Immunology

The immune system, part by part: who each cell is, how a response starts, what cytokines do, when the response does harm, what happens when it fails, and how vaccines and tests work. Linked to the 3D anatomy, Microbiology and DurgiPedia's conditions.

93 pages

• Lymphoid organs
• Immune cells
• Innate immunity
• Adaptive immunity
• Cytokines and molecules
• Hypersensitivity
• Autoimmunity
• Immunodeficiencies
• Transplant, tumors and immunotherapy
• Vaccines
• Immunology lab
• A to Z

Lymphoid organs

Where immune cells are born, mature and meet.

• Primary and secondary lymphoid organsImmune cells are born and trained in the bone marrow and thymus, then meet invaders in lymph nodes, the spleen and the mucosal tissue.Topic
• Bone marrow and hematopoiesis of immune cellsThe red bone marrow is the factory of every blood cell, including all white cells, and the school where B cells mature.Organ
• Thymus: where T cells learnThe thymus, behind the sternum, is where young T cells are tested: those that cannot see self-MHC or that attack self are removed.Organ
• Lymph node: cortex, paracortex, medullaLymph nodes are bean-shaped filters along lymph vessels where B and T cells meet antigens carried in from the tissues.Organ
• Spleen: white pulp, red pulp, aspleniaThe spleen filters the blood: its red pulp removes old red cells and its white pulp starts immune responses against blood-borne germs.Organ
• Mucosa-associated lymphoid tissue (tonsils, Peyer patches)Lymphoid tissue under the mucosa of the throat, gut and airways samples what we swallow and breathe and answers mainly with IgA.Organ

Immune cells

Who is who: function, markers and what happens when they are missing.

• NeutrophilThe most common white blood cell: a short-lived first responder that rushes to bacteria, eats them and dies, forming pus.Cell
• Monocyte and macrophageMonocytes circulate in blood and become macrophages in tissues: big eaters that clean up, kill germs, signal alarm and show antigens to T cells.Cell
• Dendritic cell (professional antigen-presenting cell)Dendritic cells are sentinels in the tissues that grab antigens, travel to the lymph node and switch on naive T cells.Cell
• Natural killer cellNK cells are innate lymphocytes that kill virus-infected and tumor cells without prior sensitization, especially cells that have lost MHC class I.Cell
• EosinophilEosinophils are granulocytes with bright red granules that fight parasitic worms and drive much of the damage in allergic asthma.Cell
• Mast cell and basophilMast cells in tissues and basophils in blood carry IgE on their surface and, when an allergen binds it, release histamine within minutes.Cell
• CD4⁺ helper T cellHelper T cells are the coordinators of the immune response: they recognize antigen on MHC class II and tell B cells, macrophages and CD8 cells what to do.Cell
• CD8⁺ cytotoxic T cellCytotoxic T cells recognize viral or tumor peptides on MHC class I and kill the cell that shows them.Cell
• Regulatory T cell (Treg, FOXP3)Regulatory T cells are the brakes of the immune system: they calm other lymphocytes and protect the body from autoimmunity.Cell
• B cell and plasma cellB cells recognize antigens with surface antibody; when activated they become plasma cells, factories that secrete antibody, or memory cells.Cell
• CD markers: the table to knowCD (cluster of differentiation) numbers name the surface molecules that identify each immune cell; a short list explains most exam questions.Topic
• Innate-like lymphocytes: ILCs, γδ T, NKT, MAIT, B-1 and marginal-zone B cellsSome lymphocytes do not wait days to learn: they react within hours to common danger signals and act as a bridge between innate and adaptive immunity.Cell
• Lymphocyte recirculation and homingLymphocytes travel all the time between blood, lymph nodes and tissues, following address labels. Some multiple sclerosis drugs work by blocking these labels.Process

Innate immunity

The first response: barriers, pattern receptors, complement and inflammation.

• Innate immunity (overview, barriers)The defenses you are born with: skin, mucus, acid, complement and cells that react within minutes to hours, before antibodies exist.Topic
• Pattern recognition: PAMPs, DAMPs, Toll-like receptorsInnate cells carry receptors that spot molecules shared by many microbes or released by damaged tissue, and sound the alarm.Process
• Complement: three pathways, MAC, regulatorsA cascade of blood proteins that coats microbes for eating, calls in white cells and punches holes in some bacteria.Process
• Acute inflammation: vascular and cellular eventsThe quick local response to infection or injury: vessels widen and leak, and white cells leave the blood to reach the problem.Process
• Phagocytosis and the respiratory burstHow neutrophils and macrophages swallow microbes and kill them with acid, enzymes and bleach-like oxygen products.Process
• Acute-phase response and fever (CRP, ESR, procalcitonin)During inflammation the liver makes alarm proteins and the brain raises body temperature; blood tests can measure these changes.Process
• Granulomatous inflammationWhen the body cannot destroy something, it walls it off with a ball of activated macrophages: a granuloma.Process

Adaptive immunity

Antigen presentation, T and B cells, antibodies and memory.

• V(D)J recombination: how a few genes make billions of receptorsEach B and T cell cuts and rejoins pieces of its own DNA to build a one-of-a-kind receptor. Without the cutting enzymes (RAG) there are no B or T cells.Process
• Immunity to microbes: which arm defends against whatEach kind of germ is controlled by a different part of the immune system, and each has its own tricks to escape. The table to know.Topic
• What antibodies do: effector functionsAntibodies do not kill germs by themselves: they block them, tag them for eating, call in complement and killer cells, and guard the mucosa.Process
• Adaptive immunity (overview: humoral vs cellular)The trained part of the immune system: T and B cells that recognize one target precisely and remember it.Topic
• MHC/HLA class I and IIDisplay molecules on our cells that show protein fragments to T cells; in humans they are called HLA and differ from person to person.Molecule
• Antigen processing and presentationCells chop proteins into small pieces and show them on MHC molecules so T cells can check for something foreign.Process
• T-cell development: positive and negative selectionYoung T cells are trained in the thymus: those that cannot see our MHC die, and those that attack our own tissues are removed.Process
• T-cell activation: two signals and superantigensA naive T cell needs to see its antigen and receive a second «go» signal; bacterial superantigens bypass this and switch on huge numbers of T cells.Process
• Th1, Th2, Th17, Tfh and TregHelper T cells specialize into types that fight different germs, each with its own set of chemical signals.Topic
• B-cell activation, class switching and affinity maturationB cells that recognize a germ get help from T cells, then improve their antibodies and change their type in lymph nodes.Process
• Antibody structure and isotypes (IgG, IgA, IgM, IgE, IgD)Antibodies are Y-shaped proteins; their tips grab one target and their tail decides what happens next, which differs among the five classes.Molecule
• Primary vs secondary response and memoryThe first time the body meets a germ it responds slowly; the second time, memory cells make a faster and stronger response.Process
• Neonatal immunity: maternal IgG and breast-milk IgANewborns are protected at first by antibodies from their mother: IgG through the placenta and IgA in breast milk.Topic

Cytokines and molecules

The messengers: which cell makes them and what they do.

• Cytokines: the table to knowCytokines are small proteins that immune cells use to talk to each other: they switch inflammation on or off and tell other cells what to become.Topic
• Interleukin-1IL-1 is an alarm cytokine made by macrophages: it causes fever and inflammation, and its excess drives rare inherited fever syndromes.Molecule
• Interleukin-2IL-2 is the growth signal T cells give themselves after they recognise an antigen; regulatory T cells also depend on it.Molecule
• IL-4, IL-5 and IL-13 (the Th2 cytokines)IL-4, IL-5 and IL-13 run allergic (type 2) inflammation: IgE, eosinophils and mucus. They are targets of modern asthma and eczema biologics.Molecule
• Interleukin-6IL-6 tells the liver to make CRP and other acute-phase proteins. Blocking its receptor is a treatment for rheumatoid arthritis and cytokine storms.Molecule
• IL-8 and the chemokinesChemokines are signals that call immune cells to a place. IL-8 (CXCL8) is the one that brings neutrophils to an infection.Molecule
• IL-10 and TGF-β (the brakes)IL-10 and TGF-β calm the immune response down after an infection and keep it from attacking the gut and the body's own tissues.Molecule
• IL-12 and IL-23IL-12 and IL-23 are sister cytokines from dendritic cells and macrophages: IL-12 creates Th1 cells and IL-23 keeps Th17 cells going.Molecule
• Interleukin-17IL-17 calls neutrophils to skin and mucosa and protects against Candida; too much of it drives psoriasis.Molecule
• TNF-αTNF-α is a powerful inflammation signal from macrophages. It holds tuberculosis granulomas together, and blocking it treats arthritis and bowel disease.Molecule
• Interferon-γInterferon-γ is the signal that turns macrophages into killers. It is what the blood test for latent tuberculosis (IGRA) measures.Molecule
• Type I interferons (α, β)Type I interferons are an early antiviral warning: an infected cell releases them so its neighbours resist the virus. In lupus they are overactive.Molecule
• Adhesion molecules: selectins and integrinsSelectins and integrins are the brakes and anchors that let white blood cells stop on a vessel wall and leave the blood to reach an infection.Molecule
• Fc receptors, BCR and TCRThe BCR and TCR let B and T cells recognise one specific antigen; Fc receptors let other cells grab antibodies that are already bound to a target.Molecule

Hypersensitivity

When the immune response does harm: types I to IV, transfusion and blood groups.

• Hypersensitivity: the four types comparedAn immune response that harms the body. There are four types, named by what does the damage: IgE, antibodies on cells, immune complexes or T cells.Topic
• Type I hypersensitivity (immediate, IgE)An allergy: the body has made IgE against something harmless, and on the next contact mast cells burst open within minutes and release histamine.Process
• Type II hypersensitivity (antibody against cells)Antibodies stick to the body's own cells or tissue. They mark them for destruction, or they switch a receptor on or off without killing the cell.Process
• Type III hypersensitivity (immune complexes)Antibodies clump with a soluble antigen in the blood. The clumps lodge in small vessels, mostly in the kidney, joints and skin, and inflame them.Process
• Type IV hypersensitivity (delayed, T cells)A slow reaction made by T cells, not antibodies. It shows up two to three days after contact, as in the tuberculin skin test or a rash from nickel.Process
• Transfusion reactionsHarmful reactions to a blood transfusion, from fever and hives to a deadly blood-type mismatch. Most serious ones start in the first minutes.Topic
• ABO and Rh blood groups, hemolytic disease of the newbornA person's blood group is set by sugars (A, B) and a protein (Rh) on red cells. A mismatch in a transfusion or between mother and baby can destroy red cells.Topic
• Latex and drug allergyLatex gloves and many medicines can cause allergy, from a skin rash to anaphylaxis. Not every side effect is an allergy.Topic

Autoimmunity

Tolerance, autoantibodies and HLA associations.

• Immune tolerance and how autoimmunity beginsTolerance is how the immune system learns not to attack the body. Autoimmunity begins when those safety checks fail.Process
• Autoantibodies: the table to knowAutoantibodies are antibodies against the body's own parts. Each disease tends to have its own, which helps doctors name it.Topic
• HLA associations with diseaseHLA genes shape which protein pieces immune cells are shown. Some HLA types raise the risk of certain autoimmune diseases or drug reactions.Topic
• Molecular mimicry and post-infectious autoimmunitySome germs carry pieces that look like our own tissue. The defence aimed at the germ can then hit the look-alike tissue, weeks after the infection.Process

Immunodeficiencies

Warning signs and the infection pattern by defect.

• Hyper-IgE (Job) syndrome, chronic mucocutaneous candidiasis and the IL-12/IFN-γ axisSome inborn defects knock out a single branch of T-cell help, giving a very specific infection pattern: Staphylococcus, Candida or mycobacteria.Topic
• How HIV destroys CD4 T cellsHIV enters and destroys the helper T cells that coordinate immunity. As their number falls, germs that are harmless to healthy people cause disease.Process
• Immunodeficiency: warning signs and the infection pattern by defectWhen infections come too often, last too long or are caused by unusual germs, the immune system may be missing a piece.Topic
• B-cell (antibody) deficiencies: XLA, CVID, IgA deficiency, hyper-IgMWhen the body cannot make enough antibodies, bacteria with a capsule keep causing ear, sinus and lung infections.Topic
• T-cell and combined deficiencies: DiGeorge, SCID, Wiskott–Aldrich, ataxia-telangiectasiaWithout working T cells, viruses and fungi cause severe infections from the first months, and B cells lose their helpers too.Topic
• Phagocyte defects: CGD, LAD, Chédiak–HigashiWhen neutrophils cannot reach, swallow or kill germs, deep abscesses and fungal infections appear, often with little pus.Topic
• Complement deficiencies and hereditary angioedemaMissing complement proteins cause repeated Neisseria or capsule infections, lupus-like disease, or episodes of deep swelling.Topic
• Secondary immunodeficiency: HIV, malnutrition, drugs, aspleniaMost weak immune systems are acquired, from HIV, poor nutrition, medicines, cancer or losing the spleen, not inherited.Topic
• The neutropenic and immunosuppressed patient (nursing)With very few neutrophils, a fever may be the only sign of a dangerous infection, so prevention and fast action matter.Topic

Transplant, tumors and immunotherapy

Rejection, graft-versus-host disease, immunosuppressants and monoclonal antibodies.

• Cancer immunotherapy: checkpoint inhibitors, CAR-T and vaccinesSome cancer treatments do not attack the tumour directly: they release the brakes of the immune system or train the patient's own T cells to find the cancer.Topic
• Transplant rejection: hyperacute, acute, chronicThe body sees a donated organ as foreign and attacks it, within minutes, weeks or slowly over years.Process
• Graft-versus-host diseaseAfter a donor stem cell transplant, donor immune cells can attack the patient's skin, liver and gut.Process
• Immunosuppressants by mechanism (classes)Medicines that calm the immune system to protect a transplant or control autoimmune disease, at the cost of more infections.Topic
• Monoclonal antibodies and biologics: naming and targetsLab-made antibodies hit one target, such as TNF, CD20 or HER2; the end of the drug name tells you what kind of molecule it is.Topic
• Tumor immunology and checkpoint inhibitorsThe immune system can find and kill cancer cells; tumors learn to hide or switch immune cells off, and new drugs release the brakes.Process

Vaccines

Vaccine types, Colombia's PAI schedule, the cold chain and passive immunization.

• Vaccine types: live, inactivated, subunit, toxoid, mRNA, vectorVaccines teach the immune system to recognize a germ without causing the disease. They carry a weakened germ, a killed one, a piece of it or its instructions.Topic
• Colombia's PAI schedule (which vaccines, at what age)Colombia's Expanded Programme on Immunization (PAI) gives free vaccines from birth. This page sums up what each age is protected against, per the Ministry.Topic
• Live vaccines: who should not receive themLive vaccines carry a weakened germ. With very weak defences or in pregnancy they can be dangerous, so they have clear contraindications.Topic
• The cold chainVaccines are damaged by heat, light or freezing. The cold chain keeps them between 2 and 8 °C from the factory to the person's arm.Topic
• Passive immunization: immunoglobulins and antitoxinsIn passive immunization a person receives ready-made antibodies. They protect at once, but last weeks or months and leave no memory.Topic
• Herd immunity and outbreak controlWhen nearly everyone is vaccinated, the germ cannot find anyone to infect, and that also protects people who cannot be vaccinated.Topic
• Events after vaccination (ESAVI) and how they are reportedAn ESAVI is any health problem that appears after vaccination. The vaccine is not always the cause, so it is reported and investigated.Topic

Immunology lab

How to read serology, ELISA, flow cytometry and the Coombs test.

• Serology: IgM vs IgG, seroconversion, aviditySerology looks for antibodies in the blood. Their type and amount suggest whether an infection is recent, past, or whether there was vaccination.Topic
• ELISA, western blot and rapid testsELISA uses an enzyme that makes colour when an antibody binds its target. It underlies many screening tests, such as HIV tests.Topic
• Flow cytometry and the CD4 countFlow cytometry counts and sorts cells one by one with lasers and fluorescent antibodies. It is how the CD4 count in HIV is measured, for example.Topic
• Direct and indirect Coombs testThe Coombs test looks for antibodies against red blood cells: stuck to them (direct) or free in the plasma (indirect).Topic
• Immunofluorescence and the ANA testThe ANA test looks for antibodies against the nucleus of the body's own cells. It is read with a fluorescence microscope and points toward autoimmune disease.Topic
• Tuberculin skin test and IGRATwo tests show whether a person has had a tuberculosis infection: one on the skin (tuberculin), one on blood (IGRA). Neither says if the disease is active.Topic

A to Z

• ABO and Rh blood groups, hemolytic disease of the newbornHypersensitivity · Topic
• Acute inflammation: vascular and cellular eventsInnate immunity · Process
• Acute-phase response and fever (CRP, ESR, procalcitonin)Innate immunity · Process
• Adaptive immunity (overview: humoral vs cellular)Adaptive immunity · Topic
• Adhesion molecules: selectins and integrinsCytokines and molecules · Molecule
• Antibody structure and isotypes (IgG, IgA, IgM, IgE, IgD)Adaptive immunity · Molecule
• Antigen processing and presentationAdaptive immunity · Process
• Autoantibodies: the table to knowAutoimmunity · Topic
• B cell and plasma cellImmune cells · Cell
• B-cell (antibody) deficiencies: XLA, CVID, IgA deficiency, hyper-IgMImmunodeficiencies · Topic
• B-cell activation, class switching and affinity maturationAdaptive immunity · Process
• Bone marrow and hematopoiesis of immune cellsLymphoid organs · Organ
• Cancer immunotherapy: checkpoint inhibitors, CAR-T and vaccinesTransplant, tumors and immunotherapy · Topic
• CD markers: the table to knowImmune cells · Topic
• CD4⁺ helper T cellImmune cells · Cell
• CD8⁺ cytotoxic T cellImmune cells · Cell
• Colombia's PAI schedule (which vaccines, at what age)Vaccines · Topic
• Complement deficiencies and hereditary angioedemaImmunodeficiencies · Topic
• Complement: three pathways, MAC, regulatorsInnate immunity · Process
• Cytokines: the table to knowCytokines and molecules · Topic
• Dendritic cell (professional antigen-presenting cell)Immune cells · Cell
• Direct and indirect Coombs testImmunology lab · Topic
• ELISA, western blot and rapid testsImmunology lab · Topic
• EosinophilImmune cells · Cell
• Events after vaccination (ESAVI) and how they are reportedVaccines · Topic
• Fc receptors, BCR and TCRCytokines and molecules · Molecule
• Flow cytometry and the CD4 countImmunology lab · Topic
• Graft-versus-host diseaseTransplant, tumors and immunotherapy · Process
• Granulomatous inflammationInnate immunity · Process
• Herd immunity and outbreak controlVaccines · Topic
• HLA associations with diseaseAutoimmunity · Topic
• How HIV destroys CD4 T cellsImmunodeficiencies · Process
• Hyper-IgE (Job) syndrome, chronic mucocutaneous candidiasis and the IL-12/IFN-γ axisImmunodeficiencies · Topic
• Hypersensitivity: the four types comparedHypersensitivity · Topic
• IL-10 and TGF-β (the brakes)Cytokines and molecules · Molecule
• IL-12 and IL-23Cytokines and molecules · Molecule
• IL-4, IL-5 and IL-13 (the Th2 cytokines)Cytokines and molecules · Molecule
• IL-8 and the chemokinesCytokines and molecules · Molecule
• Immune tolerance and how autoimmunity beginsAutoimmunity · Process
• Immunity to microbes: which arm defends against whatAdaptive immunity · Topic
• Immunodeficiency: warning signs and the infection pattern by defectImmunodeficiencies · Topic
• Immunofluorescence and the ANA testImmunology lab · Topic
• Immunosuppressants by mechanism (classes)Transplant, tumors and immunotherapy · Topic
• Innate immunity (overview, barriers)Innate immunity · Topic
• Innate-like lymphocytes: ILCs, γδ T, NKT, MAIT, B-1 and marginal-zone B cellsImmune cells · Cell
• Interferon-γCytokines and molecules · Molecule
• Interleukin-1Cytokines and molecules · Molecule
• Interleukin-17Cytokines and molecules · Molecule
• Interleukin-2Cytokines and molecules · Molecule
• Interleukin-6Cytokines and molecules · Molecule
• Latex and drug allergyHypersensitivity · Topic
• Live vaccines: who should not receive themVaccines · Topic
• Lymph node: cortex, paracortex, medullaLymphoid organs · Organ
• Lymphocyte recirculation and homingImmune cells · Process
• Mast cell and basophilImmune cells · Cell
• MHC/HLA class I and IIAdaptive immunity · Molecule
• Molecular mimicry and post-infectious autoimmunityAutoimmunity · Process
• Monoclonal antibodies and biologics: naming and targetsTransplant, tumors and immunotherapy · Topic
• Monocyte and macrophageImmune cells · Cell
• Mucosa-associated lymphoid tissue (tonsils, Peyer patches)Lymphoid organs · Organ
• Natural killer cellImmune cells · Cell
• Neonatal immunity: maternal IgG and breast-milk IgAAdaptive immunity · Topic
• NeutrophilImmune cells · Cell
• Passive immunization: immunoglobulins and antitoxinsVaccines · Topic
• Pattern recognition: PAMPs, DAMPs, Toll-like receptorsInnate immunity · Process
• Phagocyte defects: CGD, LAD, Chédiak–HigashiImmunodeficiencies · Topic
• Phagocytosis and the respiratory burstInnate immunity · Process
• Primary and secondary lymphoid organsLymphoid organs · Topic
• Primary vs secondary response and memoryAdaptive immunity · Process
• Regulatory T cell (Treg, FOXP3)Immune cells · Cell
• Secondary immunodeficiency: HIV, malnutrition, drugs, aspleniaImmunodeficiencies · Topic
• Serology: IgM vs IgG, seroconversion, avidityImmunology lab · Topic
• Spleen: white pulp, red pulp, aspleniaLymphoid organs · Organ
• T-cell activation: two signals and superantigensAdaptive immunity · Process
• T-cell and combined deficiencies: DiGeorge, SCID, Wiskott–Aldrich, ataxia-telangiectasiaImmunodeficiencies · Topic
• T-cell development: positive and negative selectionAdaptive immunity · Process
• Th1, Th2, Th17, Tfh and TregAdaptive immunity · Topic
• The cold chainVaccines · Topic
• The neutropenic and immunosuppressed patient (nursing)Immunodeficiencies · Topic
• Thymus: where T cells learnLymphoid organs · Organ
• TNF-αCytokines and molecules · Molecule
• Transfusion reactionsHypersensitivity · Topic
• Transplant rejection: hyperacute, acute, chronicTransplant, tumors and immunotherapy · Process
• Tuberculin skin test and IGRAImmunology lab · Topic
• Tumor immunology and checkpoint inhibitorsTransplant, tumors and immunotherapy · Process
• Type I hypersensitivity (immediate, IgE)Hypersensitivity · Process
• Type I interferons (α, β)Cytokines and molecules · Molecule
• Type II hypersensitivity (antibody against cells)Hypersensitivity · Process
• Type III hypersensitivity (immune complexes)Hypersensitivity · Process
• Type IV hypersensitivity (delayed, T cells)Hypersensitivity · Process
• V(D)J recombination: how a few genes make billions of receptorsAdaptive immunity · Process
• Vaccine types: live, inactivated, subunit, toxoid, mRNA, vectorVaccines · Topic
• What antibodies do: effector functionsAdaptive immunity · Process

Educational content on the immune system; not a treatment or individual vaccination guide and no substitute for a health professional's advice. No doses are given.

Representative model, for educational purposes only.