Chapter 5 Diseases of immunity Nonspecific immunity- do not require previous contact with a specificmicroorganism physical barriers Antibacterial Agents

ts Commensal Microorganisms Ongoing Phagocytosis Inflammatory Response Fever Specific Immunity- required after birth Recognition-discovering a new pathogen Learning- what to do when there is a second or subsequent exposureto pathogen Memory- improved response to pathogen Self-discrimination- able to discriminate between foreign substancesand those that make up our own body, and to direct its attack only againstintrudersLymphocytesTLymphocytes o Produced in bone marrow or thymus( mature here) o T-cell receptors recognize antigens and immunogenic o Able to recognize foreign substances particularly the surface features of microorganisms, because their receptor shapes match, allowing them to bindtogether. o Antigenic Determinants or epitopes the billions of binding sites for theT-cell Why we may have an allergic response to something harmless May confuse nonself-antigens with self-antigens o Are looking for trouble from foreign substances B-Lymphocytes o Antibody producing cells o Mature in the bone marrow

o React to specific epitopes o Antibodies- y shaped linkers who limit repertoire of defenses to the hostof invaders that threaten us Antigen-binding fragment (FAB)- can attach and mark any of a billionepitopes; and can neutralize toxic substances The Fc (crystallizable fragment)- the stalk of the Y, this will bring about theproduction of masses of antigen-specific antibodies that can bind to theantigen Macrophages, PMNs and eoxinophils have Fc receptors o These antibodies produce a first line of defense: IgM- a normal immune response IgG- most prevalent in blood IgE-allergies and worms IgA- GI related (gut checker) IgD- antigen receptor on lymphocyte membranes Natural killer cells (NK cells) o Large granular lymphocytes that are killers of foreign substances o Antibody-dependent cellular cytotoxicity (ADCC) shared withneutrophils, macrophages, and eosinophils o Tumor surveillance- recognize if a cell is becoming abnormal, thenengage and kill itLymphoid Tissue Primary- red bone marrow and thymus, where T & B lymphocytes areformed Secondary- lymph nodes, spleen, tonsils, Peyers patches in theintestines o Draining lymph enters blood circulation then can reenter othersecondary lymphoid tissues o The lymphoid tissue are strategically placed to locate and encounterantigens shortly after it violates the bodys outer defenses o

Lymphocyte traffic increases chances of running into an antigen in thebody FilterImmune Response A macrophage is usually a quick responder to foreign substance o Once it has destroyed a foreign substance , the antigens, are thendisplayed on the surface of the macrophage, which presents them to T cells o Of the T-cells, one will have T-cell receptor that corresponds to anepitope of the antigen o This T-cell is called a helper T cell (Th cell) matching this th cell is calledclonal selection o The Th cell is activated into clonal expansion along with memory cells Cytotoxic T cells are activated which can identify and kill virus- or parasiteinfected cells With the expansion of Th cells it initiates the movement of NK cells &macrophages o Antigen presenting cells stimulate B-cells (starting with IgM and thenIgG) to produce antibodies and form memory cells allowing for fasterresponse to the antigen in the future o Cytotokines is a mediating factor that will communicate between cells Stimulates nearby immune cells to become active and promoteinflammation o Overview of Immune response Figure 5.12 Immunization is the preventive technique of artificially inducing an immune response. Itstimulates the immune system without exposing it to an infection. Inducing a toxins antigeniccomponent is known as a vaccine The purpose of a vaccine is to induce a primary antibody response with the long-termretention provided by memory T and B cells. Measles, Mumps, Rubella are immunized with attenuated viruses (children 15-19 monthsold) Diphtheria is immunized with diphtheria toxoid and Pertussis, Tetanus are immunized withbordetella pertussis, tetanus toxoid (children 2-3 months old)Vaccine induced immunities are said to be active and passive immunity is ready madeantibodies from outside the system. Hypersensitivity

- reactions involve deleterious effects caused by the immune systemresulting in tissue damage. There are four types of reactions. Type 1 Immediate hypersensitivity : Contact with antigen results in plasma cellproduction of IgE antibody. This binds to the Fc receptors on mucosal, dermal, or perivascular mast cells, thus arming them. This results in mast cell degranulation and synthesis of secondarymediators. Primary mediator of mast cell degranulation is histamineTypical manifestationsinclude hay fever, asthma, hives, food allergies, and eczema. Type 2 Cytotoxic Hypersensitivity : Ab directed against cell surface antigens mediatescell destruction via complement activation. Includes blood transfusion reactions, autoimmunehemolytic anemia. Type 3 Complex-Mediated Hypersensitivity : Induce complement activation andensues inflammatory response mediated by massive infiltration of neutrophils. Includes serumsickness, rheumatoid arthritis, and systemic lupus erythematosus Type 4 Cell-mediated Hypersensitivity : Cytokines that activate macrophages or Tccells which mediate direct cellular damage. Includes dermatitis, tubercular lesions, and graftrejection Graft rejection : Antigen presenting cells facilitate T-cell sensitization, which enhancescomplement deposition and platelet aggregation and in turn phagocytosis. Antibody bindingmakes possible antibody-dependent cellular cytotoxicity by NK cells. NK cells attack thetransplant tissue, while sensitized and activated T cells mobilize a chronic attack on the grafttissue. Primary Immune Deficiencies result when one or more components of immune systemfunction are deficient or lacking, often because of a genetic defect, with a resulting characteristicpattern of infection. B-cell deficiencies result in recurrent infections by viruses that are normally neutralized byantibody or bacteria that can resist phagocytosis. This B-cell deficit produces lower gammaglobulin levels. e ) e ediated toxicity sible changesfibers get biggerplasia- extra cellshange one cell type to another cell type alteration of cells growth patternproduction beyond the bodys neednomous growthof contact inhibitioning indepedentlyof response to ECMt o d e r m layer; skin/nervous systerm