Introduction to the Immune System Flashcards
Leukocytes:
Complete cells, <1% of blood (4,800-10,800/μl).
Function: Defense, immune/inflammatory responses.
Leave capillaries via diapedesis, move through tissue spaces by amoeboid motion and + chemotaxis.
Mnemonic:
Never Let Monkeys Eat Bananas
Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils.
Leukocytosis: WBC > 11,000/μl.
Major Categories:
Granulocytes: Neutrophils, Eosinophils, Basophils.
Agranulocytes: Lymphocytes, Monocytes.
Proteins 7%, water 91 %, other 2%, platelets <1%, Erthroyctes >99%
Granulocytes:
Larger than RBCs, lobed nuclei, phagocytic.
Types: Neutrophils, Eosinophils, Basophils.
Neutrophils:
Most numerous (50-70%).
Multi-lobed nuclei, bacteria slayers.
Kill microbes via defensins and respiratory burst.
Functions as a phagocyte
Indistinct granules
Pale blue cytoplasmic granules
Eosinophils:
2-4% of WBCs, bilobed nucleus, cytoplasmic granules.
Digest parasitic worms, involved in allergies and asthma.
functions in attacking parasitic worms and plays complex roles in inflammatory diseases like allergies and asthma.
Basophils:
Rarest WBCs (0.5-1%).
Contain histamine, involved in inflammation.
Contains a U- or an S-shaped nucleus; granules stain very dark; releases histamine and heparin.
Bilobed nucleus, purplish-black, cytoplasmic granuels.
Erythrocyte:
Transports CO2 and oxygen.
Agranulocytes:
No visible granules, spherical/kidney-shaped nuclei.
Types: Lymphocytes, Monocytes.
Lymphocytes (small):
Found in lymphoid nodes and spleen.
2nd most numerous (25%).
T cells: Attack virus/tumor cells.
B cells: Produce antibodies.
Large spherical nucleus
Rim of pale blue cytoplasm
Monocytes:
Largest WBC (3-8%).
Differentiate into macrophages, phagocytic.
Crucial for viruses, bacteria, chronic infections
Kidney-shaped nucleus, pale (more) and blue cytoplasm
Leukopoiesis:
Hormone-regulated (ILs & CSFs).
Leukocytes come from hemocytoblast stem cells.
Pathways:
Lymphoid: Produces lymphocytes.
Myeloid: Produces other leukocytes.
Bone marrow stores more granulocytes than blood.
Granulocyte lifespan: 0.5-9 days.
See D.
Leukemias:
Abnormal WBC overproduction.
Acute: Fast, affects kids.
Chronic: Slow, affects adults.
Treatment: Radiation, drugs, transplant.
Infectious Mononucleosis:
Epstein-Barr virus.
Symptoms: Fatigue, sore throat, fever.
Resolves in 4-6 weeks.
Leukopenia:
Low WBC count, often due to drugs.
See the immune system categories
Immune System:
Innate (Nonspecific) Defense:
1st line: Skin, mucosa.
2nd line: Antimicrobial proteins, phagocytes, inflammation.
Adaptive (Specific) Defense:
3rd line: Targets specific invaders using lymphocytes.
T-cell and NK T cells common between innate and adaptive immunity
Innate Defenses:
First Line: Skin, mucous membranes.
Second Line (internal defenses): Phagocytes, NK cells, inflammation, interferons, antimicrobial proteins, fever.
Phagocytes:
Neutrophils: Abundant, die after fighting.
Macrophages: Robust, from monocytes.
Phagocytosis:
Phagocytes bind to pathogen’s signature.
Opsonization: Antibodies/complement coat pathogens.
Respiratory Burst: T cells trigger free radicals and chemicals to kill tough pathogens.
Defensins: Neutrophils pierce pathogen membranes.
Natural Killer Cells:
Lymphocytes that recognize stressed cells.
Kill cancer/virus-infected cells.
Induce apoptosis and enhance inflammation.
Inflammation Benefits:
Prevents spread of damage.
Disposes of debris/pathogens.
Prepares for repair.
Alerts adaptive immune system.
Signs of Inflammation:
Redness, heat, swelling, pain (and impaired function).
Inflammation Stages:
Chemical Release: Histamine, kinins, PGs, cytokines attract phagocytes.
Vasodilation: Causes redness, heat, and swelling.
Phagocyte Mobilization:
Leukocytosis: Neutrophils released.
Margination: Neutrophils stick to vessel walls.
Diapedesis: Neutrophils enter tissues.
Chemotaxis: Chemicals guide neutrophils.
Antimicrobial Proteins:
Functions: Attack microbes directly or inhibit reproduction.
Key Proteins:
Interferons (IFN):
Secreted by virus-infected cells to warn neighbors.
Stimulate antiviral proteins in nearby cells.
Activate macrophages & natural killer cells.
INF-γ activates macrophages for immune mobilization.
Complement System:
~20 proteins (C1-C9, factors B, D, and P, regulatory proteins) that destroy invaders and enhance immunity (innate and adaptive).
Activation: Classical, Lectin, and Alternative pathways.
Classical: Antibodies bind to invaders and activate complement.
Lectin: Lectins bind to sugars on invaders, activating complement.
Alternative: Activation occurs spontaneously on foreign invaders.
See D.
erythropoiesis
Innate Defense: Fever
High body temperature response to microorganisms.
Setpoint reset by pyrogens from leukocytes/macrophages.
Benefit of Fever
Boosts immune response by aiding T lymphocyte/monocyte migration.
Increases metabolism for faster repair and T lymphocyte production.
Limits bacterial growth by restricting metal ion access.
High fever is dangerous because it can cause severe dehydration, organ damage, and disrupt normal bodily functions if left untreated.
Beginning of AI
Antibody-Mediated Immunity
B cells create antibodies to neutralize pathogens.
Cell-Mediated Immunity
T cells attack infected cells with antigens.
Adaptive Immunity
Memory B and T cells provide long-term protection.
Adaptive Immune System
Specific defense, eliminates pathogens/abnormal cells.
Amplifies inflammation, activates complement, needs priming.
Characteristics
Involves B and T lymphocytes.
Specific: Targets specific antigens.
Systemic: Affects whole body.
Memory: Stronger response on subsequent exposures
Adaptive Immune System
Two arms: Humoral and Cellular immunity.
Humoral Immunity
Antibodies from lymphocytes in body fluids.
Inactivate targets and mark for destruction.
Targets extracellular pathogens.
Cellular Immunity
Lymphocytes kill infected cells or release chemicals.
Targets infected cells.
Antigens
Trigger immune response, mobilize adaptive defenses.
Non-self, large, complex molecules.
Complete Antigens
Immunogenicity: Stimulate lymphocyte growth.
Reactivity: React with lymphocytes/antibodies.
Examples: Foreign proteins, lipids, polysaccharides.
Incomplete Antigens (Haptens)
Too small to trigger immunity alone.
Become immunogenic when attached to body proteins (e.g., poison ivy).
Antigenic Determinants
Parts of antigens that antibodies or lymphocytes bind to.
Genetic Immunity
Genes, not antigens, determine immune recognition.
~25,000 genes code for proteins, creating up to a billion lymphocyte receptors.
Self-Antigens: MHC Proteins
Surface proteins unique to each individual, not antigenic to self.
MHC proteins display self or foreign antigens.
T Lymphocyte Recognition
T cells recognize antigens on MHC proteins.
Self-marker (MHC) labels body cells as “friend,” foreign antigens as “foes.”
Adaptive Immune System Cells
B Cells: Humoral immunity.
T Cells: Cellular immunity (cytotoxic, helper, memory, regulatory).
APCs: Assist in immunity, not antigen-specific.
Lymphocyte Development
Origin: B and T cell precursors start in red bone marrow.
Maturation:
T cells mature in the thymus.
B cells mature in the bone marrow.
Develop immunocompetence and self-tolerance.
Seeding Secondary Organs: Immunocompetent, naive lymphocytes circulate to secondary organs.
Activation: Lymphocytes are activated when binding specific antigens.
Proliferation & Differentiation: Activated lymphocytes multiply and become effector and memory cells.
Lymphocyte Development & Activation
T and B lymphocytes follow similar steps.
1. Origin: Both originate in red bone marrow.
2. Maturation:
B cells mature in bone marrow, T cells in thymus.
Education:
Immunocompetence: Recognize one specific antigen.
Self-tolerance: Don’t react to own antigens.
Lymphocyte Development & Activation (cont.)
3. Seeding Secondary Organs:
Naive lymphocytes migrate to secondary organs, increasing antigen encounter.
- Antigen Encounter & Activation:
Naive lymphocytes bind their antigen, triggering activation (clonal selection). - Proliferation & Differentiation:
Activated lymphocytes proliferate, forming clones.
Most clones become effector cells, some become memory cells for faster future response.
T Cell Maturation
Positive Selection: T cells that recognize self-MHC are selected.
Negative Selection: T cells that bind self-antigens undergo apoptosis, ensuring self-tolerance.
See diagram
B Cells:
Present antigens to helper T cells.
Don’t activate naive T cells.
Dendritic Cells:
Found in tissues, phagocytize pathogens, and present antigens to T cells.
Link innate and adaptive immunity.
Macrophages:
Found in connective tissues, present antigens to T cells.
Activate T cells, trigger inflammation, and become phagocytic killers.
Humoral Immune Response
B Cell Activation: B cells bind antigens, trigger clonal selection.
Plasma Cells: Secrete antibodies (~2000/sec for 4-5 days).
Memory Cells: Provide faster future responses.
Immunological Memory
Primary Response: 3-6 day lag, peak in 10 days.
Secondary Response: Faster, stronger, peak in 2-3 days.
Vaccines: Stimulate primary response, create memory cells.
Active vs. Passive Humoral Immunity
Active Humoral Immunity:
Naturally Acquired: From infection.
Artificially Acquired: From vaccines (dead/attenuated pathogens or mRNA).
Vaccine Benefits: Provide antigens, prevent symptoms.
Passive Humoral Immunity:
Naturally Acquired: Antibodies from mother (placenta/milk).
Artificially Acquired: Injection of antibodies (e.g., gamma globulin).
No Memory: Protection is temporary.
Antibodies (Immunoglobulins - Igs)
Function: Secreted by plasma cells, bind to antigens.
Structure: Y-shaped, with 2 heavy and 2 light chains; antigen-binding sites at variable regions.
Classes:
IgM: First in primary response, activates complement, agglutinates.
IgA: Found in body secretions, prevents pathogen attachment.
IgD: B cell receptor.
IgG: Most abundant, protects against infections, crosses placenta.
IgE: Triggers allergic reactions, involved in parasitic infections.
Antibodies
Class Switching: B cells switch from IgM to IgG, IgA, or IgE, keeping specificity.
IgM: First in primary response, IgG in secondary responses.
Functions
Neutralization: Blocks toxin/virus binding.
Agglutination: Clumps antigens.
Precipitation: Forms complexes for phagocytosis.
Complement Activation: Triggers cell lysis and inflammation.
Cell-Mediated Immunity
T cells respond to processed antigen fragments on infected or abnormal cells.
Types of T Cells
Helper T (CD4): Activate/regulate immune cells.
Regulatory T (CD4): Control immune responses.
Cytotoxic T (CD8): Kill infected or abnormal cells.
Activation
CD4 → helper/regulatory T cells, CD8 → cytotoxic T cells.
Cellular immune response from here
T Cells in Cellular Immune Response
T Cell Types
CD4 (Helper T): Activate B cells, T cells, macrophages; can become regulatory or memory T cells.
CD8 (Cytotoxic T): Destroy infected/cancerous cells; can become memory T cells.
Naive T cells: Simply CD4 or CD8, before activation.
T Cells in Cellular Immunity
CD4 (Helper T): Activate immune cells, can become regulatory or memory T cells.
CD8 (Cytotoxic T): Destroy infected/cancerous cells, can become memory T cells.
Naive T cells: Unactivated CD4 or CD8.
MHC Proteins
Class I MHC: On all cells, displays endogenous antigens, activates CD8.
Class II MHC: On APCs, displays exogenous antigens, activates CD4.
Function
Class I: Alerts CD8 to destroy infected cells.
Class II: Alerts CD4 to help immune response.
T Cell Activation and Differentiation
Antigen Binding: TCRs bind to antigen-MHC complex on APC (double recognition of MHC and antigen).
Co-stimulation: T cell must bind co-stimulatory signals on APC. Without it, T cells become anergic (inactive).
Proliferation and Differentiation: Activated T cells proliferate, differentiate, and peak within 1 week. Memory cells remain for secondary response.
Cytokines
Chemical messengers (e.g., interferons, interleukins) that regulate immune responses.
Effector T Cells Roles
Helper T Cells (TH): Activate B cells and T cells, secrete cytokines, amplify innate immunity, and help activate CD8 cells.
Cytotoxic T Cells (TC): Destroy infected/cancer cells using perforins and granzymes, target Class I MHC antigens.
Regulatory T Cells (TReg): Suppress immune responses, prevent autoimmunity, and aid in transplants and autoimmune diseases.
