Lectures 7 and 8 so far — Disorders in Immunity and Diagnosing Infections. ★ = emphasized in the lecture recording. Exam 2 (Lectures 7–13) is Friday 23 October 2026.
| Term | What you need to know |
|---|---|
| ★ Learn this table | The four-hypersensitivity summary table (slide 9): “a chart you should pay attention to.” |
| ★ The one mechanism | Desensitization works by raising allergen-specific immunoglobulin G that BLOCKS the allergen from the immunoglobulin E on mast cells. |
| ★ No type I | Type I plays NO part in graft rejection or in autoimmunity. Both use II, III and IV. |
| ★ B cell vs T cell defect | B cell defect (agammaglobulinemia) → recurrent BACTERIAL infections. T cell defect → fungal, viral, protozoan. |
| Not to memorize | Helminth-allergen pairings (slide 6) · graft versus host grades (slide 50) · autoimmune disease charts (slides 58–60) · the order of the transformation sequence (slide 67). Oncogenic virus table (slide 68) deferred to the virus lectures. |
| Term | What you need to know |
|---|---|
| Four immunopathologies | OVER: allergy/hypersensitivity, autoimmunity (typically). UNDER: immunodeficiency, cancer (both a cause and an effect of immune dysfunction). |
| Hypersensitivity | Exaggerated, misdirected response to an allergen using the SAME mechanisms as protective immunity. I, II, III = B cell mediated; IV = T cell mediated. |
| Type I | IMMEDIATE. Immunoglobulin E on mast cells, basophils, eosinophils is crosslinked → mediators. Hay fever, hives, anaphylactic shock. |
| Type II | Immunoglobulin G/M against CELL SURFACE antigen → complement, lysis by membrane attack complex, phagocytosis. Transfusion reactions, Rh disease, autoimmune hemolytic anemia, myasthenia gravis. |
| Type III | Immunoglobulin G/M against SOLUBLE antigen → immune complexes in basement membranes. Needs lots of antigen; delayed hours to days; joints, skin, kidney. Serum sickness, Arthus reaction, post-streptococcal glomerulonephritis, lupus, rheumatoid arthritis. |
| Type IV | DELAYED, T cell mediated. Infectious allergy (tuberculosis, leprosy, syphilis, histoplasmosis, toxoplasmosis, candidiasis), tuberculin test, contact dermatitis, graft rejection. |
| Hygiene hypothesis | Helminths give the allergic profile without allergy: nonspecific immunoglobulin E crowds Fc receptors and regulatory T cells suppress. Remove the worms and the immune system is underused and poorly regulated. |
| Asthma crosses types | Acute = type I (bronchospasm, mucus). Chronic = TYPE IV (cytokines, eosinophil granules). |
| Term | What you need to know |
|---|---|
| Sensitizing vs provocative dose | FIRST contact: immunoglobulin E made and parked on mast cells, no symptoms. LATER contact: allergen crosslinks it → degranulation. 10,000–40,000 immunoglobulin E per cell. |
| Skin | Urticaria = skin mast cells + histamine. Angioedema = DEEPER mast cells. Eczema = PROLONGED response. Food urticaria: antigen carried to the skin in blood. |
| Anaphylaxis | Cutaneous = wheal and flare (used in diagnosis). Systemic = fluid leaves blood → pressure falls → swelling → asphyxiation. 500–1000 deaths a year in the United States. |
| Epinephrine (5 actions) | Reseals endothelial tight junctions · relaxes bronchi · reduces airway mucosal edema · stimulates heart · suppresses histamine release. |
| Late phase | About 6 HOURS after the immediate reaction; synthesized mediators such as leukotrienes; eosinophils; tissue more sensitive next time. |
| Diagnosis | Allergy or infection? Skin prick/intradermal (wheal and flare) · blood: specific immunoglobulin E, basophils · supervised food challenge · PATCH test = contact dermatitis (type IV). |
| Drugs | Corticosteroids ↓ immunoglobulin E via lymphocytes · cromolyn blocks degranulation · montelukast blocks leukotriene synthesis · omalizumab = anti-immunoglobulin E antibody · antihistamines block receptors. |
| Desensitization | Subcutaneous immunotherapy most common; ~80% improve. Also regulatory T cells. Sublingual: under the tongue; peanut dose 1/75 of a kernel. |
| Term | What you need to know |
|---|---|
| Why ABO | Red cells carry NO major histocompatibility complex molecules. You make antibody against the ABO antigens you LACK. |
| Cross-match | RECIPIENT serum against DONOR red cells — never the reverse (too little donor antibody to react). |
| Consequences | Complement lysis → blocked glomeruli, fever, jaundice; coated cells also cleared by natural killer cells and macrophages. |
| Rh disease | Rh-negative mother, Rh-positive fetus. First pregnancy sensitizes; later ones hemolytic (erythroblastosis fetalis). |
| Rhogam timing | Passive anti-Rh antibody prevents sensitization. 26–28 WEEKS · within 72 HOURS of birth · after invasive tests, abdominal injury, accidental exposure. |
| Term | What you need to know |
|---|---|
| Graft types | Autograft = self · isograft = identical twin · allograft = same species · xenograft = other species. |
| ★ Rejection by type | Hyperacute = II (preexisting antibody; engorged, purple graft) · acute = IV (T cells vs human leukocyte antigen differences) · chronic = III (thickened vessel walls) · graft versus host = IV. |
| Chronic rejection | Months to years; fails MORE THAN HALF of kidney and heart transplants after 10+ years. |
| Acute rejection route | Graft dendritic cells → SPLEEN → activate effector T cells → back via blood → graft destroyed. |
| Cornea | First organ transplanted; succeeds WITHOUT a human leukocyte antigen match — eye downregulates T cells, macrophages, neutrophils, complement. |
| Liver | Human leukocyte antigens NOT assessed; ABO IS. Hepatocytes: little class I, no class II. |
| Bone marrow | MOST sensitive to mismatch → graft versus host disease (skin, muscle, liver, gut) in ~30%. |
| Preventing rejection | Tissue typing, mixed lymphocyte reaction; purine analogs, corticosteroids, tacrolimus, cyclosporine, rapamycin (sirolimus). |
| Term | What you need to know |
|---|---|
| Autoimmunity | Lost tolerance → autoantibodies and sensitized T cells. All types EXCEPT I. Runs in families; WOMEN more often. |
| Sequestered antigen | Privileged tissue (central nervous system, lens, thyroid, testes) damaged later releases unseen antigen. One injured eye → T cells attack BOTH. |
| Molecular mimicry | Rheumatic fever (strep → heart) · Lyme arthritis (Borrelia) · reactive arthritis (Shigella, Salmonella, Campylobacter) · type 1 diabetes (coxsackie A/B, echovirus, rubella). |
| Thymic senescence | Thymus involutes to fat; premature aging in young people with autoimmunity; less output → infection, cancer, autoimmunity. |
| Slide 61 diseases | Graves' (stimulates follicle cells → hyper) · Hashimoto's (destroys them → hypo) · myasthenia gravis (acetylcholine receptors) · multiple sclerosis (myelin; T cells + antibody; Epstein-Barr link). |
| Primary vs secondary | PRIMARY = congenital, genetic. SECONDARY = acquired after birth: human immunodeficiency virus (T helper cells), chemotherapy, radiation, blood cell cancers. |
| Primary examples | Agammaglobulinemia (B, no antibody) · DiGeorge (T, no thymus) · severe combined immunodeficiency (both limbs, no adaptive response) · complement, phagocyte defects. |
| Term | What you need to know |
|---|---|
| Transformation | ONE cell with MULTIPLE accumulated mutations; oncogenes activated by radiation, chemicals, oncogenic viruses. Benign = contained; malignant = spreads. |
| Cancer cell traits | Self-stimulating · ignore stop signals · no apoptosis · angiogenesis · metastasis · constant replication · evade immunity. |
| Tumor antigens | SPECIFIC = tumor only. ASSOCIATED = tumor + normal cells (less). |
| Evasion | Shed the natural killer stress ligand · secrete transforming growth factor beta → regulatory T cells (+ interleukin 10). More regulatory T cells = WORSE prognosis. |
| Checkpoint inhibitors | Block the T cell OFF signal; do not kill directly. Melanoma, some lung cancers. |
| Adoptive cell therapy | Patient's cells engineered and returned. CAR-T (chimeric antigen receptor T cells) APPROVED for blood cancers; tumor infiltrating lymphocytes in development; chimeric antigen receptor natural killer cells in trials. |
| Antibodies & cytokines | 100+ monoclonal antibodies, diagnosis AND therapy; conjugates carry drug or radionuclide. Interleukin 2 → T and natural killer cells (kidney, melanoma). Interferon alpha → natural killer and dendritic cells. Erythropoietin = red cells; interleukin 11 = platelets. |
| Coley · viruses · vaccines | Coley's toxins (1890s; killed strep + Serratia; displaced by radiation and chemotherapy). Oncolytic viruses replicate only in tumor cells; mumps natural. Prophylactic: hepatitis B, papillomavirus. Therapeutic: bacillus Calmette-Guérin (bladder), sipuleucel-T (prostate). |
| Term | What you need to know |
|---|---|
| Scope note | The objectives are the course-wide list; the lecture teaches diagnostic METHODS. Sort every technique into one of three. |
| Phenotypic | Observable traits (phenotype = physical expression of genes): morphology, biochemistry, chemistry, drug sensitivity. Needs culture → SLOWER. |
| Genotypic | Genetic makeup; NO culture needed — slow Mycobacterium, hard Legionella. Faster diagnosis → timely treatment. |
| Immunological | Antigen-antibody specificity; culture optional. Rapid strep 10–15 minutes, but you need a hypothesis first. |
| Specimens | ALL potentially infectious. Results depend on collection, handling, transport, storage. Universal precautions MITIGATE, not eliminate. |
| Results | Direct tests or culture-isolation-identification; results PRESUMPTIVE or CONFIRMATORY. |
| Term | What you need to know |
|---|---|
| Morphology | Microscopic: shape, size, stain (Gram, flagellar, acid-fast), structures. Macroscopic: colony texture, size, shape, pigment. |
| Biochemical | Presence or absence of enzymes/pathways: fermentation, amino acids, hydrolysis, catalase, oxidase, coagulase, hemolysins. |
| ★ Blood agar | Detects HEMOLYSIS — the lecturer's “take-home message”, especially for pathogenic Gram-positives. |
| Other media | Chocolate agar: “mainly anaerobic culturing” (slide's wording) · mannitol salts: selects salt tolerance, differentiates mannitol · citrate: blue = pH up · urea: hot pink = urease. |
| Normal flora? | Is the recovered organism the cause, or normal flora? Koch's postulates reasoning. |
| Kirby-Bauer | Disk diffusion: WHICH drug and at WHAT dose; LARGER zone = more effective. Minimum inhibitory concentration strips give the concentration. |
| Term | What you need to know |
|---|---|
| Polymerase chain reaction | Thermal cycler amplifies nucleic acid; Kary Mullis. Guanine + cytosine content = taxonomy, not specific identification. |
| Ribosomal ribonucleic acid | 16S for bacteria, 18S for eukaryotes → phylogenetic trees. Restriction fragment length polymorphism = “fingerprinting.” |
| Serology | In vitro testing of serum; titer in binding antibody units. Serotyping = known antibody identifies an unknown microbe. |
| Agglutination vs precipitation | Agglutination = WHOLE-CELL/insoluble antigen, clumps, MORE sensitive (blood typing, syphilis, Weil-Felix, pregnancy, rapid strep). Precipitation = SOLUBLE antigen, needs gel/liquid (Ouchterlony, immunoelectrophoresis → antibody class). |
| Blots | Southern = deoxyribonucleic acid (the man's name) · Northern = ribonucleic acid · WESTERN = PROTEIN, second test for human immunodeficiency virus · Eastern = other epitopes. |
| Complement fixation | 4 parts: antigen, antibody, complement, sheep red cells. NO hemolysis = POSITIVE. Hemolysis = negative. |
| Fluorescent · immunoassay · in vivo | Dye-labeled monoclonal antibody, direct or indirect. Immunoassays detect TRACE amounts (radioimmunoassay; enzyme-linked immunosorbent assay, 96-well). In vivo: tuberculin, allergy tests. |
| Viruses | Not cells; need a host cell → labor intensive to culture; rapid antigen-antibody tests. |