Describe the components of Innate and adaptive immune response?8 mark

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Components of Innate and Adaptive Immune Response

Principal components and kinetics of innate and adaptive immune responses

FIG. 5.1 - Robbins & Kumar Basic Pathology: Principal components and kinetics of innate vs. adaptive immune responses

I. INNATE IMMUNITY

Innate immunity is the first line of defense - it acts within minutes to hours of infection. It uses a fixed set of receptors that recognize conserved molecular patterns shared by microbes rather than fine structural differences. It does not improve with repeated exposure.

A. Physical and Chemical Barriers

The epithelial surfaces (skin, mucosae) form a mechanical barrier that prevents microbial entry. Chemical products at these surfaces include:

Antimicrobial peptides (defensins)
Lysozyme in secretions
Mucus trapping in respiratory and GI tracts

These are the "first-contact" barriers that prevent most pathogens from ever entering the body.

B. Cellular Components

Cell Type	Origin	Key Function
Neutrophils	Bone marrow	First recruited phagocytes; kill bacteria via ROS, enzymes, NETs
Macrophages	Monocytes	Tissue-resident phagocytes; secrete cytokines (TNF, IL-1, IL-6); activate adaptive immunity
Dendritic cells (DCs)	Bone marrow	Sentinels in tissue; capture antigens; bridge innate to adaptive by presenting antigen to T cells
NK cells	Bone marrow	Kill virus-infected cells and tumor cells without prior sensitization; release IFN-γ
Mast cells	Bone marrow	Tissue-resident; release histamine, cytokines on activation; important in allergy and parasitic defense
Innate lymphoid cells (ILCs)	Bone marrow	Non-antigen-specific lymphoid cells; support mucosal defense and tissue repair

C. Pattern Recognition Receptors (PRRs)

Innate immune cells detect microbes through PRRs that recognize:

PAMPs (Pathogen-Associated Molecular Patterns) - e.g., bacterial LPS, flagellin, viral dsRNA
DAMPs (Damage-Associated Molecular Patterns) - signals from necrotic cells (uric acid, ATP, HMGB1)

Major PRR classes:

Toll-Like Receptors (TLRs): Best-characterized PRRs. Plasma membrane TLRs detect bacterial products (LPS). Endosomal TLRs detect viral/bacterial nucleic acids. Activation stimulates NF-kB -> cytokine production and costimulator upregulation.
NOD-Like Receptors (NLRs): Cytosolic receptors; NOD-1/NOD-2 detect bacterial peptidoglycans. Several NLRs signal via the inflammasome, activating caspase-1 -> cleaves pro-IL-1β to active IL-1β -> fever and inflammation. Relevant to gout (urate crystal detection) and autoinflammatory syndromes.
C-type Lectin Receptors: On macrophages and DCs; detect fungal/bacterial polysaccharides -> phagocytosis.
RIG-like Receptors (RLRs): Cytosolic sensors for viral RNA -> trigger type I interferon production.
Cytosolic DNA Sensors: Detect viral/bacterial DNA in the cytoplasm -> interferons. Dysregulation causes interferonopathies.
G protein-coupled receptors: On neutrophils/macrophages; detect N-formylmethionyl peptides (bacterial) -> chemotaxis.

D. Plasma Proteins

Complement system (C1-C9): Three pathways (classical, alternative, lectin) converge to produce opsonins (C3b), chemotactic factors (C5a), and the membrane attack complex (MAC). ~100 different innate receptors recognize a few thousand molecular patterns.
Acute phase proteins: CRP, mannose-binding lectin (MBL), fibrinogen - opsonize microbes and activate complement.
Interferons (type I, IFN-α/β): Secreted by virus-infected cells; induce antiviral state in neighboring cells; degrade viral nucleic acids.

E. Reactions of Innate Immunity

Inflammation - cytokines + complement fragments recruit leukocytes that destroy pathogens and clear dead cells
Antiviral defense - type I interferons block viral replication
Bridging to adaptive immunity - DCs upregulate MHC molecules and costimulators; innate cytokines (IL-12) direct the type of adaptive response

II. ADAPTIVE IMMUNITY

Adaptive immunity develops over days to weeks, is mediated by lymphocytes, and improves dramatically with each encounter (immunological memory). It recognizes an enormous variety of distinct antigens.

Cardinal Features

Specificity: Each lymphocyte clone recognizes a single epitope (clonal selection theory, Burnet 1957)
Diversity: ~10^7 - 10^9 distinct antigenic specificities in the lymphocyte repertoire
Memory: Secondary responses are faster, greater in magnitude, and qualitatively superior
Self-tolerance: Lymphocytes reactive to self-antigens are normally eliminated or suppressed

A. Humoral Immunity (B Lymphocytes)

B cells originate and mature in bone marrow. They carry surface immunoglobulin as their B-cell receptor (BCR) - a transmembrane antibody with two heavy and two light chains linked by disulfide bonds. BCR can directly recognize native (unprocessed) antigens in the blood, lymph, and mucosal secretions.

On activation (usually with T-cell help):

B cells proliferate and differentiate into plasma cells (antibody-secreting factories)
Some become long-lived memory B cells

Functions of antibodies:

Neutralization - block microbial attachment to host cells
Opsonization - coat pathogens for phagocytosis (via Fc receptors)
Complement activation - via the classical pathway
ADCC - Antibody-dependent cellular cytotoxicity (NK cells kill Ab-coated targets)

Antibody classes (Isotypes): IgM (first responder), IgG (most abundant, crosses placenta), IgA (mucosal), IgE (allergy/parasites), IgD (B-cell surface receptor)

B. Cell-Mediated Immunity (T Lymphocytes)

T cells mature in the thymus and constitute 60-70% of peripheral blood lymphocytes. Unlike B cells, T cells cannot recognize free antigen - they only see peptide fragments presented by MHC molecules on antigen-presenting cells (APCs).

T-cell receptor (TCR): Heterodimer of α and β chains, each with a variable (antigen-binding) and constant region. Diversity generated by somatic V(D)J recombination.

Two Major T-cell Subsets:

1. CD4+ Helper T cells (Th)

Recognize antigen presented by MHC class II (on APCs: dendritic cells, macrophages, B cells)
Secrete cytokines that help B cells produce antibodies and help macrophages destroy phagocytosed microbes
HIV destroys CD4+ cells -> severe combined immunodeficiency
Further differentiate into:
- Th1: secrete IFN-γ -> activate macrophages (intracellular pathogen defense)
- Th2: secrete IL-4, IL-5, IL-13 -> eosinophil activation, IgE production (allergy/parasites)
- Th17: secrete IL-17 -> neutrophil recruitment (extracellular bacteria/fungi)
- T follicular helper (Tfh): assist B cells in germinal centers

2. CD8+ Cytotoxic T Lymphocytes (CTLs)

Recognize antigen on MHC class I (on all nucleated cells)
Directly kill virus-infected cells, tumor cells, and graft cells
Kill via perforin/granzyme pathway and Fas-FasL interactions

Regulatory T cells (Tregs)

CD4+CD25+FoxP3+ cells
Suppress immune responses; maintain peripheral tolerance
Prevent autoimmunity

C. Antigen-Presenting Cells (APCs)

APC	Key Features
Dendritic cells	Most potent APCs; tissue sentinels; express high MHC II + costimulators; bridge innate/adaptive
Macrophages	Present antigen to T cells AND effector function (phagocytosis)
B cells	Present antigen to Th cells to receive help for antibody production

APCs provide two signals for T-cell activation:

Signal 1: Antigen-MHC binds TCR
Signal 2 (Costimulation): B7 (CD80/CD86) on APC binds CD28 on T cell

Without Signal 2, T cells become anergic (tolerant).

D. Cytokines - Soluble Mediators

Cytokines coordinate both arms:

Cytokine	Source	Function
IL-1, IL-6, TNF	Macrophages	Inflammation, fever, acute phase response
IL-12	DCs, macrophages	Drive Th1 responses; activate NK cells
IFN-γ	Th1, NK cells	Activate macrophages; antiviral
IL-4	Th2 cells	B-cell class switching to IgE; Th2 differentiation
IL-17	Th17 cells	Neutrophil recruitment
TGF-β, IL-10	Tregs	Anti-inflammatory, tolerance

Summary Comparison Table

Feature	Innate Immunity	Adaptive Immunity
Response time	Minutes to hours	Days to weeks
Specificity	Broad (PAMPs/DAMPs)	Exquisitely specific (individual epitopes)
Memory	None	Long-lived memory cells
Receptors	PRRs (TLRs, NLRs, etc.) - germline encoded	TCR, BCR - somatically rearranged
Key cells	Neutrophils, macrophages, NK cells, DCs	T cells, B cells
Mediators	Complement, interferons, cytokines	Antibodies, cytokines
Diversity	~100 receptors, few thousand patterns	10^7 - 10^9 specificities

Sources: Robbins & Kumar Basic Pathology, p. 155-160; Cellular and Molecular Immunology, p. 32-35

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