🛡️ Immunity
Immunity
Immunity — Overview
Immunity is the ability of the body to resist or fight infections caused by pathogens — organisms such as bacteria, viruses, fungi, and parasites that can cause disease. Every living organism is constantly exposed to potential invaders, and the immune system acts as the body's defense force, identifying and neutralizing threats before they can cause harm.
The human immune system is broadly divided into two major arms: innate immunity (the defense you are born with) and acquired immunity (the defense you develop over your lifetime through exposure to pathogens).
Classification of Immunity
Immunity
├── Innate (Non-specific / Natural)
│ ├── Physical barriers
│ ├── Physiological barriers
│ ├── Cellular barriers
│ └── Cytokine barriers
└── Acquired (Specific / Adaptive)
├── Active immunity
│ ├── Natural active (infection)
│ └── Artificial active (vaccination)
└── Passive immunity
├── Natural passive (maternal IgG, colostrum IgA)
└── Artificial passive (antiserum injection)
NOTE
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Immunity
Immunity — Overview
Immunity is the ability of the body to resist or fight infections caused by pathogens — organisms such as bacteria, viruses, fungi, and parasites that can cause disease. Every living organism is constantly exposed to potential invaders, and the immune system acts as the body's defense force, identifying and neutralizing threats before they can cause harm.
The human immune system is broadly divided into two major arms: innate immunity (the defense you are born with) and acquired immunity (the defense you develop over your lifetime through exposure to pathogens).
Classification of Immunity
Immunity
├── Innate (Non-specific / Natural)
│ ├── Physical barriers
│ ├── Physiological barriers
│ ├── Cellular barriers
│ └── Cytokine barriers
└── Acquired (Specific / Adaptive)
├── Active immunity
│ ├── Natural active (infection)
│ └── Artificial active (vaccination)
└── Passive immunity
├── Natural passive (maternal IgG, colostrum IgA)
└── Artificial passive (antiserum injection)
NOTE
The key difference between innate and acquired immunity is specificity: innate immunity responds the same way to all pathogens, while acquired immunity generates a tailored response for each specific pathogen.
Innate Immunity
Innate immunity is present from birth and does not improve with repeated exposure to the same pathogen. It is non-specific, meaning it acts against all pathogens in the same general manner. Think of it as the body's first line of defense — always on guard, always ready.
Four Barriers of Innate Immunity
| Barrier Type | Components | Mechanism |
|---|---|---|
| Physical barriers | Skin (stratum corneum), mucous membranes, cilia, cerumen (earwax) | Skin pH 3–5 (acidic) prevents microbial growth; mucus traps pathogens; cilia sweep away particles |
| Physiological barriers | Body temperature (fever), pH, secretions (tears, saliva, gastric juice) | Fever inhibits pathogen growth; lysozyme in tears/saliva destroys bacterial cell walls; HCl in stomach (pH 1.5–3.5) kills most ingested microbes |
| Cellular barriers | Phagocytes (neutrophils, macrophages), NK cells (Natural Killer cells) | Phagocytosis — engulf and destroy pathogens; NK cells kill virus-infected and tumor cells |
| Cytokine barrier | Interferons (IFNs), TNF (Tumor Necrosis Factor), Interleukins | Interferons protect uninfected cells from viral attack; TNF promotes inflammation; TIP (Toll-like receptor-Induced Proteins) activate immune responses |
More on Physical Barriers
The skin is the largest organ of the body and serves as a remarkably effective physical barrier. The outermost layer — the **stratum corneum** — consists of dead, keratinized cells that pathogens cannot easily penetrate. Additionally, secretions like **sweat** (contains lysozyme and salt) and **sebum** (oily secretion that lowers skin pH) further discourage microbial colonization. **Cerumen** (earwax) traps dust and microbes in the ear canal, while **cilia** in the respiratory tract create a wave-like motion that sweeps trapped pathogens upward and out of the airways.Acquired Immunity
Acquired immunity (also called adaptive immunity) develops after exposure to a pathogen or antigen. Unlike innate immunity, it is specific — each immune response is tailored to a particular pathogen. Acquired immunity has four hallmark features:
Key Features
- Specificity — each antibody or T-cell recognizes a specific antigen. A response against the measles virus will not protect against the polio virus.
- Diversity — the immune system can respond to millions of different antigens, thanks to the enormous variety of lymphocyte receptors generated through gene rearrangement.
- Discrimination — the system distinguishes self from non-self. When this mechanism fails, it leads to autoimmunity (the body attacking its own tissues).
- Memory — upon re-exposure to the same antigen, the response is faster and stronger. This is the principle behind vaccination.
Primary vs Secondary Immune Response
| Feature | Primary Response | Secondary Response |
|---|---|---|
| First/subsequent exposure | First contact with antigen | Re-exposure to same antigen |
| Response time | Slow (5–7 days lag period) | Rapid (1–2 days) |
| Antibody level | Low peak | Much higher peak |
| Duration | Short-lived | Long-lasting |
| Antibody type | Mainly IgM | Mainly IgG |
| Memory cells | Generated | Memory cells activated |
IMPORTANT
The secondary immune response is the basis of vaccination — the first vaccine dose triggers a primary response and generates memory cells, so that when the real pathogen arrives, the body mounts a rapid, powerful secondary response.
Active vs Passive Immunity
| Feature | Active Immunity | Passive Immunity |
|---|---|---|
| How acquired | Exposure to antigen (infection or vaccine) | Pre-formed antibodies transferred |
| Antibody production | By the individual's own immune system | No; antibodies from external source |
| Response time | Slow (days to weeks) | Immediate |
| Memory | Yes (long-term) | No |
| Duration | Long-lasting (years to lifelong) | Short-lived (weeks to months) |
| Examples | Infection recovery; vaccination | Maternal IgG via placenta; antiserum injection |
| Booster possible | Yes | No |
Why newborns have passive immunity
During pregnancy, the mother's **IgG antibodies** cross the placenta and enter the fetal bloodstream, providing the newborn with temporary protection against infections the mother has encountered. After birth, **IgA antibodies** in the mother's **colostrum** (first milk) protect the infant's gut lining. This passive immunity wanes over the first few months of life, which is why the vaccination schedule begins early — to stimulate the baby's own active immunity.Immune Organs
The organs of the immune system are classified into primary (where immune cells originate and mature) and secondary (where immune responses are initiated).
Primary Lymphoid Organs
| Organ | Function |
|---|---|
| Bone marrow | Site of origin of all blood cells (haematopoiesis); B-cell maturation occurs here |
| Thymus | T-cell maturation; located behind the sternum; largest in childhood, involutes (shrinks) with age — this is why children generally have a more active immune system |
Secondary Lymphoid Organs
| Organ | Function |
|---|---|
| Spleen | Largest lymphoid organ; filters blood; removes old RBCs; activates B and T cells. It acts as a "blood filter" just as lymph nodes filter lymph. |
| Lymph nodes | Filter lymph; trap antigens carried by lymphatic fluid; site of immune response initiation. They swell during infections because immune cells are actively multiplying inside them. |
| MALT (Mucosa-Associated Lymphoid Tissue) | Constitutes ~50% of all lymphoid tissue; includes tonsils, Peyer's patches (in the small intestine), and the appendix. MALT guards the body's mucosal surfaces — the most common entry points for pathogens. |
Lymphocytes
Lymphocytes are the key cells of adaptive immunity. They are divided into T-cells and B-cells, each with distinct roles.
T-Cells (Thymus-dependent)
- Mature in the thymus
- Comprise 60–70% of circulating lymphocytes
- Responsible for cell-mediated immunity (CMI) — they directly attack infected cells rather than producing antibodies
| Type | Function |
|---|---|
| T-helper cells (Th / CD4+) | The "commanders" of the immune system — they activate B-cells, cytotoxic T-cells, and macrophages by secreting cytokines |
| T-killer / Cytotoxic cells (Tc / CD8+) | Directly kill virus-infected cells, tumor cells, and transplanted (foreign) cells by releasing perforin and granzymes |
| T-suppressor cells (Ts) | Regulate and suppress immune response after the threat is cleared; prevent autoimmunity by keeping the immune system in check |
| T-memory cells | Long-lived cells that "remember" a pathogen; provide rapid response on re-exposure — the cellular basis of immunological memory |
B-Cells (Bone marrow-derived)
- Mature in bone marrow
- Comprise 10–20% of circulating lymphocytes
- Responsible for humoral immunity (antibody-mediated immunity — "humoral" refers to body fluids where antibodies circulate)
- Upon activation → differentiate into plasma cells (the antibody factories that produce thousands of antibodies per second) and memory B-cells (for future encounters)
TIP
Remember: B = Bone marrow = aBody production (humoral). T = Thymus = cell-mediaTed immunity.
Antibodies (Immunoglobulins)
Antibodies (also called immunoglobulins, abbreviated as Ig) are Y-shaped protein molecules produced by plasma cells (activated B-cells). They specifically bind to antigens and neutralize or mark them for destruction.
Structure
- Y-shaped protein molecule
- Composed of 2 Heavy (H) chains + 2 Light (L) chains (H₂L₂)
- Chains linked by disulphide bonds
- Each arm has a variable region (antigen-binding site / paratope — this is unique for each antibody and determines what antigen it can bind) and a constant region (same within each antibody class)
- Fab region (Fragment antigen-binding) — the 2 arms of the Y; this is where the antibody grabs the antigen
- Fc region (Fragment crystallizable) — the stem of the Y; determines the antibody class and its biological function (e.g., whether it can cross the placenta or activate complement)
Five Classes of Antibodies
| Class | % in Serum | Molecular Weight | Location / Function |
|---|---|---|---|
| IgA | ~10% | 1,70,000 | Found in mucous membranes (saliva, tears, breast milk); first line in mucosal immunity; exists as a dimer (secretory IgA) |
| IgD | 1–3% | 1,85,000 | Found on the surface of B-lymphocytes; functions as a B-cell receptor; plays a role in B-cell activation |
| IgE | 0.05% | 1,88,000 | Bound to mast cells and basophils; triggers allergic reactions (histamine release); also important in defense against parasites (helminths) |
| IgG | 75–80% | 1,46,000 | Most abundant antibody in blood; the only antibody that crosses the placenta (provides passive immunity to fetus); activates complement; opsonization; long-lasting protection |
| IgM | 5–10% | 9,60,000 | Largest antibody (pentamer — 5 units joined together); first to be produced in a primary immune response; activates complement; strong at agglutination |
IMPORTANT
For exams, remember: IgG = most abundant + crosses placenta. IgM = largest + first produced. IgE = allergies. IgA = mucosal defense. IgD = B-cell receptor.
Antibody Functions
- Agglutination — clumping of antigens (making them easier for phagocytes to engulf)
- Opsonization — coating pathogens to enhance phagocytosis (like "tagging" them for destruction)
- Neutralization — blocking toxins and viral binding sites so they cannot infect cells
- Complement activation — triggering the complement cascade, a series of proteins that punch holes in pathogen membranes causing lysis
- Precipitation — making soluble antigens insoluble for easier clearance
Vaccines
A vaccine is a biological preparation that provides active acquired immunity against a specific pathogen. It contains a weakened, killed, or partial form of the pathogen that stimulates the immune system without causing the disease.
Types of Vaccines
| Type | Description | Examples |
|---|---|---|
| Live attenuated | Weakened (but live) pathogen; strong immune response; may not be suitable for immunocompromised individuals | BCG (TB), OPV (polio), MMR (measles, mumps, rubella), yellow fever |
| Killed / Inactivated | Dead pathogen; safer but weaker response; may need boosters | IPV (polio), rabies, influenza, typhoid (injectable) |
| Toxoid | Inactivated toxin (not the pathogen itself, but its harmful product) | DPT — Diphtheria and Tetanus components are toxoids |
| Recombinant / Subunit | Genetically engineered antigen; very specific and safe | Hepatitis B (HBsAg), HPV |
TIP
DPT vaccine contains: Diphtheria toxoid + Pertussis (killed bacteria) + Tetanus toxoid. Note that only D and T are toxoids; P is a killed whole-cell component.
HLA / MHC System
The HLA (Human Leukocyte Antigen) system is the human version of the MHC (Major Histocompatibility Complex). These are cell-surface proteins that present antigen fragments to T-cells, essentially acting as the "identity cards" of your cells.
- Genes located on chromosome 6 (short arm)
- Most polymorphic genes in the human genome — meaning they have the greatest variety of alleles, which is why finding a matching organ donor is so difficult
- Two main classes:
- MHC Class I (HLA-A, B, C) — present on all nucleated cells; recognized by CD8+ T-cells (cytotoxic). These display fragments of intracellular proteins — if a cell is infected, viral peptides appear on MHC I, alerting killer T-cells.
- MHC Class II (HLA-DR, DP, DQ) — present on APCs (antigen-presenting cells: macrophages, dendritic cells, B-cells); recognized by CD4+ T-cells (helper). These display fragments of engulfed pathogens.
- Haplotype: the set of HLA alleles inherited together from one parent (you inherit one haplotype from each parent)
- Tissue typing: matching HLA antigens before organ transplantation to minimize rejection risk
Transplantation
When tissue or organs are transferred from one body to another, the immune system may recognize the foreign MHC molecules and mount an attack. The success of transplantation depends on how closely the donor and recipient tissues match.
| Type | Donor → Recipient | Example |
|---|---|---|
| Autograft | Self → Self | Skin graft from thigh to face |
| Isograft | Genetically identical individual (identical twin) → Self | Between monozygotic twins |
| Allograft / Homograft | Same species, different individual | Kidney transplant between siblings |
| Xenograft / Heterograft | Different species → Self | Pig heart valve in human |
- Graft rejection — the immune system recognizes foreign MHC on the transplanted tissue and mounts a T-cell mediated destruction. This is why allografts and xenografts are most likely to be rejected.
- Immunosuppressants are used to prevent rejection. The most important is cyclosporin A, obtained from the fungus Trichoderma polysporum. It selectively suppresses T-cell activity without broadly shutting down the entire immune system.
NOTE
Autografts and isografts are never rejected because the MHC molecules are identical to the recipient's own cells.
Allergies
An allergy (or hypersensitivity) is an exaggerated immune response to a normally harmless substance called an allergen. The immune system essentially overreacts to something that poses no real threat.
- Mediated by IgE antibodies
- IgE binds to mast cells and basophils → upon re-exposure to the allergen, these cells release histamine → symptoms such as itching, sneezing, rash, swelling, watery eyes
- Anaphylactic shock — a severe, life-threatening systemic allergic reaction characterized by a sudden drop in blood pressure, bronchospasm (airway constriction), and can be fatal without immediate treatment
- Treatment: antihistamines (block histamine receptors), epinephrine/adrenaline (emergency treatment for anaphylaxis), corticosteroids (reduce inflammation)
- Common allergens: pollen, dust mites, animal dander, certain foods (peanuts, shellfish), drugs (penicillin)
Why do allergies happen?
In allergic individuals, the first exposure to an allergen causes B-cells to produce IgE antibodies, which then coat mast cells throughout the body (this is called **sensitization**). On subsequent exposures, the allergen cross-links IgE molecules on mast cells, triggering **degranulation** — the explosive release of histamine and other inflammatory mediators. This is why allergic reactions typically do not occur on the very first exposure but on the second or later exposures.Autoimmune Disorders
Autoimmune disorders occur when the immune system attacks the body's own tissues — a failure of self-tolerance. Normally, the immune system is trained during development to ignore self-antigens, but when this mechanism breaks down, the results can be devastating.
| Disease | Target / Feature |
|---|---|
| Myasthenia gravis | Antibodies against acetylcholine receptors at the neuromuscular junction → progressive muscle weakness and fatigue |
| Pernicious anemia | Antibodies against intrinsic factor → inability to absorb vitamin B₁₂ → megaloblastic anemia |
| Hashimoto's thyroiditis | Antibodies against the thyroid gland → destruction of thyroid tissue → hypothyroidism |
| Rheumatoid arthritis | Antibodies attack synovial joints → chronic inflammation and joint destruction |
| Type 1 Diabetes (IDDM) | T-cells destroy insulin-producing β-cells of the pancreas → absolute insulin deficiency |
| Multiple sclerosis | Immune attack on the myelin sheath of neurons → impaired nerve signal transmission → neurodegeneration |
| Tay-Sachs disease | A genetic lysosomal storage disorder caused by deficiency of the enzyme hexosaminidase A → accumulation of GM2 ganglioside in neurons → neurodegeneration (often grouped with immune/genetic disorders) |
AIDS (Acquired Immunodeficiency Syndrome)
AIDS is the most advanced stage of infection with the Human Immunodeficiency Virus (HIV). It represents a progressive destruction of the immune system, leaving the body vulnerable to infections that a healthy immune system would easily control.
Causative Agent: HIV (Human Immunodeficiency Virus)
- Family: Retroviridae
- Type: ssRNA retrovirus (contains 2 copies of single-stranded RNA)
- Key surface proteins: GP-120 (binds to CD4 receptor on T-helper cells — this is how the virus gains entry) and GP-41 (mediates membrane fusion between virus and host cell)
- Core proteins: P-24 (capsid protein) and P-17 (matrix protein)
- Key enzyme: Reverse transcriptase (converts viral RNA → DNA, which then integrates into the host genome — this is why it's called a retrovirus)
- Target cells: CD4+ T-helper cells, macrophages, dendritic cells
- Receptor: CD4 protein on T-helper cells — the virus specifically targets the cells that coordinate the entire immune response, which is why HIV is so devastating
Stages of HIV Infection
| Stage | Duration | Features |
|---|---|---|
| Acute / Primary | 2–6 weeks | Flu-like symptoms; high viral load; rapid CD4 decline |
| Clinical latency / Asymptomatic | 2–15 years | Few or no symptoms; slow CD4 decline; virus continues replicating silently |
| AIDS | Variable | CD4 count <200/μL (normal is 500–1500/μL); opportunistic infections (TB, Pneumocystis pneumonia, candidiasis, Kaposi's sarcoma) |
WARNING
A person with HIV can transmit the virus even during the asymptomatic stage, which can last for years. This is why testing is crucial — infected individuals may feel perfectly healthy while spreading the virus unknowingly.
Diagnosis
- ELISA (Enzyme-Linked Immunosorbent Assay) — screening test (detects antibodies against HIV; fast and inexpensive but can give false positives)
- Western Blot — confirmatory test (more specific; confirms a positive ELISA result)
- PCR (Polymerase Chain Reaction) — detects viral RNA directly; most sensitive test; used for early detection (before antibodies develop) and in newborns
Treatment
- HAART (Highly Active Antiretroviral Therapy) — a combination of drugs from different classes:
- Reverse transcriptase inhibitors (e.g., AZT/zidovudine — the first anti-HIV drug approved)
- Protease inhibitors (block viral protein processing)
- Integrase inhibitors (prevent viral DNA from integrating into host genome)
- There is no cure yet; treatment controls viral load and extends life significantly
Transmission
- Sexual contact (most common route worldwide)
- Contaminated blood/needles (sharing needles, unsafe transfusions)
- Mother to child (transplacental during pregnancy, during delivery, or through breastfeeding)
- NOT transmitted by: casual contact, mosquito bites, sharing food/utensils, hugging, or shaking hands
Image Generation Prompts
Image Generation Prompt 1: Immune System Overview — Innate vs Adaptive
An educational infographic diagram showing the two branches of the human immune system. Left side labeled "Innate Immunity (Non-specific)" with four boxes: Physical barriers (skin, mucous membranes, cilia — illustrated with a skin cross-section), Physiological barriers (fever, pH, lysozyme, gastric acid), Cellular barriers (neutrophils and macrophages shown phagocytosing bacteria, NK cells attacking virus-infected cell), and Cytokine barriers (interferons, TNF shown as signaling molecules). Right side labeled "Adaptive Immunity (Specific)" branching into: Humoral immunity (B-cells differentiating into plasma cells producing Y-shaped antibodies) and Cell-mediated immunity (T-cells — T-helper CD4+ activating other cells, T-killer CD8+ destroying infected cells). Show arrows connecting innate to adaptive (innate activates adaptive). Further subdivide adaptive into Active (natural via infection, artificial via vaccination) and Passive (natural via maternal IgG/colostrum IgA, artificial via antiserum). Clean educational poster style with icons and color coding.
Image Generation Prompt 2: Antibody Structure — Y-Shaped IgG
A detailed structural diagram of a Y-shaped immunoglobulin G (IgG) antibody molecule. Show the two heavy chains (H chains, drawn in blue, each running the full length of the Y) and two light chains (L chains, drawn in green, each forming one arm of the Y). Label the variable regions (V) at the tips of both arms — these form the antigen-binding sites (paratopes), shown with a complementary antigen fitting in like a lock-and-key. Label the constant regions (C) forming the stem and lower arms. Mark the hinge region in the middle where the arms meet the stem, showing flexibility. Show disulfide bonds (S-S) linking the heavy chains to each other and light chains to heavy chains. Label the Fab region (Fragment antigen-binding — each arm) and Fc region (Fragment crystallizable — the stem, which determines antibody class and effector function). Include annotations for the N-terminus (top) and C-terminus (bottom). Clean molecular biology textbook illustration style.
Summary Cheat Sheet
| Concept / Topic | Key Details / Explanation |
|---|---|
| Immunity | Body's ability to resist/fight infections caused by pathogens |
| Innate immunity | Present from birth; non-specific; does not improve with repeated exposure |
| Physical barriers | Skin (pH 3-5), mucous membranes, cilia, cerumen (earwax) |
| Physiological barriers | Lysozyme (in tears/saliva — destroys bacterial cell walls), HCl in stomach (pH 1.5-3.5), fever |
| Cellular barriers | Phagocytes (neutrophils, macrophages), NK cells (kill virus-infected & tumor cells) |
| Cytokine barriers | Interferons (protect uninfected cells from viruses), TNF, interleukins |
| Acquired immunity | Develops after pathogen exposure; specific; has memory |
| 4 features of acquired immunity | Specificity, Diversity, Discrimination (self vs non-self), Memory |
| Primary immune response | First exposure; slow (5-7 days); low antibody; mainly IgM |
| Secondary immune response | Re-exposure; rapid (1-2 days); high antibody; mainly IgG; basis of vaccination |
| Active immunity | Body produces own antibodies; long-lasting; has memory (e.g., infection, vaccination) |
| Passive immunity | Pre-formed antibodies transferred; immediate but short-lived; no memory (e.g., maternal IgG, antiserum) |
| Bone marrow | Site of B-cell maturation and origin of all blood cells |
| Thymus | Site of T-cell maturation; largest in childhood; involutes (shrinks) with age |
| Spleen | Largest lymphoid organ; filters blood; removes old RBCs |
| MALT | ~50% of all lymphoid tissue; includes tonsils, Peyer's patches, appendix |
| T-cells | Mature in thymus; 60-70% of lymphocytes; responsible for cell-mediated immunity (CMI) |
| T-helper (CD4+) | "Commanders" — activate B-cells, cytotoxic T-cells, macrophages via cytokines |
| T-killer (CD8+) | Directly kill virus-infected cells using perforin and granzymes |
| B-cells | Mature in bone marrow; 10-20% of lymphocytes; responsible for humoral immunity (antibody-mediated) |
| Antibody structure | Y-shaped; 2 Heavy + 2 Light chains (H₂L₂); linked by disulphide bonds; Fab (antigen-binding) + Fc (effector function) |
| IgG | 75-80% of serum; only Ig that crosses placenta; activates complement |
| IgM | Largest antibody (pentamer, MW 9,60,000); first produced in primary response |
| IgE | 0.05%; mediates allergic reactions (histamine release from mast cells); defense against parasites |
| IgA | ~10%; found in mucous membranes (saliva, tears, breast milk); mucosal immunity |
| IgD | 1-3%; B-cell receptor on surface of B-lymphocytes |
| Antibody functions | Agglutination, Opsonization, Neutralization, Complement activation, Precipitation |
| Live attenuated vaccines | Weakened pathogen; strong response: BCG (TB), OPV (polio), MMR |
| Killed/Inactivated vaccines | Dead pathogen; safer: IPV (polio), rabies |
| Toxoid vaccines | Inactivated toxin: DPT (D = diphtheria toxoid, P = killed pertussis, T = tetanus toxoid) |
| Recombinant vaccines | Genetically engineered antigen: Hepatitis B (HBsAg), HPV |
| HLA/MHC system | Genes on chromosome 6; most polymorphic genes; MHC I on all nucleated cells (CD8+), MHC II on APCs (CD4+) |
| Autograft | Self → Self (never rejected) |
| Isograft | Identical twin → Self (never rejected) |
| Allograft | Same species, different individual (e.g., kidney transplant) |
| Xenograft | Different species → Self (e.g., pig heart valve) |
| Cyclosporin A | Immunosuppressant from Trichoderma polysporum; selectively suppresses T-cells |
| Allergy | Exaggerated response to allergen; mediated by IgE; mast cells release histamine; treated with antihistamines |
| Anaphylactic shock | Severe systemic allergic reaction; life-threatening; treated with epinephrine |
| Autoimmune disorders | Immune system attacks own tissues: Myasthenia gravis (acetylcholine receptors), Rheumatoid arthritis (joints), Type 1 diabetes (β-cells), Hashimoto's (thyroid) |
| HIV | ssRNA retrovirus; family Retroviridae; surface proteins: GP-120 (binds CD4), GP-41 (fusion); key enzyme: reverse transcriptase |
| HIV target | CD4+ T-helper cells; AIDS when CD4 count <200/μL |
| HIV diagnosis | ELISA (screening), Western Blot (confirmatory), PCR (most sensitive, detects viral RNA) |
| HAART | Highly Active Antiretroviral Therapy; includes reverse transcriptase inhibitors (AZT), protease inhibitors, integrase inhibitors; no cure |
| HIV transmission | Sexual contact (most common), contaminated blood/needles, mother to child; NOT by casual contact or mosquito bites |
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