{"id":2029,"date":"2024-07-23T14:50:26","date_gmt":"2024-07-23T18:50:26","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&p=2029"},"modified":"2025-12-07T23:28:42","modified_gmt":"2025-12-08T04:28:42","slug":"specific-adaptive-immunity-sensitization-of-b-cells-and-activation-of-b-cells-by-helper-t-cells","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/specific-adaptive-immunity-sensitization-of-b-cells-and-activation-of-b-cells-by-helper-t-cells\/","title":{"raw":"5p6 Specific (Adaptive) Immunity - Sensitization of B Cells and Activation of B cells by Helper T Cells","rendered":"5p6 Specific (Adaptive) Immunity – Sensitization of B Cells and Activation of B cells by Helper T Cells"},"content":{"raw":"

1. Sensitization of B cells<\/strong><\/h1>\r\nB cells become sensitized<\/strong> after they phagocytose either pathogen (bacteria, virus) or pathogen antigens.\u00a0 \u00a0This is done with the help of IgD antibody receptors (B cell receptors, BCRs)<\/strong> that bind to specific non-self antigens.\u00a0 Most often these non-self antigens belong to pathogens such as bacteria.\u00a0 Once the bacteria is phagocytosed, the bacteria is degraded and bacterial peptides are bound to <\/span>MHC II molecule<\/strong>s and sent to the B cell surfaces for display.\u00a0 <\/span>The B cell is now termed \u201csensitized\u201d.\u00a0<\/span>\r\n\r\nBCRs actually have a dual role<\/strong>, in that not only do they assist in internalizing pathogens, once they attach to a pathogen, they also stimulate DNA expression of genes required for B cell activity.\r\n

2. Activation of Sensitized B cells that are Displaying Non-Self Antigens by\u00a0<\/strong>CD4+ Helper T cells<\/strong><\/h1>\r\nOnce sensitized, B cells can be activated by activated Helper CD4+ T cells<\/strong>, which do this by using their TCR<\/strong> and CD4<\/strong> co-receptors to bind to the peptide-MHC II molecules<\/strong> on the surface of the B cell.\u00a0 This recognition of a non-self peptide<\/strong> display by the B cell's MHC II, triggers the Helper CD4+ T cell to release cytokines (e.g. lymphokines, specifically interleukins) that activate the B cell.\u00a0 The activated B cell<\/strong> will proliferate producing 2 types of daughter cells:\r\n
    \r\n \t
  • \r\n
      \r\n \t
    • Plasmablasts<\/strong> which differentiate (mature) into Plasma cells<\/strong> that become antibody factories, producing antibodies against the specific bacterial antigens.\u00a0 Plasma cells can produce \u00ac100 million antibodies per hour.\u00a0 The release of different cytokines by Helper T cells is thought to help stimulate which type of antibodies are produced (IgG, IgA, IgE) in addition to the two antibodies that are most predominant in circulating the blood, IgM and IgD.<\/li>\r\n \t
    • Memory B cells<\/strong> that express the specific BCRs that were able to bind to the bacterial antigens.<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\nNote:\u00a0 <\/strong>Helper T cells are essential for the activation of B cells.\u00a0 This becomes apparent in cases of human immunodeficiency virus (HIV), in that the HIV virus can destroy Helper T cells, leading to the inability of B cells to launch an effective humeral immunity.\u00a0 Additionally, this lack of Helper T cells, leads to\u00a0 diminished cytotoxic T cell mediated immune responses.\u00a0 As such, individuals afflicted with HIV can become immunosuppressed and are vulnerable to both opportunistic infections and cancer.\r\n\r\n \r\n

      Summary in Point Form:<\/h1>\r\n
        \r\n \t
      • CD4+ Helper T Cell Activation of Sensitized B Cells<\/strong>\r\n
          \r\n \t
        • Sensitized B Cells<\/strong>\r\n
            \r\n \t
          • B cells use their cell surface IgD receptors (BCRs<\/strong>) to bind to specific pathogens, which the B cells can then phagocytose<\/strong> and destroy, displaying pathogen (e.g., bacterial) peptides on their cell surfaces using MHC II<\/strong><\/li>\r\n \t
          • B cells become sensitized<\/strong> after they have phagocytosed<\/strong> and displayed pathogen antigens.\u00a0 BCRs<\/strong> stimulate DNA expression for B cell activity.<\/li>\r\n \t
          • Sensitized B cells can then be activated<\/strong> by Helper CD4+ T cells<\/li>\r\n \t
          • Once activated by Helper T cells, B cells go through mitosis producing daughter B memory cells<\/strong> and plasmablasts<\/strong> (which mature into plasma cells)<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
          • Activation Process<\/strong>\r\n
              \r\n \t
            • Helper CD4+ T cells use TCR and CD4 co-receptors to bind peptide-MHC II on B cell<\/li>\r\n \t
            • Helper CD4+ T cells then release cytokines (e.g., interleukins) to activate B cells<\/li>\r\n \t
            • Activated B cells proliferate into plasmablasts and memory B cells<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
            • Plasmablasts and Plasma Cells<\/strong>\r\n
                \r\n \t
              • Plasmablasts differentiate into plasma cells, produce antibodies<\/li>\r\n \t
              • Plasma cells can produce ~100 million antibodies per hour<\/li>\r\n \t
              • Cytokines help determine antibody types (IgG, IgA, IgE, IgM, IgD)<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
              • Memory B Cells<\/strong>\r\n
                  \r\n \t
                • Express specific BCRs that bind infecting pathogen\u2019s antigens, maintain memory pool<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t
                • Impact of HIV on Immune Response<\/strong>\r\n
                    \r\n \t
                  • HIV destroys Helper T cells, leading to impaired B cell activation and reduced CD8+ T cell activation<\/li>\r\n \t
                  • Results in diminished humoral immunity and cytotoxic T cell-mediated responses<\/li>\r\n \t
                  • Individuals with HIV are vulnerable to opportunistic infections and cancer<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n ","rendered":"

                    1. Sensitization of B cells<\/strong><\/h1>\n

                    B cells become sensitized<\/strong> after they phagocytose either pathogen (bacteria, virus) or pathogen antigens.\u00a0 \u00a0This is done with the help of IgD antibody receptors (B cell receptors, BCRs)<\/strong> that bind to specific non-self antigens.\u00a0 Most often these non-self antigens belong to pathogens such as bacteria.\u00a0 Once the bacteria is phagocytosed, the bacteria is degraded and bacterial peptides are bound to <\/span>MHC II molecule<\/strong>s and sent to the B cell surfaces for display.\u00a0 <\/span>The B cell is now termed \u201csensitized\u201d.\u00a0<\/span><\/p>\n

                    BCRs actually have a dual role<\/strong>, in that not only do they assist in internalizing pathogens, once they attach to a pathogen, they also stimulate DNA expression of genes required for B cell activity.<\/p>\n

                    2. Activation of Sensitized B cells that are Displaying Non-Self Antigens by\u00a0<\/strong>CD4+ Helper T cells<\/strong><\/h1>\n

                    Once sensitized, B cells can be activated by activated Helper CD4+ T cells<\/strong>, which do this by using their TCR<\/strong> and CD4<\/strong> co-receptors to bind to the peptide-MHC II molecules<\/strong> on the surface of the B cell.\u00a0 This recognition of a non-self peptide<\/strong> display by the B cell’s MHC II, triggers the Helper CD4+ T cell to release cytokines (e.g. lymphokines, specifically interleukins) that activate the B cell.\u00a0 The activated B cell<\/strong> will proliferate producing 2 types of daughter cells:<\/p>\n

                      \n
                    • \n
                        \n
                      • Plasmablasts<\/strong> which differentiate (mature) into Plasma cells<\/strong> that become antibody factories, producing antibodies against the specific bacterial antigens.\u00a0 Plasma cells can produce \u00ac100 million antibodies per hour.\u00a0 The release of different cytokines by Helper T cells is thought to help stimulate which type of antibodies are produced (IgG, IgA, IgE) in addition to the two antibodies that are most predominant in circulating the blood, IgM and IgD.<\/li>\n
                      • Memory B cells<\/strong> that express the specific BCRs that were able to bind to the bacterial antigens.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n

                        Note:\u00a0 <\/strong>Helper T cells are essential for the activation of B cells.\u00a0 This becomes apparent in cases of human immunodeficiency virus (HIV), in that the HIV virus can destroy Helper T cells, leading to the inability of B cells to launch an effective humeral immunity.\u00a0 Additionally, this lack of Helper T cells, leads to\u00a0 diminished cytotoxic T cell mediated immune responses.\u00a0 As such, individuals afflicted with HIV can become immunosuppressed and are vulnerable to both opportunistic infections and cancer.<\/p>\n

                         <\/p>\n

                        Summary in Point Form:<\/h1>\n
                          \n
                        • CD4+ Helper T Cell Activation of Sensitized B Cells<\/strong>\n
                            \n
                          • Sensitized B Cells<\/strong>\n
                              \n
                            • B cells use their cell surface IgD receptors (BCRs<\/strong>) to bind to specific pathogens, which the B cells can then phagocytose<\/strong> and destroy, displaying pathogen (e.g., bacterial) peptides on their cell surfaces using MHC II<\/strong><\/li>\n
                            • B cells become sensitized<\/strong> after they have phagocytosed<\/strong> and displayed pathogen antigens.\u00a0 BCRs<\/strong> stimulate DNA expression for B cell activity.<\/li>\n
                            • Sensitized B cells can then be activated<\/strong> by Helper CD4+ T cells<\/li>\n
                            • Once activated by Helper T cells, B cells go through mitosis producing daughter B memory cells<\/strong> and plasmablasts<\/strong> (which mature into plasma cells)<\/li>\n<\/ul>\n<\/li>\n
                            • Activation Process<\/strong>\n
                                \n
                              • Helper CD4+ T cells use TCR and CD4 co-receptors to bind peptide-MHC II on B cell<\/li>\n
                              • Helper CD4+ T cells then release cytokines (e.g., interleukins) to activate B cells<\/li>\n
                              • Activated B cells proliferate into plasmablasts and memory B cells<\/li>\n<\/ul>\n<\/li>\n
                              • Plasmablasts and Plasma Cells<\/strong>\n
                                  \n
                                • Plasmablasts differentiate into plasma cells, produce antibodies<\/li>\n
                                • Plasma cells can produce ~100 million antibodies per hour<\/li>\n
                                • Cytokines help determine antibody types (IgG, IgA, IgE, IgM, IgD)<\/li>\n<\/ul>\n<\/li>\n
                                • Memory B Cells<\/strong>\n
                                    \n
                                  • Express specific BCRs that bind infecting pathogen\u2019s antigens, maintain memory pool<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n
                                  • Impact of HIV on Immune Response<\/strong>\n
                                      \n
                                    • HIV destroys Helper T cells, leading to impaired B cell activation and reduced CD8+ T cell activation<\/li>\n
                                    • Results in diminished humoral immunity and cytotoxic T cell-mediated responses<\/li>\n
                                    • Individuals with HIV are vulnerable to opportunistic infections and cancer<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n

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