Innate immunity is the body's immediate, non-specific defense system against pathogens.

Characteristics:

• Rapid response (minutes–hours)
• No antigen specificity
• No memory
• Recognizes conserved microbial patterns

Innate immunity bridges into adaptive immunity.

See also:

• Adaptive Immunity
• Cytokines Overview

Innate immunity consists of:

• Physical barriers
• Cellular defenses
• Soluble mediators

• Skin
• Mucosal epithelium
• Tight junctions
• Gastric acid
• Mucus
• Ciliary clearance
• Antimicrobial peptides (defensins)

Barrier disruption is often the first step in infection and inflammation.

Innate immune cells recognize pathogens using PRRs.

PRRs detect:

• PAMPs (Pathogen-Associated Molecular Patterns)
• DAMPs (Damage-Associated Molecular Patterns)

Major PRRs:

• Toll-Like Receptors (TLRs)
• NOD-like receptors
• RIG-I-like receptors

Activation of PRRs leads to:

• NF-κB activation
• Cytokine production
• Interferon production

TLRs recognize conserved microbial structures.

Examples:

• TLR4 → LPS (Gram-negative bacteria)
• TLR3 → Viral dsRNA
• TLR7/8 → Viral ssRNA
• TLR9 → Bacterial DNA

TLR activation triggers:

• TNF-α release
• IL-1 release
• IL-6 release
• Type I interferons

See:

• Interferons
• TNF Family

• First responders
• Phagocytosis
• Reactive oxygen species
• NET formation

Dominant in acute bacterial infections.

• Tissue-resident phagocytes
• Cytokine producers
• Antigen presentation (bridge to adaptive immunity)

Key cytokines:

• TNF-α
• IL-1
• IL-6

• Professional antigen-presenting cells
• Activate naive T cells
• Link innate → adaptive immunity

See:

• Antigen Presentation & MHC

• Kill virus-infected cells
• Kill tumor cells
• Recognize reduced MHC-I expression

Mechanism:

• Perforin
• Granzymes

Complement is a plasma protein cascade that:

• Opsonizes pathogens
• Recruits inflammatory cells
• Forms membrane attack complex (MAC)

Major functions:

• C3b → Opsonization
• C5a → Chemotaxis
• C5b-9 → Membrane attack complex

See full page:

• Complement System

Early inflammatory cytokines:

• TNF-α
• IL-1
• IL-6

Effects:

• Fever
• Increased vascular permeability
• Leukocyte recruitment
• Acute phase reactant production (CRP)

See:

• Cytokines Overview

1. PRR activation 2. Cytokine release (TNF, IL-1, IL-6) 3. Endothelial activation 4. Neutrophil recruitment 5. Pathogen clearance

If dysregulated → sepsis or chronic inflammation.

Drugs targeting innate pathways:

• TNF Inhibitors
• IL-1 Inhibitors
• Complement Inhibitors
• NSAIDs (prostaglandin inhibition)

Innate dysregulation is central to:

• Sepsis
• Rheumatoid arthritis
• IBD
• Psoriasis

• Innate immunity is immediate and non-specific.
• PRRs detect conserved microbial patterns.
• TNF-α, IL-1, and IL-6 drive early inflammation.
• Complement C3b opsonizes; C5a recruits; MAC lyses.
• Innate immunity activates adaptive immunity via dendritic cells.