Innate and Adaptive Immunity PDF

**Innate (Nonspecific) Immunity** **Definition**: This type of immunity is the body\'s first line of defense against infection and disease. It is present at birth and provides a generalized response to any type of invading agent.12 **Key Features**: ○ **Non-specific**: Targets a wide range of pa...

**Innate (Nonspecific) Immunity** **Definition**: This type of immunity is the body\'s first line of defense against infection and disease. It is present at birth and provides a generalized response to any type of invading agent.12 **Key Features**: ○ **Non-specific**: Targets a wide range of pathogens without prior exposure.1 ○ **Immediate**: Responds rapidly to threats.1 ○ **No memory**: Does not provide long-term immunity to specific pathogens.13 **Adaptive (Specific) Immunity** **Definition**: This type of immunity develops after exposure to specific pathogens. It involves the coordinated action of T cells and B cells, providing a highly targeted response.12 **Key Features**: ○ **Specific**: Targets specific pathogens based on their unique antigens.13 ○ **Delayed**: Requires time to develop a response upon first exposure.13 ○ **Memory**: Provides long-term immunity due to the formation of memory cells.13 **Structures of Body Defenses** **Innate (Nonspecific) Defenses** The sources highlight seven major categories of nonspecific defenses:2 1. **Physical Barriers**: The first line of defense includes the skin, mucous membranes, hair, and epithelial layers of internal passageways. These structures prevent pathogen entry. Secretions like sweat, mucus, and urine flush away materials, while enzymes, antibodies, and stomach acid kill or inhibit microorganisms.24 2. **Phagocytes**: These cells engulf and destroy pathogens. Two classes of phagocytes are:24 ○ **Microphages**: Neutrophils and eosinophils leave the bloodstream and enter peripheral tissues to fight infections.4 ○ **Macrophages**: Large phagocytic cells derived from monocytes, distributed throughout the body and make up the monocyte--macrophage system (reticuloendothelial system). They respond to pathogens by engulfing and destroying them with lysosomal enzymes, binding to them so other cells can destroy them, or releasing toxic chemicals into the interstitial fluid.45 ○ **Types of Macrophages**:5 **Fixed Macrophages (Histiocytes)**: Reside in specific tissues or organs like the dermis and bone marrow.5 **Free Macrophages (Wandering Macrophages)**: Travel throughout the body.5 ○ **Special Histiocytes**: Microglia are found in the central nervous system, while Kupffer cells are found in liver sinusoids.6 ○ **Movement and Phagocytosis**: Macrophages move through capillary walls (emigration) and are attracted or repelled by chemicals in surrounding fluids (chemotaxis). Phagocytosis begins when the phagocyte attaches to the target (adhesion), engulfs it to form a phagosome, and then fuses with a lysosome to form a phagolysosome. Lysosomal enzymes digest the particles, leaving a residual body that is expelled by exocytosis.67 3. **Immune Surveillance**: Carried out by natural killer (NK) cells that identify and attach to abnormal cells (nonselective). The Golgi apparatus in NK cells forms perforin vesicles, which release perforins that lyse the abnormal plasma membrane. NK cells attack cancer cells and cells infected with viruses.78 ○ **Cancer Cells**: Tumor-specific antigens identify cancer cells as abnormal, allowing NK cells to identify and destroy them. However, some cancer cells evade NK cells (immunological escape).9 ○ **Viral Infections**: Cells infected with viruses display abnormal proteins on their plasma membranes, which are recognized and destroyed by NK cells.9 4. **Interferons (IFNs)**: A family of immune modulating proteins released by activated lymphocytes, macrophages, and fibroblasts. They trigger the production of antiviral proteins in normal cells to block viral replication without killing viruses.910 ○ **Types of Interferons**:11 **Interferon alpha (α)**: Produced by virus-infected cells, attracts and stimulates NK cells, and enhances resistance to viral infection.11 **Interferon beta (β)**: Secreted by fibroblasts, slows inflammation in a damaged area.11 **Interferon gamma (γ)**: Secreted by T cells and NK cells, stimulates macrophage activity.11 5. **Complement System**: A group of 30 special complement (C) proteins in plasma that enhance both innate and adaptive defenses. They work together in cascades, with three pathways activating the system.1213 ○ **Complement Pathways**:13 **Classical Pathway**: Antibodies bind to invading organisms and then to complement components, activating them (complement fixation), triggering an activation cascade.13 **Lectin Pathway**: Lectins, produced by the innate system to recognize foreign invaders, bind to specific sugars on the invaders and activate complement.13 **Alternative Pathway**: The complement cascade is activated spontaneously when certain complement factors bind directly to the foreign invader. The lack of inhibitors on the microorganism\'s surface allows the process to proceed.1314 ○ **Effects of Complement Activation**:141516 **Cell lysis**: C3b binds to the target cell, triggering the insertion of the membrane attack complex (MAC) into the cell's membrane, forming a hole, causing an influx of water, and lysis.1415 **Enhancement of phagocytosis by opsonization**: Complements work with antibodies (opsonins) to coat pathogen surfaces.16 **Histamine release**: Increases blood vessel permeability and attracts phagocytes by chemotaxis.16 6. **Inflammatory Response**: A localized response triggered by tissue injuries due to trauma, heat, chemicals, or infections.17 ○ **Benefits**:17 Prevents the spread of damaging agents. Disposes of cell debris and pathogens. Alerts the adaptive immune system. Sets the stage for repair. ○ **Cardinal Signs and Symptoms**: Swelling (tumor), redness (rubor), heat (calor), and pain (dolor).18 ○ **Effects**:18 Temporary repair and a barrier against pathogens. Retardation of pathogen spread into surrounding areas. Mobilization of local and systemic defenses and facilitation of repairs (regeneration). ○ **Products**:19 **Necrosis**: Local tissue destruction in the area of injury.19 **Pus**: A mixture of debris and necrotic tissue.19 **Abscess**: Pus accumulated in an enclosed space.20 7. **Fever**: A maintained body temperature above 37.2°C (99°F), triggered by pyrogens.20 ○ **Pyrogens**: Substances that cause the hypothalamus to raise body temperature. They can be circulating pathogens, toxins, antibody complexes, or endogenous pyrogens like interleukin-1 (IL-1) released by active macrophages.20 **Adaptive (Specific) Defenses** **Cells Involved**:20 ○ **T cells**: Provide cell-mediated immunity, defending against abnormal cells and pathogens inside cells.3 ○ **B cells**: Provide antibody-mediated immunity, defending against antigens and pathogens in body fluids.3 **Forms of Immunity**:3 ○ **Innate**: Present at birth.3 ○ **Adaptive**: Develops after birth.3 ○ **Active**: Antibodies develop after exposure to an antigen.3 **Naturally acquired**: Through environmental exposure to pathogens.21 **Artificially induced**: Through vaccines containing pathogens.21 ○ **Passive**: Antibodies are transferred from another source.3 **Naturally acquired**: Antibodies acquired from the mother.21 **Artificially induced**: By injection of antibodies.21 **Properties of Immunity**:21 ○ **Specificity**: Each T or B cell responds only to a specific antigen.21 ○ **Versatility**: The body produces many types of lymphocytes to fight different antigens. Active lymphocytes clone themselves.21 ○ **Memory**: Some active lymphocytes (memory cells) stay in circulation, providing immunity against new exposure.22 ○ **Tolerance**: The immune system ignores \'normal\' antigens (self-antigens).22 **T Cells and Immunity** **Major Types of T Cells**:23 ○ **Cytotoxic T cells (TC cells)**: Attack cells infected by viruses and are responsible for cell-mediated immunity.23 ○ **Memory T cells**: Clone themselves in response to a \'remembered\' antigen.24 ○ **Helper T cells (TH cells)**: Stimulate the function of T cells and B cells.24 ○ **Suppressor T cells (TS cells)**: Inhibit the function of T cells and B cells.24 **Antigen Presentation**: T cells recognize antigens bound to MHC proteins on plasma membranes.24 ○ **MHC Proteins**: Membrane glycoproteins that bind to antigens, genetically coded in chromosome 6 (major histocompatibility complex, MHC) and differ among individuals.24 ○ **Classes of MHC Proteins**:25 **Class I**: Found in membranes of all nucleated cells. They pick up small peptides in the cell and carry them to the surface. Abnormal peptides or viral proteins activate T cells to destroy the cell.2526 **Class II**: Found in membranes of antigen-presenting cells (APCs) and lymphocytes. Antigenic fragments from antigen processing bind to Class II proteins and are inserted into the plasma membrane to stimulate T cells.2527 **Antigen-Presenting Cells (APCs)**: Activate T cells against foreign cells and proteins.27 ○ **Phagocytic APCs**: Free and fixed macrophages in connective tissues, Kupffer cells of the liver, and microglia in the CNS.28 ○ **Non-phagocytic APCs**: Langerhans cells in the skin and dendritic cells in lymph nodes and spleen.28 **Antigen Recognition**: Inactive T cell receptors recognize Class I or Class II MHC proteins and a specific antigen. Binding occurs when the MHC protein matches the antigen.2829 **CD Markers**: Also called cluster of differentiation markers, found in T cell membranes. There are over 70 types, each designated by an identifying number.29 ○ **CD3 Receptor Complex**: Found in all T cells.29 ○ **CD8 Markers**: Found on cytotoxic T cells and suppressor T cells, respond to antigens on Class I MHC proteins.29 ○ **CD4 Markers**: Found on helper T cells, respond to antigens on Class II MHC proteins.30 ○ **CD8 or CD4 Markers**: Bind to the CD3 receptor complex and prepare the cell for activation.30 **Costimulation**: T cells require costimulation to be activated, achieved by binding to a stimulating cell at a second site, confirming the first signal.30 **Activation of CD8 T Cells**: Triggered by exposure to antigens on MHC proteins. One response is rapid, producing cytotoxic T cells and memory T cells, while the other is slow, producing suppressor T cells.31 ○ **Cytotoxic T (TC) Cells**: Immediately destroy target cells by releasing perforin to destroy the antigenic plasma membrane, secreting poisonous lymphotoxin, or activating genes in the target cell that cause cell death.313233 ○ **Memory TC Cells**: Produced with cytotoxic T cells, stay in circulation, and immediately form cytotoxic T cells if the same antigen appears again.33 ○ **Suppressor T Cells**: Secrete suppression factors that inhibit T and B cell responses, acting after the initial immune response to limit the reaction to a single stimulus.3334 **Activation of CD4 T cells**: Produces active helper T cells (TH cells) that secrete cytokines, and memory helper (TH) cells that remain in reserve.34 **Functions of Cytokines**:35 ○ Stimulate T cell divisions, producing memory TH cells and accelerating cytotoxic T cell maturation.35 ○ Attract and stimulate macrophages.35 ○ Attract and stimulate cytotoxic T cells.35 ○ Promote B cell activation.35 **B Cells and Immunity** **Function**: Responsible for antibody-mediated immunity, attacking antigens by producing specific antibodies. Millions of populations exist, each with different antibody molecules.36 **B Cell Sensitization**: When corresponding antigens in interstitial fluids bind to B cell receptors, the B cell prepares for activation (sensitization). During sensitization, antigens are taken into the B cell, processed, and reappear on the surface bound to Class II MHC proteins.37 **Role of Helper T Cells**: A sensitized B cell needs a helper T cell activated by the same antigen to become fully activated. The helper T cell binds to the MHC complex and secretes cytokines that promote B cell activation and division.38 **B Cell Activation and Differentiation**:3839 ○ An activated B cell divides into: **Plasma cells**: Synthesize and secrete antibodies into interstitial fluid.39 **Memory B cells**: Remain in reserve to respond to the next infection.39 **Antibody Structure** **Composition**:39 ○ Two parallel pairs of polypeptide chains: one pair of heavy chains and one pair of light chains.39 ○ Each chain contains constant segments and variable segments.39 **Five Heavy-Chain Constant Segments**:39 ○ Determine the five types of antibodies: IgG, IgE, IgD, IgM, IgA.39 **Variable Segments**:40 ○ Determine the specificity of the antibody molecule.40 ○ **Binding Sites**: Free tips of two variable segments form antigen-binding sites that bind to antigenic determinant sites on the antigen molecule.40 **Antigen--Antibody Complex**:40 ○ Formed when an antibody binds to an antigen.40 ○ **Complete Antigen**: Has at least two antigenic determinant sites and binds to both antigen-binding sites of the antibody\'s variable segments. Exposure to a complete antigen leads to B cell sensitization and an immune response.4041 ○ **Hapten (Partial Antigen)**: Must attach to a carrier molecule to act as a complete antigen. Antibodies produced will attack both the hapten and the carrier molecule, which can lead to attacks on normal cells if the carrier is \'normal\' (e.g., penicillin allergy).4142 **Classes of Antibodies (Immunoglobulins, Igs)** **Types**: IgG, IgD, IgE, IgM, IgA, found in body fluids and determined by constant segments. They have no effect on antibody specificity.4243 **IgG**:43 ○ Largest and most diverse class of antibodies (80% of all antibodies).43 ○ Responsible for resistance against many viruses, bacteria, and bacterial toxins.43 ○ Can cross the placenta, providing passive immunity to the fetus.43 ○ Anti-Rh antibodies produced by Rh-negative mothers are IgG antibodies and can cause hemolytic disease of the newborn.43 **IgE**:44 ○ Attaches to basophils and mast cells.44 ○ When an antigen binds to IgE, the cell releases histamine and other chemicals that accelerate inflammation.44 ○ Important in the allergic response.44 **IgD**:44 ○ Found on the surfaces of B cells, where it binds antigens in the extracellular fluid.44 ○ Plays a role in B cell sensitization.44 **IgM**:4445 ○ The first class of antibody secreted after antigen encounter.44 ○ Concentration declines as IgG production accelerates.44 ○ Circulates as a five-antibody starburst.45 ○ Anti-A and anti-B antibodies responsible for blood type incompatibility are IgM antibodies.45 ○ May attack bacteria insensitive to IgG.45 **IgA**:4546 ○ Found primarily in glandular secretions (mucus, tears, saliva, semen).45 ○ Attacks pathogens before they gain access to internal tissues.45 ○ Circulates in blood as individual molecules or in pairs.45 ○ Epithelial cells absorb IgA from the blood, attach a secretory piece for solubility, and secrete it onto the epithelial surface.46 **Functions of Antigen--Antibody Complexes** 1. Neutralization of antigen-binding sites.46 2. Precipitation and agglutination (formation of immune complex).46 3. Activation of complement.46 4. Attraction of phagocytes.46 5. Opsonization (increasing phagocyte efficiency).46 6. Stimulation of inflammation.46 7. Prevention of bacterial and viral adhesion.46 **Primary and Secondary Immune Responses** **Primary Response**:4748 ○ Occurs upon the first exposure to an antigen.47 ○ Slow to develop, taking time for antigens to activate B cells, plasma cells to differentiate, and antibody titer to rise.47 ○ Peak response takes about two weeks and declines rapidly.4748 ○ IgM is produced faster than IgG but is less effective.48 **Secondary Response**:4749 ○ Triggered by subsequent exposure to the same antigen.47 ○ More extensive and prolonged due to memory cells being primed.47 ○ Memory B cells are activated at lower antigen concentrations and secrete antibodies in massive quantities.48 ○ IgG rises very high and very quickly, remaining elevated for an extended time.49 ○ IgM production is also quicker and slightly extended.49 **Combined Responses to Infections** **Bacterial Infection**:50 ○ Neutrophils and NK cells begin killing bacteria.50 ○ Cytokines draw phagocytes to the area.50 ○ Antigen presentation activates helper T cells and cytotoxic T cells.50 ○ B cells activate and differentiate.50 ○ Plasma cells increase antibody levels.50 **Viral Infection**:51 ○ Similar to bacterial infection, but cytotoxic T cells and NK cells are activated by contact with virus-infected cells.51 **Immune System Development** **Fetal Development**:52 ○ The fetus can produce an immune response (immunocompetence) after exposure to antigens at about three to four months.52 ○ Fetal thymus cells migrate to tissues that will form T cells.52 ○ The liver and bone marrow produce B cells.52 ○ A four-month fetus produces IgM antibodies.52 **Before Birth**:53 ○ Maternal IgG antibodies cross the placenta, providing passive immunity to the fetus.53 **After Birth**:53 ○ Mother\'s milk provides IgA antibodies while passive immunity from the mother is lost.53 ○ The infant produces IgG antibodies through exposure to antigens.53 ○ Antibody, B cell, and T cell levels slowly rise to adult levels by about age 12.53 **Cytokines of the Immune System** **Definition**: Chemical messengers (hormones and paracrine-like glycoproteins) involved in cellular immunity.53 **Examples**: Interferons, interleukins, tumor necrosis factors (TNFs).54 **Interleukins**:5455 ○ **Functions**: Increase T cell sensitivity to antigens on macrophage membranes.54 Stimulate B cell activity, plasma cell formation, and antibody production.54 Enhance nonspecific defenses by stimulating inflammation, scar tissue formation by fibroblasts, elevating body temperature, stimulating mast cell formation, and promoting ACTH secretion.55 Moderate the immune response by suppressing immune function and shortening the response.55 ○ **IL-1 and IL-2**: Important in stimulating and maintaining the immune response by stimulating the activities of other immune cells and the secreting cell, creating a positive feedback loop that recruits more immune cells.55 **Tumor Necrosis Factors (TNFs)**:56 ○ Slow tumor growth and kill tumor cells.56 ○ Activated macrophages secrete one type of TNF and carry the molecules in their plasma membranes.56 ○ Cytotoxic T cells produce a different type of TNF.56 ○ Stimulate granular leukocyte production, promote eosinophil activity, cause fever, and increase T cell sensitivity to interleukins.56 **Phagocyte-Activating Chemicals**:57 ○ Coordinate immune defenses by adjusting phagocytic cell activities.57 ○ Attract free macrophages and microphages and prevent their premature departure from the site of injury.57 **Colony-Stimulating Factors (CSFs)**:57 ○ Produced by active T cells, cells of the monocyte--macrophage system, endothelial cells, and fibroblasts.57 ○ Stimulate blood cell production in red bone marrow and lymphocyte production in lymphoid tissues and organs.57 **Classification by Origin**:58 ○ **Lymphokines**: Produced by lymphocytes.58 ○ **Monokines**: Secreted by active macrophages and other APCs.58 ○ These terms can be misleading as lymphocytes and macrophages may secrete the same cytokines.58 ○ Cells involved in adaptive immunity and tissue repair also secrete cytokines.58 **Immune Disorders** **Types**: Autoimmune disorders, immunodeficiency diseases, allergies.58 **Autoimmune Disorders** **Definition**: Malfunction of the system that recognizes and ignores \'normal\' antigens, leading to activated B cells making autoantibodies against body cells.59 **Examples**: Thyroiditis, rheumatoid arthritis, insulin-dependent diabetes mellitus (IDDM).59 **Treatment**:60 ○ Suppress the entire immune system with anti-inflammatory drugs (e.g., corticosteroids).60 ○ Block cytokine action.60 ○ Block costimulatory molecules.60 **Research**: Focuses on activating regulatory T cells, inducing self-tolerance using vaccines, and directing antibodies against self-reactive immune cells.60 **Mechanisms**:61 ○ Weakly self-reactive lymphocytes may be activated by:61 Foreign antigens resembling self-antigens. Antibodies against foreign antigens may cross-react with self-antigens.61 New self-antigens appearing due to gene mutations, changes in self-antigens by hapten attachment or infectious damage, or release of novel self-antigens by trauma.61 **Immunodeficiency Diseases** **Causes**:59 ○ Problems with embryological development of lymphoid tissues, resulting in severe combined immunodeficiency disease (SCID).59 ○ Viral infections like HIV, resulting in AIDS.59 ○ Immunosuppressive drugs or radiation treatments, leading to complete immunological failure.62 **Allergies** **Definition**: Inappropriate or excessive immune responses to antigens.62 **Allergens**: Antigens that trigger allergic reactions.62 **Categories**: Immediate hypersensitivity (Type I), cytotoxic reactions (Type II), immune complex disorders (Type III), delayed hypersensitivity (Type IV).62 **Type I Allergy (Immediate Hypersensitivity)**:6364 ○ A rapid and severe response to the presence of an antigen.63 ○ Severity depends on individual sensitivity and locations involved.63 ○ Allergens in the bloodstream can cause anaphylaxis.63 ○ The most commonly recognized allergy type, including allergic rhinitis (environmental allergies).63 ○ Sensitization leads to the production of large quantities of IgE antibodies distributed throughout the body.63 ○ Second exposure leads to massive inflammation of affected tissues.64 ○ **Anaphylaxis**:6465 Potentially fatal, affecting cells throughout the body.64 Changes capillary permeability, producing swelling (hives) on the skin.64 Causes smooth muscle contraction in the respiratory system, making breathing difficult.64 Peripheral vasodilation can cause circulatory collapse (anaphylactic shock).64 **Treatment**: Epinephrine.66 **Stress and the Immune Response**:67 ○ **Glucocorticoids**: Secreted to limit the immune response, but long-term secretion (chronic stress) inhibits the immune response and lowers resistance to disease.67 ○ **Functions of Glucocorticoids**: Depression of the inflammatory response, reduction in phagocyte abundance and activity, inhibition of interleukin secretion.67 **Immunodeficiencies**:68 ○ **Definition**: Congenital or acquired condition impairing immune cell or molecule function or production.68 ○ **Congenital Immunodeficiencies**:68 **Severe Combined Immunodeficiency (SCID) Syndrome**: A genetic defect causing a marked deficit in B and T cells. Defective adenosine deaminase (ADA) enzyme leads to the accumulation of metabolites lethal to T cells. Fatal if untreated, treated with bone marrow transplants.68 ○ **Autoimmune Diseases**:68 The immune system loses the ability to distinguish self from foreign, producing autoantibodies and sensitized TC cells that destroy body tissues.68 **Examples**: Multiple sclerosis, myasthenia gravis, Graves\' disease, type 1 diabetes mellitus, systemic lupus erythematosus (SLE), glomerulonephritis, rheumatoid arthritis.68 **Hypersensitivities**:61 ○ **Definition**: Immune responses to perceived harmless threats causing tissue damage.61 ○ **Types**: Distinguished by time course and whether antibodies or T cells are involved.61 Antibodies cause immediate and subacute hypersensitivities.61 T cells cause delayed hypersensitivity.61 ○ **Immediate Hypersensitivity**:69 **Acute (type I) hypersensitivities (allergies)** begin seconds after contact with an allergen.69 Initial contact is asymptomatic but sensitizes the person.69 Reaction may be local or systemic.69 The mechanism involves IL-4 secreted by TH2 cells, stimulating B cells to produce IgE, which binds to mast cells and basophils, causing a histamine release and an inflammatory response.69 Subsequent encounters with the same allergen trigger an allergic reaction.69 **Reactions**: Can be local or systemic.70 **Local**: Mast cells of the skin and respiratory and gastrointestinal mucosa release histamines, causing dilated and leaky blood vessels, leading to symptoms like a runny nose, hives, and watery eyes. Inhaled allergens can cause asthma, which is controlled with antihistamines.70 **Systemic**: Anaphylactic shock.70 ○ **Anaphylactic Shock**:6670 A systemic response to an allergen that enters the blood and circulates rapidly.70 Basophils and mast cells throughout the body release histamine.70 Can cause bronchiole constriction, tongue swelling, sudden vasodilation, fluid loss from the bloodstream, circulatory collapse (hypotensive shock), and death.70 **Treatment**: Epinephrine.66 ○ **Subacute Hypersensitivities**:66 Caused by IgM and IgG transferred via blood plasma or serum.66 Slow onset (1--3 hours) and long duration (10--15 hours).66 **Cytotoxic (type II) reactions**: Antibodies bind to antigens on specific body cells, stimulating phagocytosis and complement-mediated lysis of cellular antigens. Example: mismatched blood transfusion reaction.66 **Immune complex (type III) hypersensitivity**:66 Antigens are widely distributed in the body or blood.66 Insoluble antigen-antibody complexes form and cannot be cleared from a particular area.66 Intense inflammation, local cell lysis, and cell killing by neutrophils occur.66 Example: Systemic lupus erythematosus (SLE).66 ○ **Delayed Hypersensitivities (Type IV)**:71 Slow onset (one to three days).71 Mechanism depends on helper T cells.71 Cytokine-activated macrophages and cytotoxic T cells cause damage.71 Example: Allergic contact dermatitis (e.g., poison ivy).71 Agents act as haptens.71 The TB skin test depends on this reaction.71 **Effects of Aging on the Immune System** **Immune System Decline**:71 ○ Increases vulnerability to infections and cancer.71 ○ **Effects of Aging**:71 Thymic hormone production is greatly reduced.71 T cells become less responsive to antigens.71 Fewer T cells reduce B cell responsiveness.71 Immune surveillance against tumor cells declines.71 **Immune System Integration** **Nervous and Endocrine Systems**:72 ○ Interact with thymic hormones.72 ○ Adjust the sensitivity of the immune response.72 Please note that this study guide is based solely on the information provided in the sources you gave. You may want to supplement this with information from your textbook or other class materials. copy\_all thumb\_up thumb\_down keep\_pinSave to note