antigen binding.

Avidity

Overall strength of binding between a multivalent antibody and a multivalent antigen.

Complement Receptor 1 (CR1)

Phagocyte receptor that binds C3b/C4b-coated particles to promote clearance and immune complex removal.