Immunity in Class Part 2 (PDF)

Humoral vs cell mediated immunity In class Immunity Humoral Immunity and Cell‐ Mediated Immunity B cells are responsible for humoral immunity T cells are responsible for cell‐mediated immunity the success of the immune system depends on interaction between the humor...

Humoral vs cell mediated immunity In class Immunity Humoral Immunity and Cell‐ Mediated Immunity B cells are responsible for humoral immunity T cells are responsible for cell‐mediated immunity the success of the immune system depends on interaction between the humoral and cell‐ mediated responses  eliminate bacteria, responsible for neutralize Immunity humoral immunity bacterial toxins, prevent viral infection B cell surface LYMPHOCY they deal with contains: immunoglobulins TES antigens that are easily “seen” (that act as antigen receptors), MHC class II molecules, complement receptors specific CD molecules (CD 4)  Immunity B LYMPHOCYTES a B cell is activated when it encounters antigen complementary to their surface immunoglobulin receptor and receives chemical signals (cytokines) from T helper cells once activated, B cells proliferate and differentiate into antibody‐secreting plasma cells; some B cells differentiate into memory cells the proliferation of a single type of B‐cell is called clonal selection memory cells live longer than plasma cells; they reside in peripheral tissues in preparation for subsequent antigen exposure  Immunity B LYMPHOCYTES B cells can also function as an APC by engulfing the immunoglobulin/antigen complex, digesting the antigen into small fragments, and presenting the small fragments g on an MHC II molecule on its cell surface T‐helper cells bind to the MHC II/antigen complex and will release cytokines that will stimulate the proliferation of B cells Immunity ANTIBODIE S Function: once secreted, antibodies will circulate through blood and lymph, where they will bind to antigens antibodies cannot destroy antigens themselves formation of antibody‐antigen complex (also known as immune complex) will lead to ‐ neutralization, agglutination, precipitation or complement fixation Antibodies Neutralization – Agglutination blocking specific (clumping) – sites on bacterial antibody‐antigen toxins or viruses, so complexes forming that they cannot clump together by injure cells; complex is cross‐linking with eventually degraded other antibody‐antigen by phagocytes complexes Antibodies Complement Fixation – Precipitation – soluble used against cellular molecules are cross‐ antigens (e.g. linked into large bacteria); binding of complexes that settle antibody to antigenic out of solution; determinant of cell precipitated antigen is triggers fixation of easier for phagocytes to complement and lysis of bind and engulf target cell  Immunity HUMORAL IMMUNITY Primary and Secondary Responses: Humoral immunity depends on maturation of B lymphocytes into plasma cells, which produce and secrete antibodies Two types of responses occur in the development of humoral immunity: Primary and Secondary responses  Humoral immunity a primary response occurs when the antigen is first introduced in the body a lag period (about 1 week) occurs before antibody can be detected in blood lag period is due to time needed for cytokine secretion from T‐helper cell to trigger proliferation of B cells into plasma cells that produce the antibody at the same time that plasma cells are produced, a small portion of the activated B cells will produce memory cells  Immunity a secondary response occurs upon second or subsequent exposures to the antigen rise in antibody occurs sooner and reaches a higher level because of memory cells produced at time of primary response memory cells recognize the antigen and respond more efficiently to manufacture antibody Adaptive defenses Humoral immunity Primary response Antigen (initial encounter Antigen binding with antigen) to a receptor on a specific B lymphocyte Proliferation to (B lymphocytes with Activated B cells form a clone non-complementary receptors remain inactive) Plasma cells Memory B cell— (effector B cells) primed to Secreted respond to same antibody antigen molecules Figure 20.11 (1 of 2)  Adaptive defenses Humoral immunity Primary response Antigen (initial encounter Antigen binding with antigen) to a receptor on a specific B lymphocyte (B lymphocytes with Proliferation to non-complementary receptors remain Activated B cells form a clone inactive) Plasma cells Memory B cell— primed to respond (effector B cells) to same antigen Secreted antibody molecules Subsequent challenge by Secondary response Clone of cells same antigen (can be years later) identical to results in more ancestral cells rapid response Plasma cells Secreted antibody Memory molecules B cells Figure 20.11  Secondary immune response to Primary immune antigen A is faster and larger; primary response to antigen immune response to antigen B is A occurs after a delay. similar to that for antigen A. Anti- Anti- bodies bodies to A to B First exposure Second exposure to antigen A; to antigen A first exposure to antigen B Time (days) Figure 20.12 Immunity Active and Passive Humoral Immunity: immunity can be acquired naturally or artificially and it can be active or passive active immunity can be acquired naturally when someone is exposed to a pathogen (ahchoo!!!!) or artificially when someone is immunized (vaccinated) passive immunity can be acquired naturally when antibodies are transferred from mother through placenta or breast milk (thanks mom!) or artificially if and individual is administered antibodies from another source (thanks dude!)  Humoral immunity Active Passive Naturally Artificially Naturally Artificially acquired acquired acquired acquired Infection; Vaccine; Antibodies Injection of contact dead or pass from immune with attenuated mother to serum pathogen pathogens fetus via (gamma placenta; globulin) or to infant in her milk Figure 20.13 Cell mediated immunity T LYMPHOCYTES different types of T cells exist that take part in different aspects of the immune response maturation of different types occurs in thymus gland; mature T cells circulate to peripheral lymphoid tissues in anticipation of binding to antigen T cell receptor (TCR) consists of two polypeptide chains that fold to form a groove that interacts with processed antigen/MHC complexes  possess CD4 molecule on cell surface activation of these cells requires binding to antigen associated with MHC Class II molecule Immunity these cells help activate other cells of immune T‐helper system by secreting stimulating cytokines: B‐cells, T‐cytotoxic cells (CD8), Natural cells Killer cells, & macrophages are activated by T‐ helper cells  possess CD8 molecule on the cell surface become activated after binding to Immunity antigen associated with MHC Class I on abnormal cells as well receiving cytokines from T‐helper cells T‐ abnormal cells are usually body cells infected with virus or transformed by Cytotoxic cancer Cells neighbouring host cells that have MHC Class I molecule without antigen or with a “self‐peptide” will be left alone by T‐cytotoxic cells Immunity T‐regulatory cells release cytokines that will suppress the activity of B cells and other T cells when antigen has been inactivated or destroyed important for winding down immune response also known as T‐suppressor cells T‐Memory cells responsible for secondary response Immunity CYTOKINES regulatory proteins synthesized by many cell types of the immune response; produced primarily by T helper cells and macrophages some cytokines mediate inflammation by inducing fever (e.g. Interleukin‐1. Tumor Necrosis Factor) or act as chemotactic molecules (e.g. Interleukin – 8) most interleukin cytokines function in cell communication between T cells, B cells, macrophages and other immune cells Examples of cytokines Interleukin‐1 > helps to activate T helper cells; secreted by activated macrophages Interleukin‐2 > necessary for proliferation and function of T helper cells, T cytotoxic cells, B and NK cells; secreted by T helper cells Interleukin‐6 > induces differentiation of B cells into plasma cells Tumor Necrosis Factor – alpha > helps activate T cells and phagocytes; secreted by activated macrophages CELL‐MEDIATED IMMUNITY provided by T cells with help from Antigen Presenting Cells activation of T helper cells by binding to antigen/MHC Class II complexes on APCs will lead to proliferation of T helper cells (induced by cytokines) T cytotoxic cells are stimulated to proliferate and differentiate when their receptors binds to antigen/MHC Class I complexes CELL‐MEDIATED IMMUNITY differentiation of T helper cells (in response to cytokines) leads to production of other cytokines which enhance the activity of T‐cytotoxic cells and macrophages destroy target cells by releasing cytolytic enzymes, toxic cytokines, and perforins (pore‐ forming molecules) or by triggering apoptosis in the target cell T‐cytotoxic cells are important for destroying virus‐infected cells, so the virus will not replicate; antibodies cannot perform this function because they cannot penetrate living cells!!!