Chapter 40 Immune Response. Non-Specific vs Specific Response 1.Non-specific immune response...

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Chapter 40 Immune Respons e

Transcript of Chapter 40 Immune Response. Non-Specific vs Specific Response 1.Non-specific immune response...

Page 1: Chapter 40 Immune Response. Non-Specific vs Specific Response 1.Non-specific immune response a.Barriers (skin or mucous lining) b.Stomach secretions,

Chapter 40

Immune Respons

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Page 2: Chapter 40 Immune Response. Non-Specific vs Specific Response 1.Non-specific immune response a.Barriers (skin or mucous lining) b.Stomach secretions,

Non-Specific vs Specific Response

1. Non-specific immune responsea. Barriers (skin or mucous lining)

b. Stomach secretions, tears, and lysozyme

c. Inflammation due to injured cells

2. Specific immune responsea. Cell-mediated immunity

b. Antibody-mediated (Humoral) immunity- complement proteins involved after release of antibodies

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Inflammation response

(Histamines)

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Complement

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Our book calls these effector B cells

Our book calls these effector cytotoxic T cells

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The Immune Story1. Pathogens, either bacteria or viruses, enter the body and begin to

reproduce rapidly.

2. Some pathogens are engulfed by macrophages (large phagocytic cells)

3. As it engulfs the pathogen, the macrophage removes some of the pathogen’s antigens and displays them on its own surface along with its own antigens (antigen-MHC complex)

4. Among the millions of different types of helper T cells that developed in the thymus gland and then were released, a few have receptors that make a perfect “fit” with the antigens displayed on the macrophage membrane.

5. Helper T cells couple with the macrophage causing the macrophage to produce a chemical, interleukin-1 (IL-1). IL-1 is a pyrogen (causes fever) and activates the helper T cells to produce interleukin-2 (IL-2)

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The Immune Story (cont’d)6. IL-2 stimulates the growth and multiplication of vast numbers of identical

helper and cytotoxic T cells. Eventually, the cytotoxic T cells are exposed to the antigens displayed by the macrophage. Cytotoxic T cells (“killer T cells”) chemically puncture pathogens or infected cells.

7. Helper T cells secrete other chemicals that cause B cells to multiply and differentiate into memory B cells and effector B cells.

8. Effector B cells produce antibodies that have binding sites that match the pathogen’s antigens. Some antibodies “stick” to pathogens, slowing them down so they can be easily engulfed by macrophages. Some antibodies can actually help puncture the pathogen’s membrane.

9. As the battle is won, many T and B cells die out, but the memory cells continue to live. These cells circulate for years to prevent a future pathogen of the same type from ever getting started, in other words, producing immunity.

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2nd Exposure to a Pathogen