Cells of the Immune System – Vocabulary Flashcards

Classification Schemes for Immune Cells

• Four complementary ways to group leukocytes (white-blood cells):

  • Developmental lineage

  • \text{Lymphoid} \rightarrow B cells, T cells, NK cells

  • \text{Myeloid} \rightarrow granulocytes, monocytes, macrophages, dendritic cells, mast cells, platelets, erythrocytes

  • Arm of immunity

  • \text{Innate} (rapid, non-specific)

  • \text{Adaptive} (delayed, antigen-specific, immunological memory)

  • Cytoplasmic granularity

  • \text{Granulocytes} (neutrophils, eosinophils, basophils, mast cells)

  • \text{Agranulocytes} (lymphocytes, monocytes, macrophages, dendritic cells)

  • Dominant function

  • Phagocytosis, antigen presentation, cell-mediated cytotoxicity, antibody-dependent cell-mediated cytotoxicity (ADCC)

Blood Cell Overview & Haematopoiesis

• All blood cells derive from pluripotent haematopoietic stem cells (HSCs) in the bone marrow.

• Major formed elements:

  • Erythrocytes (RBCs) – gas transport

  • Leukocytes (WBCs) – immunity

  • Platelets – haemostasis

Innate vs. Adaptive Immune Cells

• Innate leukocytes: neutrophils, eosinophils, basophils, mast cells, monocytes, macrophages, dendritic cells, natural-killer (NK) cells

• Adaptive leukocytes: B lymphocytes (→ plasma cells), T lymphocytes (CD4^+ Th & CD8^+ Tc)

Granulocytes vs. Agranulocytes

• Granulocytes (multi-lobed nuclei, cytoplasmic granules): neutrophils, eosinophils, basophils, mast cells

• Agranulocytes (round nuclei, scant granules): lymphocytes, monocytes → macrophages & dendritic cells

Functional Classification

Phagocytes & Phagocytosis

• Professional phagocytes: neutrophils, monocytes, macrophages, dendritic cells, immature B cells, eosinophils (limited)

• Four sequential stages

  1. Adherence (pattern-recognition receptors engage PAMPs or opsonins)

  2. Ingestion → phagosome formation

  3. Digestion → phagolysosome (fusion with granules/lysosomes)

  4. Exocytosis of debris

• Cellular prerequisites: actin cytoskeleton rearrangement, abundant lysosomes, oxidative burst enzymes, low pH vacuole.

Professional Antigen-Presenting Cells (APC)

• Dendritic cells, macrophages, B cells

• Express \text{MHC II} constitutively → present exogenous peptides to CD4^+ T helper cells.

Cell-Mediated Cytotoxicity

• Cells able to trigger apoptosis of infected or malignant host cells

  • Innate: NK cells

  • Adaptive: cytotoxic T lymphocytes (CTL, CD8^+)

Antibody-Dependent Cell-Mediated Cytotoxicity (ADCC)

• Bridge between humoral & cellular arms

• Mechanism

  • Antibodies bind antigens on target cell → Fc portion exposed.

  • FcγR (for IgG) on NK cells, macrophages, neutrophils OR FcεR (for IgE) on eosinophils engage Fc.

  • Cross-linking → cell activation → apoptosis of antibody-coated target

• Participating effector cells: NK cells, macrophages, neutrophils, eosinophils.

Innate Immune Cell Profiles

Neutrophils

• Most abundant leukocyte (≈50-70 % of WBCs)

• First responders at infection/injury (chemotaxis via IL-8, C5a)

• Granules

  • Primary/azurophilic: peroxidase, lysozyme, acid hydrolases

  • Secondary/specific: collagenase, lactoferrin, additional lysozyme, \text{NADPH} oxidase components

• Functions

  • Phagocytosis & respiratory burst

  • NETs (neutrophil extracellular traps) – chromatin-based microbicidal webs

Monocytes → Macrophages & Dendritic Cells

• Monocytes circulate ≈8 h, then extravasate and differentiate.

• Macrophage differentiation changes

  • ↑ cell size (×5–10), more lysosomes, RER, Golgi, secretory vesicles.

• Macrophage types

  • Resident tissue macrophages with specialised names & roles:

  • Kupffer (liver): tissue repair & detox

  • Mesangial (kidney): support glomerular filtration

  • Wandering/inflammatory macrophages – recruited during infection

• Functions: phagocytosis, cytokine secretion, APC activity (MHC II)

Dendritic Cells (DC)

• Sentinel phagocytes in peripheral tissues; most potent APCs.

• Express MHC I & II, co-receptors CD80/86, CD4, CD8.

• Lifecycle

  1. Capture antigen by phagocytosis/macropinocytosis.

  2. Maturation (↑MHC, ↓phagocytosis).

  3. Migration via lymphatics to T-cell zones of lymph node/spleen.

  4. Present peptide–MHC II to naïve CD4^+ T cells → adaptive priming.

Eosinophils

• 1–3 % of circulating WBCs; abundant in mucosal & connective tissues.

• Granules rich in major basic protein, eosinophil cationic protein, peroxidase → toxic to helminths, protozoa.

• Functions

  • Parasite & fungal defense, late-phase allergic reactions.

  • Release ROS, lipid mediators (prostaglandins, leukotrienes) & cytokines → amplify inflammation & recruit other leukocytes.

  • Express complement receptors, cytokine receptors, and FcεR for IgE → ADCC against large parasites.

Basophils

• <1 % of WBCs; non-phagocytic granulocytes.

• Recruited from blood to infected tissues.

• Express FcεR (IgE) & cytokine receptors.

• Effector molecules: histamine, heparin → ↑vascular permeability; IL-4, IL-13 → Th2 skewing.

• Cooperate with eosinophils in anti-parasite responses; mediate type I hypersensitivity.

Mast Cells

• Arise from bone-marrow progenitors but complete maturation in tissues (skin, mucosae, perivascular & perineural sites).

• Granules contain histamine, proteases, TNF-α.

• Surface FcεR high for IgE → degranulation on cross-linking by allergens → immediate hypersensitivity.

• Secrete cytokines & lipid mediators; major orchestrators of local inflammation and vascular changes.

Natural Killer (NK) Cells

• 5–10 % of circulating lymphocytes (large granular lymphocytes).

• Receptor balance model

  • Activating receptors detect stress-induced ligands on infected/tumour cells → trigger cytotoxicity.

  • Inhibitory receptors (KIR, CD94/NKG2) bind self-MHC I → suppress killing (“missing-self” recognition).

• Cytotoxic granules contain perforin (membrane pore) & granzymes (serine proteases) → apoptosis.

• Additional pathways: Fas-ligand–Fas interaction; ADCC via FcγR III (CD16).

Mechanisms of NK Cytotoxicity

• Fas-Independent (Perforin/Granzyme)

  1. Recognition & conjugate formation with target.

  2. Directed exocytosis of perforin & granzymes.

  3. Detachment; target undergoes apoptosis (caspase cascade, mitochondrial disruption, DNA fragmentation into 200\,\text{bp} ladders).

• Fas-Dependent

  • NK/Tc cells express Fas-ligand → bind Fas (CD95) on target → caspase-8 activation → apoptosis.

• Both mechanisms are silent (no lytic inflammation) and discriminate cells with reduced MHC I.

Adaptive Immune Cell Profiles

Lymphocyte Similarities

• Small, round, 8{-}10\,\mu\text{m}; large nucleus, scant cytoplasm.

• Originate in bone marrow; circulate between blood and secondary lymphoid organs.

• Express unique antigen receptors produced by V(D)J gene recombination:

  • B-cell receptor (BCR) – membrane Ig

  • T-cell receptor (TCR) – αβ heterodimer

Key Differences

• Maturation sites: B cells in bone marrow (and partially spleen); T cells in thymus.

• Antigen recognition

  • BCR/antibodies bind native proteins, polysaccharides, lipids, small chemicals.

  • TCR recognises peptide antigens bound to MHC only.

• Effector functions

  • B cells secrete antibodies; are phagocytic.

  • T cells produce cytokines (Th) or kill infected cells (Tc); non-phagocytic.

B-Cell Development & Fate

• Mature (naïve) B cells exit bone marrow → circulate/settle in secondary lymphoid organs.

• Upon antigen encounter + Th help → activation → clonal expansion.

• Differentiate into

  • Plasma cells – secrete high-affinity antibodies, survive 1{-}2\,\text{weeks}.

  • Memory B cells – migrate to bone marrow; long-lived, rapid recall.

T-Cell Development & Selection

• Bone-marrow progenitors migrate to thymus → rearrange TCR genes.

• Positive selection: retain cells whose TCRs recognise self-MHC moderately.

• Negative selection: delete cells with high affinity for self peptide-MHC (central tolerance).

• Surviving single-positive cells exit as

  • CD4^+ T helper (Th)

  • CD8^+ cytotoxic T (Tc / CTL)

Effector Functions (schematic)

• Th (CD4^+): secrete cytokines → activate macrophages, assist B-cell antibody production, orchestrate inflammation.

• CTL (CD8^+): recognise peptide-MHC I on infected cells → induce apoptosis (perforin/granzyme & Fas).

• B cells / plasma cells: produce soluble antibodies → neutralisation, opsonisation, complement activation, ADCC.

Key Definitions (Homework Guide)

• Leukocytes: all nucleated immune cells in blood & tissues.

• Lymphocytes: adaptive (B, T) + innate-like (NK, ILCs) agranulocytes.

• Granulocytes: polymorphonuclear leukocytes with cytoplasmic granules (neutrophils, eosinophils, basophils, mast cells).

• Agranulocytes: leukocytes lacking conspicuous granules (lymphocytes, monocytes, macrophages, dendritic cells).

• Antigen-Presenting Cells (APC): cells that display processed antigen with \text{MHC II} (DC, macrophage, B cell).

• Phagocytes: cells that ingest & degrade particles/microbes (neutrophils, macrophages, DCs, monocytes, eosinophils).

• Cytotoxic cell: cell that induces apoptosis in target cells (NK, CTL, some macrophages/eosinophils via ADCC).

• Phagocytosis: receptor-mediated endocytosis culminating in intracellular digestion.

• Cell cytotoxicity: active killing of host cells harbouring intracellular pathogens or malignancy.

• Apoptosis: programmed, caspase-mediated cell death (membrane blebbing, DNA laddering, non-inflammatory).

• Necrosis: uncontrolled cell death with membrane rupture & inflammation.

• Antigen: any molecule recognised by BCR/TCR; capable of eliciting an immune response.

Exam-Style Prompts Referenced

• List innate phagocytes; describe phagocytosis steps & enabling ultrastructural features.

• Describe distribution & molecular features of \text{MHC I} vs \text{MHC II}.

  • Exogenous vs endogenous antigen-processing pathways.

  • Immunological significance (CD4 vs CD8 activation, self-tolerance).

Suggested Further Reading

• Kuby Immunology, 8th ed., Chapters 1, 2, 7.

• Janeway’s Immunobiology, 9th ed., Chapter 1 & Chapter 6 (MHC).

• Roitt’s Essential Immunology; Parham – The Immune System (3rd ed.).

• Relevant pathogen sections in standard Medical Microbiology texts.