Transcript B cell
Immune System •Skin pH=3-5 •Secretions •Lysozyme •Tears •mucus, •saliva Mucus Membranes Phagocytic cells Migrate OUT of the blood when the sense differences in concentration of certain chemicals engulf bacteria, dead cells, etc…. Recognize surface molecules on abnormal cells (cancerous or virus infected) Pin Swelling Skin surface Bacteria Chemical signals Phagocytes and fluid move into area Phagocytes White blood cell Blood vessel 1 Tissue injury; release of chemical signals such as histamine link 2 Dilation and increased leakiness of local blood vessels; migration of phagocytes to the area 3 Phagocytes (macrophages and neutrophils) consume bacteria and cell debris; tissue heals Fig. 24-2a Pin Skin surface Bacteria Chemical signals White blood cell Blood vessel 1 Tissue injury; release of chemical signals such as histamine Fig. 24-2b Swelling Phagocytes and fluid move into area 2 Dilation and increased leakiness of local blood vessels; migration of phagocytes to the area Fig. 24-2c Phagocytes 3 Phagocytes (macrophages and neutrophils) consume bacteria and cell debris; tissue heals Lymphatic system includes: -vessels (with valves) -fluid (lymph) -organs Important cells involved are T lymphocytes and B lymphocytes These cells are responsible for specific immune responses to specific pathogens Acquired Immunity (the immune response) •Is highly specific •Produces antibodies in response to specific antigens •Antigens may be molecules on bacteria, viruses, protozoa, worms, transplanted organs •Both B and T lymphocytes have receptors on membrane that recognize different antigens B cells -mature in bone - produce antibodies -antibodies float through the blood, recognizing and attaching to antigens T cells -mature in thymus -do not produce antibodies -cytotoxic T cells - require cell/cell contact to destroy pathogen Both B cells and T cells can produce memory cells Fig. 24-5a Cell-mediated immune response Humoral immune response Bone marrow Stem cell Thymus Via blood Immature lymphocytes Antigen receptor Antigen receptor B cell T cell Via blood Lymph nodes, spleen, and other lymphatic organs Final maturation of B and T cells in lymphatic organ Fig. 24-5a Cell-mediated immune response Humoral immune response Bone marrow Stem cell Thymus Via blood Immature lymphocytes Antigen receptor Antigen receptor B cell T cell Via blood Lymph nodes, spleen, and other lymphatic organs Final maturation of B and T cells in lymphatic organ T cells are selected B cells are selected -antibody producing plasma cells are produced Person feels ill while these cells are produced Symptoms diminish as these cells do their job Response is much faster Memory cells are activated -tend to have a stronger response than the primary Fig. 24-7aa-1 Primary immune response B cells with different antigen receptors 1 Antigen receptor (antibody on cell surface) Fig. 24-7aa-2 Primary immune response B cells with different antigen receptors 1 Antigen receptor (antibody on cell surface) 2 Antigen molecules Fig. 24-7aa-3 Primary immune response B cells with different antigen receptors 1 Antigen receptor (antibody on cell surface) 2 Antigen molecules 3 First exposure to antigen Cell activation: growth, division, and differentiation Fig. 24-7aa-4 Primary immune response 1 B cells with different antigen receptors Antigen receptor (antibody on cell surface) 2 Antigen molecules 3 First exposure to antigen Cell activation: growth, division, and differentiation Antibody molecules 4 First clone Endoplasmic reticulum Plasma (effector) cells secreting antibodies Fig. 24-7aa-5 Primary immune response 1 B cells with different antigen receptors Antigen receptor (antibody on cell surface) 2 Antigen molecules 3 First exposure to antigen Cell activation: growth, division, and differentiation Antibody molecules 4 First clone 5 Endoplasmic reticulum Plasma (effector) cells secreting antibodies Memory cells Fig. 24-7aa-6 Antigen molecules 6 Second exposure to same antigen Secondary immune response (May occur long after primary immune response.) Antibody molecules Endoplasmic reticulum Second clone Plasma (effector) cells secreting antibodies Memory cells Fig. 24-12-1 1 T cells work by directly binding to infected cells and then destroying them Cytotoxic T cell binds to infected cell Self-nonself complex Infected cell Perforin molecule Foreign antigen Cytotoxic T cell Fig. 24-12-2 1 Cytotoxic T cell binds to infected cell Self-nonself complex Infected cell Foreign antigen Perforin molecule Cytotoxic T cell 2 Perforin makes holes in infected cell’s membrane and enzyme enters Hole forming Fig. 24-12-3 1 Cytotoxic T cell binds to infected cell Self-nonself complex Infected cell Foreign antigen Perforin molecule Cytotoxic T cell 2 Perforin makes holes in infected cell’s membrane and enzyme enters Hole forming 3 Infected cell is destroyed Allergies Hypersensitivity to environmental antigen (allergen) Antibodies attach to mast cells - later, allergen attaches to these antibodies on mast cells Histamine & other inflammatory agents released Fig. 24-17a B cell (plasma cell) Mast cell Antigenic determinant 1 Histamine 3 Antibodies attach to mast cell Sensitization: Initial exposure to allergen Allergen (pollen grain) 2 B cells make enters bloodstream antibodies Fig. 24-17b 4 Allergen binds to 5 Histamine is released, causing antibodies on allergy symptoms mast cell Later exposure to same allergen Anaphylactic shock Acute reaction to allergen Massive dilation of blood vessels -drop in blood pressure Counteracted by epinephrine Active immunity results from natural recovery from infections vaccinations Passive immunity Receive antibodies from someone else -IgG anitibodies cross placenta -breast milk -shots (rabies treatment) Transfusions/transplants ABO blood group -IgM doesn’t cross placenta Antibodies produced against bacterial antigens which are very similar rH factor -IgG crosses placenta Tissue graphs/ organ transplants Give drugs that suppress cell mediated immunity Bone marrow transplants Risk of graft vs host reaction Donor lymphocytes attack host cells Autoimmune diseases Immune system doesn’t recognize “self” and attacks MS Insulin dependent diabetes HIV infection of cells require CD4 -found on T cells Is a retrovirus Antibodies are ineffective because -provirus gives it “invisibility” -rapid rate of mutation -Helper T cells decrease -secondary infections Drug treatments slow viral replication -AZT (reverse transcriptase inhibitors) -protease inhibitors