Immune System

Skin Secretions Lysozyme Tears mucus, saliva Innate Defenses External defenses Skin Secretions pH=3-5 Lysozyme Tears mucus, saliva

Mucus Membranes

Internal Innate Defense: Phagocytosis Phagocytic cells Migrate OUT of the blood when the sense differences in concentration of certain chemicals engulf bacteria, dead cells, etc….

Natural Killer Cells Recognize surface molecules on abnormal cells (cancerous or virus infected)

Inflammatory response Pin Skin surface Swelling Bacteria Phagocytes and fluid move into area Phagocytes Chemical signals White blood cell Blood vessel 1 Tissue injury; release of chemical signals such as histamine 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 link

Pin Skin surface Bacteria Fig. 24-2a Pin Skin surface Bacteria Chemical signals White blood cell Blood vessel 1 Tissue injury; release of chemical signals such as histamine

Dilation and increased leakiness of local blood vessels; migration of 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

Phagocytes (macrophages and neutrophils) consume 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

-do not produce antibodies -cytotoxic T cells 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

Humoral immune response Cell-mediated immune response Fig. 24-5a Humoral immune response Cell-mediated 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

Humoral immune response Cell-mediated immune response Fig. 24-5a Humoral immune response Cell-mediated 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

Primary Immune Response 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

Secondary Immune Response Response is much faster Memory cells are activated -tend to have a stronger response than the primary

Primary immune response Antigen receptor (antibody on cell surface) Fig. 24-7aa-1 Primary immune response 1 Antigen receptor (antibody on cell surface) B cells with different antigen receptors

Primary immune response Antigen receptor (antibody on cell surface) Fig. 24-7aa-2 Primary immune response 2 1 Antigen receptor (antibody on cell surface) Antigen molecules B cells with different antigen receptors

Primary immune response Antigen receptor (antibody on cell surface) Fig. 24-7aa-3 Primary immune response 2 1 Antigen receptor (antibody on cell surface) Antigen molecules B cells with different antigen receptors 3 First exposure to antigen Cell activation: growth, division, and differentiation

Plasma (effector) cells secreting antibodies Fig. 24-7aa-4 Primary immune response 2 1 Antigen receptor (antibody on cell surface) Antigen molecules B cells with different antigen receptors 3 First exposure to antigen Cell activation: growth, division, and differentiation Antibody molecules 4 Endoplasmic reticulum First clone Plasma (effector) cells secreting antibodies

Plasma (effector) cells secreting antibodies Memory cells Fig. 24-7aa-5 Primary immune response 2 1 Antigen receptor (antibody on cell surface) Antigen molecules B cells with different antigen receptors 3 First exposure to antigen Cell activation: growth, division, and differentiation Antibody molecules 4 5 Endoplasmic reticulum First clone Plasma (effector) cells secreting antibodies Memory cells

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 T cells work by directly binding to infected cells and then destroying them 1 Cytotoxic T cell binds to infected cell Self-nonself complex Foreign antigen Infected cell Perforin molecule Cytotoxic T cell

Perforin makes holes in infected cell’s membrane and enzyme enters Fig. 24-12-2 1 Cytotoxic T cell binds to infected cell 2 Perforin makes holes in infected cell’s membrane and enzyme enters Self-nonself complex Hole forming Foreign antigen Infected cell Perforin molecule Cytotoxic T cell

Perforin makes holes in infected cell’s membrane and enzyme enters Fig. 24-12-3 1 Cytotoxic T cell binds to infected cell 2 Perforin makes holes in infected cell’s membrane and enzyme enters 3 Infected cell is destroyed Self-nonself complex Hole forming Foreign antigen Infected cell Perforin molecule Cytotoxic T cell

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

Antigenic determinant Histamine Fig. 24-17a B cell (plasma cell) Mast cell Antigenic determinant Histamine 1 Allergen (pollen grain) enters bloodstream 2 B cells make antibodies 3 Antibodies attach to mast cell Sensitization: Initial exposure to allergen

Later exposure to same allergen Fig. 24-17b 4 Allergen binds to antibodies on mast cell 5 Histamine is released, causing allergy symptoms 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 Passive 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

AIDS 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