Specific Immune response

• 1. Pathogen is engulfed and its antigens are presented by a macrophage (an antigen presenting cell)
  2. The complementary receptor of a specific T-cell binds with the presented antigen
  3. The specific T-cell is activated (clonal selection)
  4. The T-cell undergoes mitosis. This is clonal expansion.
  5. Genetically identical T-cells differentiate.
  6. Either cytotoxic T-cells, memory T-cells or T helper cells are formed.
  7. Receptors of cytotoxic T-cells bind to specific antigens presented by the infected cells. They secrete perforin and destroy these infected cells.
  8. T helper cells activate specific B cells.
• T lymphocytes are made in the bone marrow. They mature in the thymus.
• T lymphocytes- involved in the cell mediated response, which targets pathogens which have entered our cells. For example, viruses , the bacterium that causes tuberculosis or our own cells which have become abnormal (cancer cells, cells of transplanted tissues).
• B lymphocytes mature in the bone marrow.
• B lymphocytes- involved in the humoral response, which involves the production of antibodies which can attack pathogens that are in our blood or other body fluids.
• Helper T cells release chemical signals called cytokines, which stimulate phagocytes and also activate specific B cells which then divide.
• Cytotoxic T cells recognise body cells infected by pathogens because the infected cell will have some of the pathogen's antigens on its surface. The cytotoxic T cell binds to these antigens and secretes perforin, which makes holes in the cell surface membrane of the targeted cell. The cell surface membrane becomes freely permeable to all substances, so the cell dies along with any pathogens.
• 1. Pathogen is engulfed and the antigens are presented by the macrophage (an antigen Presenting cell).
  2. Specific T-cells are activated. These undergo mitosis and differentiate into T-helper cells.
  3. Meanwhile, a B-cell has specific antibodies on its cell surface membrane.
  4. The pathogen with complementary specific antigens binds to these antibodies. It enters the B-cell by endocytosis.
  5. The pathogen is then hydrolysed by enzymes and its antigens are presented on the B-cell's surface.
• 6. The specific, activated T helper cells bind to the processed antigen and activate the B-cell (clonal selection).

  7. The B-cell undergoes mitosis to form clones (clonal expansion).

  8.These differentiate into plasma B cells and memory B cells.
• Plasma B cells secrete antibodies into the blood. They are only able to survive for a few days but each can make around 2000 antibodies per second.
• Memory B cells do not produce antibodies, but can live for decades. When they encounter the same antigen, they divide rapidly and differentiate into plasma B cells and more memory B cells. This provides long term immunity.
• Because it takes less time for one of many memory B-cells to encounter the antigen then in the first exposure, the secondary immune response is much faster and produces higher levels of antibodies.
• 1. Pathogen is engulfed and its antigens are presented by a macrophage (an antigen presenting cell)
  2. The complementary receptor of a specific T-cell binds with the presented antigen
  3. The specific T-cell is activated (clonal selection)
  4. The T-cell undergoes mitosis. This is clonal expansion.
  5. Genetically identical T-cells differentiate.
  6. Either cytotoxic T-cells, memory T-cells or T helper cells are formed.
  7. Receptors of cytotoxic T-cells bind to specific antigens presented by the infected cells. They secrete perforin and destroy these infected cells.
  8. T helper cells activate specific B cells.