Q1 LONG ANSWER 10M ★ High-yield

Classify immunity. Describe the organs and cells of the immune system and the mechanisms of innate immunity.

Microbiology · 2nd Professional — Para-Clinical

Definition and Classification

Immunity is the resistance of the host to infection and to foreign substances. It is broadly innate (natural, non-specific) or adaptive (acquired, specific).

Feature	Innate immunity	Adaptive immunity
Specificity	Non-specific — recognises broad patterns (PAMPs) shared by classes of organism	Highly specific for a particular epitope
Speed	Immediate (minutes to hours)	Slow on first exposure (days), rapid thereafter
Memory	None — the response is identical every time	Present — the basis of vaccination
Components	Barriers, phagocytes, NK cells, complement, interferons, acute phase proteins, inflammation, fever	B lymphocytes and antibody; T lymphocytes
Receptors	Germ-line encoded, limited in number — TOLL-like receptors	Generated by gene rearrangement, giving enormous diversity
Diversity	Limited	Effectively unlimited
Present in	All multicellular organisms	Vertebrates only

Adaptive immunity is further classified as active (the host makes its own response, slow to develop but long-lasting, with memory) or passive (preformed antibody is transferred, giving immediate but temporary protection with no memory)
Active natural — clinical or subclinical infection; active artificial — vaccination
Passive natural — maternal IgG across the placenta and IgA in colostrum; passive artificial — immunoglobulin, antivenom, antitoxin

CLINICAL PEARL

The two systems are not alternatives; the innate response instructs the adaptive one. Dendritic cells recognising a pathogen through Toll-like receptors do not merely phagocytose it — they migrate to lymph nodes, present its antigen, and through the cytokines they release determine what kind of adaptive response follows. Without that instruction the adaptive system does not know what to make, which is why adjuvants work: they provoke innate signals.

Organs of the Immune System

Category	Organs	Function
Primary (central)	Bone marrow and thymus	Sites where lymphocytes are produced and mature, and where self-reactive cells are deleted. B cells mature in the bone marrow (the bursa equivalent); T cells mature in the thymus
Thymic education	—	Positive selection retains cells that can recognise self-MHC; negative selection deletes those reacting strongly to self antigen — the basis of central tolerance. Over 95% of thymocytes die in the process
Secondary (peripheral)	Lymph nodes, spleen, and mucosa-associated lymphoid tissue (malt, GALT, tonsils, Peyer patches)	Sites where mature lymphocytes encounter antigen and mount a response
Lymph node	—	Cortex contains B-cell follicles with germinal centres; paracortex is the T-cell zone; medulla contains plasma cells. Filters lymph
Spleen	—	Filters blood; white pulp is lymphoid; the chief site of response to blood-borne and capsulated organisms — hence the risk after splenectomy

Cells of the Immune System

Cell	Markers	Function
B lymphocyte	CD19, CD20, surface immunoglobulin	Recognises native antigen through surface immunoglobulin; differentiates into plasma cells secreting antibody, and into memory B cells
T helper (CD4)	CD3, CD4	Recognises antigen with MHC class II; the coordinator of the whole adaptive response. Subsets: Th1 (interferon-gamma; activates macrophages, cell-mediated immunity), Th2 (IL-4, IL-5; antibody and eosinophil responses), Th17 (mucosal defence against fungi and extracellular bacteria), T regulatory (suppress responses and maintain peripheral tolerance)
T cytotoxic (CD8)	CD3, CD8	Recognises antigen with MHC class I; kills virus-infected and tumour cells by perforin, granzymes and Fas
Natural killer cell	CD16, CD56; CD3 negative	Innate lymphocyte that kills without prior sensitisation and without MHC restriction; it kills cells that have lost MHC class I ("missing self"), which is how viruses and tumours evade cytotoxic T cells. Also mediates ADCC
Macrophage and dendritic cell	MHC class II, CD14 (macrophage)	Antigen-presenting cells; phagocytosis, cytokine production. The dendritic cell is the most efficient and the only one that activates a naive T cell
Neutrophil	—	Principal phagocyte in acute bacterial infection
Eosinophil	—	Parasitic (helminth) infection and allergic disease
Mast cell and basophil	High-affinity IgE receptor (FcepsilonRI)	Type I hypersensitivity — release histamine and leukotrienes

Innate Defence Mechanisms in Detail

Mechanical barriers — intact skin, mucous membranes, the mucociliary escalator, coughing, sneezing, and the flushing action of urine and tears
Chemical barriers — gastric acid, lysozyme in tears and saliva (which splits peptidoglycan), fatty acids and low pH of skin, lactoferrin sequestering iron, and defensins
Biological — the normal flora, through colonisation resistance
Phagocytosis — chemotaxis, adherence (greatly enhanced by opsonins: IgG and C3b), ingestion, and killing by oxygen-dependent (respiratory burst, myeloperoxidase) and oxygen-independent (lysozyme, lactoferrin, defensins) mechanisms
Complement, interferons, acute phase proteins (C-reactive protein, mannose-binding lectin), fever and inflammation
Pattern recognition — TOLL-like receptors recognise conserved microbial structures: TLR4 binds LPS, TLR2 peptidoglycan, TLR5 flagellin, TLR3, 7, 8 and 9 nucleic acids

Cytokines

Cytokine	Chief source	Principal action
IL-1	Macrophages	Endogenous pyrogen — fever; acute phase response; T-cell activation
IL-2	Th1 cells	T-cell growth factor — the central autocrine signal of clonal expansion; the target of calcineurin inhibitors
IL-4, IL-5	Th2 cells	IL-4 drives class switching to IgE; IL-5 activates eosinophils — together the basis of allergy and antihelminth defence
IL-6	Macrophages, T cells	Acute phase proteins; fever; a key mediator of cytokine release syndrome, blocked by tocilizumab
IL-10, TGF-beta	T regulatory cells	Anti-inflammatory — suppress the response and maintain tolerance
IL-12	Dendritic cells, macrophages	Drives Th1 differentiation
Interferon-gamma	Th1 cells, NK cells	The principal macrophage-activating cytokine; essential against intracellular organisms; up-regulates MHC
Interferon-alpha and beta	Virus-infected cells	Antiviral — induce an antiviral state in neighbouring cells
TNF-alpha	Macrophages	Inflammation, fever, cachexia; central to septic shock and to granuloma maintenance — which is why anti-TNF agents reactivate tuberculosis
Chemokines	Many cells	Direct leucocyte migration; CCR5 and CXCR4 are HIV co-receptors

Applied Aspects

Maternal IgG protects the infant for about 3 to 6 months, which is why the primary immunisation schedule begins at 6 weeks — earlier vaccination is partly neutralised by maternal antibody
Splenectomised patients are at lifelong risk from capsulated organisms — pneumococcus, meningococcus, Haemophilus — and require vaccination, penicillin prophylaxis and a warning card
Defects in phagocyte function cause recurrent pyogenic infection, as in chronic granulomatous disease, where the respiratory burst fails and catalase-positive organisms survive inside the phagocyte
Passive immunisation gives immediate protection and no memory, which is why antivenom, antitoxin and immunoglobulin are used for immediate threats and are given alongside the vaccine in post-exposure prophylaxis
Adjuvants work by provoking innate signals; alum and newer adjuvants convert a weakly immunogenic protein into an effective vaccine by supplying the danger signal that dendritic cells require
Undernutrition impairs cell-mediated immunity particularly, and is a major reason why tuberculosis, measles and diarrhoea remain lethal in Indian children who would otherwise recover

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