3 Primary Immune Response This is how immunity to disease is acquiredRequires timeTwo componentsRecognitionRequires exposure to invading agentResponseInvolves a searching effort (clonal selection)
4 Secondary Immune Response The response of the immune system to the second or subsequent occasion on which it encounters a specific antigen.
5 Lymphocytes Primary participants in the immune response Types of lymphocytes: B-cells and T-cellsBoth originate in red bone marrow (stem cells)
6 DifferentiationOccurs in the Primary Lymphoid Tissues (thymus and spleen)Lymphocytes develop special recognition sites on their membranesB-cellsDifferentiation occurs in red marrowT-cellsDifferentiation occurs in thymus
7 MigrationAfter differentiation, B-cells and T-cells migrate to Secondary Lymphoid TissuesLymph nodesSpleenAdenoidsTonsilsPeyer’s Patches: Intestinal liningMALT
8 Lymph Nodes B-cells, T-cells, and macrophages are “stored” here Lymph nodes receive fluid from tissues and bloodMay contain bacteria, viruses, etc.Brings lymphocytes in contact with these invaders, allows for immune response
10 B-Cells B-cells secrete antibodies that fight antigens Virgin B-cells Antibodies (AKA immunoglobins) are proteins that bind to specific antigensAntigen (AKA immunogen) is any molecule that can stimulate the immune response.Protein, nucleic acid, carbohydrate (5000+ u)Free molecules or part of the membrane of an invaderAntigenic determinants-localized chemical groups that trigger the formation of an antibodiesVirgin B-cellsMature B calls equipped with surface antibodiesMigrate to secondary lymphoid tissue to await invadersB-Cells
11 Structure of Antibody Make phagocytosis more effective 4 polypeptide chains2 heavy chains2 light chainsChains held together by disulfide linkagesY-shaped configurationVariable regions2 branches of the YAntigen binding SitesContained in variable regionBind antibody to antigenic determinantMillions of varietiesConstant RegionSame in all antibodies in a given classFc RegionsContained in constant regionMake phagocytosis more effective
12 Antibody Classes-Fig 40.11 IgG IgA IgM IgD IgE Differ in structure, location, target, and action
13 5 Antibody-Antigen Interactions (figure 40.12 ) 1. Neutralizing- antibodies encounter and surround free antigens, neutralizing harmful chemical effects.2. Activating Complement- When IgM and IgG bind to invaders, it activates complement and causes the lysis of cells.3. Viral binding- Antibodies bind to the host cell binding site on the virus, rendering them harmless.4. Bacterial binding- IgM is a pentamer (5 binding sites_so it can bind to lots of bacteria at once and make phagocytosis by a phagocyte easier.5. Opsonization- Multiple monomer antibodies bind to invader exposing many constant regions making phagocytosis easier.
14 T-Cells Major Histocompatibility Complex (MHC) Complex of genes found on chromosome # 6Determines our cell surface proteins2 MHC protein groups are important here-MHC class I and MHC class IIHelps us recognize our own cells as “self”T-cells have recognition sites that match MHC proteins, healthy cells are ignoredFigure 40.13Most body cells are coded as MHC class IT and B cells and macrophages are coded as class I or IIT-Cells
15 Identification of Infected Cells by T-Cells Infected cells incorporate antigenic material into MHC proteinT-cells have dual recognition sitesOne recognizes MHC site (class I or II)One recognizes antigensLots of variability in antigen site/T cellsAlmost any antigen can be recognizedFigure 40.14Cytotoxic T-cells (Tc, T8)Recognize class I MHC proteinsSeek out and attack diseased body cellsHelper T-cells (T4, Th)Recognize class II MHC proteinsRecognize T-cells, B-cells, and macrophages and interact with themCoordinate Immune responseVirgin T-cellsMature T-cells equipped with dual recognition sitesMigrate to secondary lymphoid tissue to await invaders
16 Primary Immune Response Complex set of eventsOccurs with first encounter w/new invader (antigen)Takes timeFirst Step—Clonal SelectionImmune cells with the correct antigen receptor must be locatedThose cells must multiplySecond Step--ResponseHumoral or Cell-Mediated
17 Clonal SelectionProliferation of clones from a single line of lymphocytes-This process takes time because1. cells bearing the correct antigen receptor must be found2. these cells must multiplyInvolves MacrophageEat invaders including free antigensHave both classes of MHC’s
18 Role of Macrophages in Clonal Selection Serve as an intermediary trigger (T-cells cannot be activated by antigen)Have both Class I and Class II proteins on their membranes
19 The Steps of Clonal Selection (see figure 40.17) 1. Macrophage eats invader.2. Material from invader conserved tomake sites to bind with a T-cell.3. Conserved materials from extra-cellularpathogens (bacteria) incorporated intothe macro’s Class 2 proteins4. Conserved materials from intra-cellularpathogens (viruses) are incorporatedinto the macro’s Class 1 proteins5. Surface of macro becomes thereciprocal of a T-cell dual recognition site6. The macrophage is now known as an antigen-presenting cell7. The antigen presenting cell bumpsinto virgin T-cells till it finds one whose dual receptors form a match.8. Because antigen presenting cells have both Class I and Class II MHC proteins, they can match (bind) with both Tc and Th cells.
20 Spreading The Alarm-Aroused T-Cells (figure 40.18) T cell and macrophage (antigen presenting cell) bind causing macrophage to release a chemical messenger called interleukin 1.This makes the attached T-cell undergo many cell divisionsWhen Th cells get aroused, they also release interleukin 2 that causes Tc cells to divide even more!All of these new T-cells can recognize the antigen that initiates the process.A small number of these new T-cells are set aside as memory cells
21 Tc cells –Cell Mediated Response Role is to “frisk” every cell till it finds a matching antigen.Once a diseased cell is found the Tc cell releases perforin (this chemical makes holes in the infected cell causing it to lyse.Some Tc cells release lymphotoxin (this chemical activates enzymes of viruses to fragment their own DNA, thus preventing the virus from multiplyingSome release gamma-interferon (this chemical stimulates phagocytes to clear up cellular debris)Can also fight cancer cells as long as the cancer has not metastasized.
22 Th cells—Humoral Response (figure 40.20) Two roles1. increase cell division2. activate B-cellsB-cells are aroused when the surface of a virgin B-cell binds to a matching free antigen.B-cell takes in the free antigen then makes class 2 MHC proteinsThen the B-cell matches and binds to a Th cell.The Th cell secretes interleukin 2This chemical causes B-cells to multiply (form clones)Some clones set aside as memory cellsOnce B-cell activated are called plasma cellsThese cells are short lived (4-5 days) but secrete up to 2000 antibody molecules per second!See earlier discussion of antibodies to remember the types of interactions they have with antigens.
23 B-cells Some B-cells don’t need to be activated by Th cells The B-cell randomly encounters the antigen that matches its MHC siteAntigen is taken in and triggers B-cell to divide (no chemicals)Vast array of clones are madeThese type of B cells are very limited
24 Suppressor T cells or Ts Monitors the immune system and keepsit from running out of controlBrings the Primary Immune response to a halt after danger has passed.These cells may inhibit remaining appropriate virgin T and B cells.Since their lives are short (T and B cells) Ts cells only need to suppress for a short time.
25 Memory cells and the 2o response Some of the activated T and B cells remain as memory cellsIf another invasion of the same invaders occurs these cells recognize them immediately and start their attack.We may not even notice that this is happening or the symptoms are very mild