Chapter 22 - Immunity B-cell Activation and Antibodies Lecture 3 - PDF

Part 1: From B-Cell to Plasma Cell Activation Process, and General Anatomy and Functionality of Antibodies. Part 2: The 5 Classes of Antibodies and Their Specific Functions.      Antibody-mediated immunity; secrete antibodies when “activated.” (not abundant in plasma) B-cells have 1) antibody (...

Part 1: From B-Cell to Plasma Cell Activation Process, and General Anatomy and Functionality of Antibodies. Part 2: The 5 Classes of Antibodies and Their Specific Functions.      Antibody-mediated immunity; secrete antibodies when “activated.” (not abundant in plasma) B-cells have 1) antibody (Ab) molecules on PM surface to recognize & bind foreign antigens. 2) produce MHC2 proteins - allow Helper T cells bind after phagocytosis. The initial activation process = sensitization = bind antigen to surface Ab, endocytose & process it, and attach to MHC2 starts the “activation” phase. Sensitized B-cell – B-cell with antigen presented on surface of PM via MHC2. ◦ Needs cytokine from helper T-cell to “activate” the Bcell, which leads to plasma cells    CD4, Helper T-cells secrete cytokines, which? Activates B-cells producing 2 cell types. (22.23) Plasma B-cells synthesize and secrete? ◦ Antibodies into interstitial fluid (IF).  Memory B-cells remain in reserve for subsequent infections of same pathogen w/greater response.  antigen bound to the antibody & can now function. 1) Neutralization – binding of Abs to viral & bacterial (+toxin) antigen’s surfaces disabling them from attaching to & infecting cells.  2) Prevention of Bacterial and Viral Adhesion    ◦ Abs coat epithelial surface to prevent adherence; makes it hard to penetrate body. 3) Linked antigens-antibody complexes forming precipitates (soluble toxins become insoluble) or causes agglutination (cell clumping). 4) Stimulates inflammation by activating...? ◦ Basophils + mast cells; both secrete heparin + histamines.  5) Attraction of phagocytes – ◦ Antigens covered in Abs attract phagocytes to destroy cell.  6) Activation of Complement ◦ Binding of antigen causes Ab molecular shape to change allowing it to bind compliment proteins  7) Leads to opsonization? – ◦ Ab coat attracts phagocytes + bind compliment proteins, which = enhancement of phagocytosis  The amount or levels of Abs in the blood = antibody titer ◦ Primary (initial response) takes 1-2 weeks to peak  Y-shaped molecule consisting of 2 parallel pairs of polypeptide chains; ◦ a pair of heavy chains; a pair of light chains  Constant segments of heavy chains form base of Ab. ◦ Plasma cells produce 5 constant segments = determines how it’s secreted, distributed, & the class of Ab it will be. ◦ Variable (tipped) Segments – determine specificity.  Of light & heavy chain ◦ Tips of the variable segment = antigen binding site.  Determined by AA seq.   Constant segments of the heavy chains. It is estimated that humans have 10 trillion B cells, which result in millions of B-cell populations. ◦ Highly variable.  Mature naïve B-cells undergo “class switching,” based on cytokines present.  Most antigens have multiple Antigenic Determinant Sites or Epitopes = binding site for Abs. meaning several B cells can bind to same pathogen or toxin.  When Abs bind to antigen, this forms? ◦ Antigen-Antibody Complex. Part 1: From B-Cell to Plasma Cell Activation Process, and General Anatomy and Functionality of Antibodies. Part 2: The 5 Classes of Antibodies and Their Specific Functions.  Immunoglobulins (Igs) ◦ IgG, IgD, IgE, IgM, and IgA, found in body fluids.  1) IgD = bound to B cell surfaces; binding of antigen causes? ◦ B cell sensitization; activation allows class switching  2) IgM = First Ab secreted via plasma cells after antigen encounter; likely on surface w/IgD. ◦ Circulates as a 5-Ab “starburst.” ◦ Conc. decline as IgG production accelerates.  IgM will attack bacteria insensitive to IgG. ◦ The anti-A + B Abs for blood typing are IgM Abs.  3) IgG = largest class (~80%) of Abs. ◦ resistance against viruses, bacteria, + toxins.  IgE = bound to basophils + mast cells; antigen binds causes? ◦ Release histamine + others stimulating inflammation. ◦ Part of allergic response.  IgA found in glandular secretions: ◦ mucus, tears, saliva, and semen.    Epithelial cells absorb them from blood prior to secretion; Attack pathogens prior to access into tissues. MPs: Ig’s are found w/in fluids to help fight infections. IgD & IgM present on membranes. Once activated, class switching may occur.     IgM = first class secreted; IgD = surface of B-cells IgG = most diverse and highest in blood; IgE = inflammation (mast cells)+ allergic response. IgA = glandular secretions  Initial immune response; takes 1-2 weeks to elicit strong response; response decline quickly. ◦ NOTICE: IgM released first; then IgG takes over.  exposure to the same antigen. ◦ Activation of memory B-cells even at lower antigen conc. Secrete Abs in massive quantities. (22.24)     Bacterial attack first neutrophil, NK cells, + macrophages; Cytokine release attracts phagocytes. Antigen presentation activates cytotoxic Tcells, Helper Tcells + B-cells. Ab levels increase leading to pathogen death.      Infection of cells Interferon release. Activation of cytotoxic and helper T-cells. TH-cells activate B-cells. Ab production helps destroy virus.