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Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Chapter 15 Immune System 15-1 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Chapter 15 Outline Innate Immunity Adaptive Immunity Complement System T Cells Histocompatibility Antigens Interactions Between Antigen-Presenting Cells & Lymphocytes Active Immunity Passive Immunity Immune System & Cancer Diseases Caused By Immune System 15-2 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Defense Mechanisms Against pathogens constitute the immune system Can be grouped into 2 categories: Innate (nonspecific) immunity is inherited as part of structure of each organism Adaptive (specific) immunity is a function of lymphocytes & changes with exposure 15-3 Innate Immunity 15-4 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Innate Immunity Is 1st line of defense against invading pathogens Includes epithelial barriers, high acidity of gastric juice, phagocytosis, & fever 15-5 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Phagocytosis Is triggered in response to pathogen-associated molecular patterns (PAMPs) produced only by microorganisms Best known are lipopolysaccharide (LPS) from gram-bacteria & peptidoglycan from gram+s 15-6 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Phagocytosis continued Is performed by 3 classes of phagocytic cells: Neutrophils - 1st to arrive at infection sites Mononuclear phagocytes - macrophages & monocytes Organ-specific phagocytes in liver, spleen, lymph nodes, lungs, & brain Fixed phagocytes line sinusoids of liver, spleen, & lymph nodes & remove pathogens 15-7 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Phagocytosis continued Connective tissue & blood contain mobile leukocytes (WBCs) These are attracted to infection (chemotaxis) by chemokines WBCs from blood exit capillaries by extravasation (diapedesis) & ingest pathogens Fig 15.1 15-8 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Phagocytosis continued Pseudopods from phagocyte surround pathogen Forming a vacuole Vacuole fuses with lysosomes which digest pathogen Fig 15.2 15-9 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Fever Appears to be component of innate immunity Occurs when hypothalamic thermostat is reset upwards by IL1- & other cytokines (endogenous pyrogens) Pyrogens are released by WBCs in response to endotoxin from gram– bacteria 15-10 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Interferons Are polypeptides produced by cells infected with virus that provide short-acting, non-specific resistance to viral infection in nearby cells 3 types: a, , g, interferon 15-11 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Fig 15.3 15-12 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 15-13 Adaptive Immunity 15-14 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Adaptive Immunity Is acquired ability to defend against specific pathogens by prior exposure to those pathogens Is mediated by production of specific antibodies by lymphocytes 15-15 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Antigens Are molecules that elicit production of antibodies that specifically bind those antigens Are usually large molecules that are foreign to the body Immune system can distinguish “self” molecules from non-self antigens Normally makes antibodies only against non-self antigens Large, complex molecules can have a number of antigenic determinant sites (different sites that stimulate production of, & bind to, different antibodies) 15-16 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Haptens Are small non-antigenic molecules that become antigens when bound to proteins (form an antigenic determinant site) Useful for creating antibodies for research and diagnosis 15-17 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Immunoassays Are tests that use specific antibodies to identify a particular antigen The binding of antibody to antigen causes clumping (agglutination) which can be visualized Fig 15.4 15-18 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Lymphocytes Are derived from stem cells in bone marrow Which replace selves by cell division so are not depleted Lymphocytes produced by this process seed thymus, spleen, & lymph nodes with self-replacing colonies 15-19 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. T Lymphocytes (T cells) Develop from lymphocytes that seed thymus Do not secrete antibodies Attack infected host cells, cancer cells, & foreign cells Thus they provide cell-mediated immunity Supply 65 – 85% of lymphocytes for blood & most of lymphocytes in germinal centers of lymph nodes & spleen 15-20 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. B Lymphocytes (B cells) Fight bacterial infections by secreting antibodies into blood & lymph Thus provide humoral immunity 15-21 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Thymus Is located below the thyroid gland Grows during childhood, gradually regresses after puberty Contains T cells that supply other tissues T cells can be depleted, e.g. by AIDs or chemotherapy These can only be replenished up to late childhood After that, repopulation is accomplished by production in secondary lymphoid organs 15-22 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Secondary Lymphoid Organs Consist of lymph nodes, spleen, tonsils, & Peyer’s patches Located in areas where antigens could gain entry to blood or lymph Lymphocytes migrate constantly through blood & lymph from one lymphoid organ to another Enhances chance that antibody will encounter its antigen Spleen filters blood; other lymphoid organs filter lymph 15-23 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Local Inflammation Occurs when bacteria enter a break in the skin Inflammatory reaction is initiated by nonspecific mechanisms of phagocytosis & complement activation Complement activation attracts phagocytes to area 15-24 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Local Inflammation continued As inflammation progresses, B cells produce antibodies against bacterial antigens Attachment of antibodies to antigens amplifies nonspecific responses because of complement activation & promotes phagocytic activity of neutrophils, macrophages, & monocytes (= opsinization) 15-25 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Local Inflammation continued In inflamed area, leukocytes attach to surface of endothelial cells Move by chemotaxis to inflamed site Neutrophils arrive 1st, then monocytes, then T cells Undergo extravasation Fig 15.6 15-26 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Local Inflammation continued Mast cells secrete heparin, histamine, prostaglandins, leukotrienes, cytokines, & TNF-a These produce redness, warmth, swelling, pus, & pain Recruit more leukocytes If infection continues, endogenous pyrogens are released Fig 15.5 15-27 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. B Lymphocytes (B cells) Have antibodies on surface that are receptors for antigens When bound to antigen, are stimulated to divide & secrete antibodies Fig 15.8 15-28 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. B Lymphocytes (B cells) When B cells divide, some progeny become memory cells Some become plasma cells that produce about 2000 antibodies/sec that are specific for original antigen This provides active immunity Fig 15.7 15-29 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. B Lymphocytes (B cells) Binding of B cells to antigen also triggers a cascade of reactions that activate complement proteins Complement proteins can kill antigen-bearing cells & promote phagocytosis 15-30 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Antibodies Are proteins called immunoglobulins Part of gamma globulin class of plasma proteins Antibodies have same basic structure but their differences provide for antibody specificity 15-31 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 15-32 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Antibody Structure Is in shape of “Y” 2 long heavy (H) chains are joined to 2 shorter light (L) chains When cleaved, stalk of Y becomes crystallizable fragment (Fc) Fc is constant among different antibodies Arms of Y contain antigenbinding fragment (Fab) Fab contains a variable Fig 15.10 region that confers antibody specifity 15-33 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Antibody Diversity person has about 1020 antibody molecules With a few million different specificities Likely there is an antibody specific for any antigen a person might encounter 2 mechanisms might account for diversity If a few hundred genes code for Hs & a few hundred for Ls, different combinations of these could lead to millions of different antibodies Mutations could increase diversity, especially with age Each 15-34 Complement System 15-35 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. The Complement System Is part of nonspecific defense system Activity is triggered by binding of antibodies to antigens (classic pathway) & by bacterial coat polysaccharides (alternative pathway) Binding of antibodies to antigens does not by itself destroy antigens or pathogens Antibodies label targets for complement system attack & also stimulate opsonization 15-36 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. The Complement System continued Is a series of proteins whose activation forms a membrane attack complex which perforates a cell causing it to lyse Complement proteins can be subdivided into 3 functional groups: C1 - recognition C4, C2, C3 - activation C5-C9 - attack (complement fixation) These form the membrane attack complex 15-37 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. The Complement System continued In classic pathway antibody-antigen binding activates C1 C1 hydrolyzes C4 into C4a & C4b C4b binds to cell membrane & becomes active, splitting C2 into C2a & C2b C2a attaches to C4b & cleaves C3 into C3a & C3b Alternate pathway also cleaves C3 (& so converges with classic pathway at this step) C3b converts C5 to C5a & C5b 15-38 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Fixation of Complement Proteins Fig 15.12 15-39 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Membrane Attack Complex C5b & C6 - C9 are inserted into bacterial cell membrane, forming membrane attack complex This creates large pore in membrane, causing osmotic influx of H20, lysis, & cell death Fig 15.13 15-40 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Complement Fragments That are liberated during activation have a number of effects, including Attracting phagocytes (chemotaxis) Phagocytes have receptors for C3b which can serve as bridge to victim cell C3a & C5a stimulate mast cells to secrete histamine Which increases blood flow & capillary permeability, bringing in more phagocytes 15-41 T Cells 15-42 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Killer or Cytotoxic T Cells Carry CD8 cell surface marker Destroy body cells that possess foreign antigens Usually from a pathogen, but can be from malignancy or self cells never seen by immune system Kill by cell-mediated destruction That is, must be in contact with victim cell Kill by secreting perforins which create a pore in victim's membrane & cause lysis Also secrete granzymes which cause destruction of victim's DNA 15-43 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Helper & Suppressor T Cells Helper Ts carry CD4 surface marker Indirectly participate by enhancing responses of both killer T cells & B cells Suppressor Ts decrease responses of killer Ts & B cells Fig 15.14 15-44 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Lymphokines Are cytokines secreted by lymphocytes Usually called interleukin-1, 2, 3 . . . or IL1, IL-2 . . . 15-45 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. T Cell Receptor Proteins Only protein antigens are recognized by most T cells T cell receptors cannot bind to free antigens T cells respond to foreign antigens when they are presented on surface of antigen-presenting cells Chief antigen presenting cells are macrophages & dendritic cells 15-46 Histocompatibility Antigens 15-47 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Dendritic Cells Originate in marrow, then migrate to most tissues Prominent where pathogens might enter body Engulf protein antigens, partially digest them, & display polypeptide fragments on surface for T cells to "see" 15-48 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Dendritic Cells continued Fragments are associated on surface with histocompatibility antigens which are necessary to activate Ts To increase chance of interacting with correct T cells, dendritics migrate to secondary lymphoid organs Where secrete chemokines to attract Ts Fig 15.15 15-49 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Histocompatibility Antigens Are on surface of all body's cells except mature RBCs Also called human leukocyte antigens (HLAs) Are coded for by group of 4 genes on chromosome 6 called major histocompatibility complex (MHC) 4 genes have multiple alleles creating many possible MHC types 15-50 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. MHC MHC genes produce 2 types of cell surface molecules: class-1 & class-2 Class-1s are made by all cells except RBCs Class-2s are made only by antigen-presenting cells & B cells These present class-2s together with foreign antigen to helper Ts This is only way to activate helper Ts so they can promote B cell activity 15-51 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. MHC continued In order for killer & helper Ts to function they require co-presentation of antigen with a specific MHC marker Killer Ts are activated to kill victim cell only by copresentation of antigen & class-1 marker Helper Ts require antigen & class-2 marker 15-52 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. MHC continued Co-presentation requirement comes from presence of different coreceptors on killer & helper T cells Killer T coreceptor CD8 interacts only with class-1s Helper T coreceptor CD4 interacts only with class-2s Fig 15.16 15-53 Interactions Between Antigen Presenting Cells & Lymphocytes 15-54 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. T Cell Response to a Virus When virus infects body it is phagocytized by macrophage or dendritic cell Its partially-digested polypeptide fragments are antigens that are displayed on surface Form a complex with class-2 MHC molecules that macrophages present to helper T cells Helper Ts bind & are activated Can now promote B cell activity 15-55 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Fig 15.17 15-56 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Macrophage-T cell Interaction When macrophages & T cells complex, macros secrete IL-1 & TNF (good at killing cancer cells) IL-1 stimulates cell division & proliferation of helper Ts Activated helpers secrete M-CSF & g- interferon & IL-2 Promotes activity of macrophages Activated helpers activate B cells 15-57 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Killer T cell Activity Killer Ts destroy infected cells if class-1 markers are present Fig 15.18 15-58 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Helper T cell-B cell Interactions Activated helper Ts promote humoral response of B cells by binding to their surface antigens & MHC class 2s This stimulates proliferation of Bs, their conversion to plasma cells, & their secretion of antibodies Fig 15.20 15-59 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Destruction of T cells Activated Ts must be destroyed after infection is over Occurs because Ts produce a surface receptor called FAS FAS production increases during infection After a few days, Ts begin to produce FAS ligand Binding of FAS to FAS ligand triggers apoptosis (cell suicide) 15-60 Active Immunity 15-61 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Primary & Secondary Responses On 1st exposure to pathogen, there is latency of 5-10 days before specific antibodies are made (= primary response) Antibody levels plateau after few days & decline after a few weeks Subsequent exposure to same antigen causes secondary response Antibody production is much more rapid & sustained Fig 15.22 15-62 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Clonal Selection Theory Is mechanism by which secondary responses are produced Each B cell produces only 1 kind of antibody & related antigen receptor (on its surface) Exposure to its antigen stimulates a B cell to divide until a large population of genetically identical cells (clones) is produced Some of these become plasma cells & secrete antibodies Some become memory cells that can be stimulated to produce antibodies in the secondary response 15-63 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Fig 15.23 15-64 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 15-65 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Active Immunity Development of a secondary response provides active immunity Immunizations induce primary responses by inoculating people with pathogens whose virulence has been attenuated or destroyed (vaccinations) Cause development of B cell clones that can provide secondary response 15-66 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Immunological Tolerance Ability to produce antibodies against non-self antigens while tolerating self-antigens (immunological competence) occurs during 1st month of life Tolerance requires continuous exposure to an antigen Some self-antigens, such as lens protein in eye, are normally hidden from blood Exposure to such self-antigens results in production of autoantibodies Killer T cells that attack self-antigens are called autoreactive T cells 15-67 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Immunological Tolerance continued 2 possible mechanisms for tolerance: Clonal deletion theory: tolerance occurs because T cells that recognize self-antigens are destroyed Good evidence this occurs in thymus Clonal anergy: lymphocytes directed against selfantigens are present throughout life but don't attack self-antigens Mechanism not understood Appears to underlie tolerance in B cells 15-68 Passive Immunity 15-69 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Passive Immunity Is immune protection produced by transfer of antibodies to a recipient from a donor Donor was actively immunized Person who receives these ready-made antibodies is passively immunized Used to treat snakebite, rabies, tetanus, hepatitis 15-70 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Passive Immunity Occurs naturally before & after birth Some antibodies from mother pass placenta to fetus during pregnancy & provide passive immunity During 1st 2-3 days of nursing, mother produces colostrum which is rich in her antibodies & gives her immunity to infant Immunological competence (ability to mount a specific immune response) does not develop until 1 month after birth 15-71 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 15-72 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Monoclonal Antibodies Commercially prepared for use in research & diagnostic tests Exhibit specificity for only 1 antigenic determinant Animal (usually mouse) is injected with antigen, & its B cells harvested from spleen Bs are hybridized with cancerous myeloma cells to make them immortal Individual Bs are screened & 1 that produces right antibody is selected This 1 is allowed to multiply in culture & its clones (= hybridoma) are source of large quantity of antibodies 15-73 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Fig 15.24 15-74 Immune System & Cancer 15-75 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Tumor Immunology Thought that tumor cells arise often but are normally recognized & killed by immune system When cancer develops, the immunological surveillance system of T & natural killer cells, has failed Tumor biology is similar to & interrelated with functions of immune system Most tumors are clones of single cells whose mitosis is not controlled by normal inhibitory mechanisms 15-76 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Tumor Immunology continued Tumor cells dedifferentiate (become less specialized like cells of an embryo) As dedifferentiate, produce surface antigens that are normally recognized by immunological surveillance & destroyed Because were absent at the time immunological competence was established Body treats these antigens as foreign Presence of these antigens provides basis of laboratory diagnostic tests for some cancers 15-77 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Natural Killer (NK) Cells Are lymphocytes related to T cells Provide first line of cell-mediated defense NK cells destroy tumors in a non-specific fashion; backed up by specific response of killer Ts NKs are stimulated by interferon from T cells NKs attack cells that lack class-1 MHC antigens Kill with perforins & granzymes 15-78 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Immunotherapy for Cancer Most strategies involve boosting, or directing, patients own immune responses Interferons & interleukins have been useful in treatment of some forms of cancer E.g. interleukin-2, which activates both killer T & B cells, has shown promise 15-79 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Effects of Aging and Stress Little is known about why susceptibility to cancer is so variable Cancer risks increase with age One factor may be that aging lymphocytes accumulate genetic errors that decrease effectiveness Thymus function declines with age Tumors grow faster in stressed animals Stress hormones (corticosteroids) cause decreased immune function 15-80 Diseases Caused By Immune System 15-81 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Diseases Caused by Immune System Can be grouped into 3 categories: autoimmune diseases, immune complex diseases, & allergies All caused by abnormal functioning of immune system 15-82 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Autoimmune Diseases Are produced by failure of immune system to recognize & tolerate self-antigens Autoreactive T cells are formed & B cells produce autoantibodies Afflicts women twice as often as men 15-83 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Autoimmune Diseases continued Failure of self-tolerance may be due to: An antigen that does not normally circulate in blood being presented to immune system E.g. in Hashimoto's thyroiditis, antibodies are stimulated to attack thyroglobulin (which is normally hidden from immune surveillance) 15-84 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Autoimmune Diseases continued Failure of self-tolerance may be due to: Combination of a self-antigen, that is otherwise tolerated, with a foreign hapten E.g. in thrombocytopenia (low platelet count), platelets are destroyed because they combine with victim's medications 15-85 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Autoimmune Diseases continued Failure of self-tolerance may be due to: Antibodies being produced that are directed against other antibodies Happens with rheumatoid arthritis 15-86 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Autoimmune Diseases continued Failure of self-tolerance may be due to: Antibodies against foreign antigens cross-reacting with self-antigens This can happen with rheumatic fever 15-87 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Autoimmune Diseases continued Failure of self-tolerance may be due to: Self-antigens being presented to helper T cells together with class-2 MHC molecules This happens in Type I diabetes 15-88 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Immune Complex Diseases Involve formation of immune complexes that are free & not attached to a cell These activate complement proteins & promote inflammation Can result from infections by bacteria, parasites, viruses Can result from formation of complexes between selfantigens & autoantibodies This occurs in rheumatoid arthritis & lupus 15-89 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Allergy (Hypersensitivity) Is an abnormal immune response to allergens Comes in 2 forms: immediate & delayed hypersensitivity Immediate is due to abnormal B cell response to allergen; causes effects in secs to mins Caused by foods, bee stings, pollen Delayed is abnormal T cell response that causes symptoms 24-72 hrs after exposure 15-90 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Immediate Hypersensitivity Dendritic cells stimulate a class of helper Ts to secrete interleukin-4 & -13 which cause B & plasma cells to secrete IgE antibodies Do not circulate in blood; are attached to mast cells & basophils When re-exposed to same allegen, antibodies on mast cells & basophils bind it & stimulate secretion of histamine, leukotrienes, & prostaglandin D Producing allergy symptoms 15-91 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Immediate Hypersensitivity continued Fig 15.26 15-92 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Delayed Hypersensitivity Symptoms take longer to develop (hrs to days) Is a cell-mediated T cell response Symptoms caused by secretion of lymphokines, not histamine Antihistamines provide little benefit Examples include contact dermatitis caused by poison ivy, oak, or sumac 15-93