Immunity (Innate and Acquired)

Innate (Natural, Nonspecific) Immunity

Present from birth. No prior exposure needed. Fast (minutes-hours). NO memory, doesn’t improve with repeat exposure.

Physical/mechanical barriers: skin, mucous membranes, mucus trapping, ciliary sweeping, cough/sneeze, tears/saliva/urine flushing, gastric acid/vaginal pH.

Chemical barriers: lysozyme (tears/saliva/mucus — digests peptidoglycan), sebum/sweat fatty acids, gastric acid, defensins, normal flora antimicrobial products.

Cellular components:

• Neutrophils — first responders, phagocytose+kill (ROS, lytic enzymes)
• Macrophages — phagocytose, present antigen, secrete cytokines
• NK cells — kill virus-infected/tumor cells, no prior sensitization needed
• Eosinophils — main defense vs helminths
• Dendritic cells — innate recognition + bridge to acquired immunity

Humoral innate components: Complement (alternative/lectin pathway — antibody-independent activation), Acute phase proteins (CRP, liver-produced), Interferons (antiviral state induction).

Recognition: Pattern Recognition Receptors (PRRs) — mainly Toll-like receptors (TLRs) — bind Pathogen-Associated Molecular Patterns (PAMPs, e.g. LPS, peptidoglycan) — conserved across pathogen CLASSES, not specific to one organism. = broad + immediate but NOT specific.

Inflammation: vasodilation + ↑vascular permeability (redness, heat, swelling) — brings plasma proteins + phagocytes. Mediators: histamine, prostaglandins, C3a/C5a.

Acquired (Adaptive, Specific) Immunity

Develops after specific antigen exposure. Slower first time (days). HIGHLY specific. MEMORY = defining feature (faster/stronger 2nd response).

Mediated by lymphocytes (T, B cells).

2 arms:

• Humoral — B cells + antibodies — extracellular organisms/toxins
• Cell-mediated — T cells — intracellular organisms/tumor cells

Classification (2 axes)

Active: own immune system response. Slow onset. LONG-lasting, memory present. Passive: transferred ready-made Ab. IMMEDIATE. SHORT-lived, NO memory — protects only current exposure, not future.

Integration

Not sequential — integrated system. Innate response (inflammation, phagocytosis, APC antigen processing) KICKSTARTS acquired immunity — APCs must process/present antigen to naive T cells first.

Innate = buys time (hours-days). Acquired = slower but sharper + remembers (long-term clearance + future protection).

Defining Immunity

Immunity is the collective set of defence mechanisms that protect the body against disease, broadly by recognizing and eliminating anything identified as foreign. It splits into two systems that differ fundamentally in speed, specificity, and memory — innate immunity, the body’s rapid first line, and acquired immunity, the slower but far more precise and adaptable system that develops over the course of an individual’s life.

Innate (Natural, Nonspecific) Immunity

Innate immunity is present from birth, requires no prior exposure to a pathogen, acts within minutes to hours, and — critically — does not improve with repeated exposure, since it carries no memory. It operates through layered barriers, each catching what the previous one lets through.

Physical and mechanical barriers are the first line: intact skin and mucous membranes physically exclude most organisms; mucus traps particles; ciliary action in the respiratory tract sweeps trapped material outward; coughing and sneezing expel material forcibly; the flushing action of tears, saliva, and urine washes surfaces clean; and the low pH of gastric acid and vaginal secretions is directly hostile to many organisms.

Chemical barriers work alongside these: lysozyme in tears, saliva, and mucus digests bacterial peptidoglycan; sebum and sweat carry antimicrobial fatty acids; gastric acid, defensins (antimicrobial peptides at epithelial surfaces), and the antimicrobial products of normal microbiota all contribute.

Cellular components provide active, mobile defence once a barrier is breached: neutrophils, the first responders to acute bacterial infection, phagocytose and kill via reactive oxygen species and lytic enzymes; macrophages phagocytose, present antigen, and secrete inflammatory cytokines; NK cells kill virus-infected and tumour cells without needing prior sensitization; eosinophils are the principal defence against helminths; and dendritic cells, while primarily antigen-presenting bridges into acquired immunity, also participate in innate recognition.

Humoral components of innate immunity include the complement system (which can be activated directly by microbial surfaces via the alternative and lectin pathways, independent of antibody), acute-phase proteins (C-reactive protein, produced by the liver in response to inflammation), and interferons (produced by virus-infected cells, inducing an antiviral state in neighbouring cells).

Innate immune cells recognize pathogens through pattern recognition receptors (PRRs) — most importantly Toll-like receptors (TLRs) — which bind conserved microbial structural motifs shared across whole classes of pathogen (pathogen-associated molecular patterns, PAMPs, such as bacterial LPS or peptidoglycan) rather than any one pathogen’s unique antigen. This is exactly why innate immunity is broad and immediate but not specific: the same receptor recognizes the same class of molecular pattern on any organism carrying it, with no fine discrimination between individual strains or antigens.

Inflammation is innate immunity’s signature tissue-level response to injury or infection — vasodilation and increased vascular permeability (redness, heat, swelling) bring plasma proteins and phagocytes to the site, driven by mediators including histamine, prostaglandins, and complement fragments (C3a, C5a).

Acquired (Adaptive, Specific) Immunity

Acquired immunity develops only after exposure to a specific antigen, is slower to mount on first contact (days), but is highly specific to that antigen and — its defining advantage over innate immunity — generates immunological memory, so subsequent exposure to the same antigen triggers a faster, stronger secondary response. It is mediated by lymphocytes (T and B cells) and their products.

Acquired immunity itself splits into two arms, mirroring the distinction covered in depth under the Immune Response topic: humoral immunity, mediated by B lymphocytes and the antibodies they secrete, effective against extracellular organisms and toxins; and cell-mediated immunity, mediated by T lymphocytes, effective against intracellular organisms and abnormal (tumour) cells.

Acquired immunity is further classified by how it is obtained, along two independent axes — active versus passive, and natural versus artificial:

Active immunity is generated by the individual’s own immune system responding to antigen (whether from natural infection or vaccination), takes time to develop, but is long-lasting and carries memory. Passive immunity is antibody transferred ready-made from another source (mother or an immunoglobulin preparation), acts immediately, but is short-lived and generates no memory of its own — a distinction with direct clinical weight, since passive immunization protects only against the immediate exposure, never against future ones.

Why the Distinction Matters

Innate and acquired immunity are not sequential alternatives but a genuinely integrated system: innate immunity’s initial response — inflammation, phagocytosis, antigen processing by dendritic cells and macrophages — is what actually gets acquired immunity started, since APCs must first process and present antigen to naive T cells before any acquired response can begin. The speed/specificity trade-off between the two systems is also what shapes vaccine design and the timeline of every infection: the innate response buys time in the first hours to days of an infection, while the acquired response — slower to arrive but sharper and longer-lasting — ultimately clears the pathogen and remembers it for next time.

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