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Microbiology Chap.15
Host Defenses 2: Specific Immunity and Immunization
| Term | Definition |
|---|---|
| Specific Immunity | The Third and final Line of defense |
| Specific Immunity | Acquired only after an immunizing event example: Infection or Vaccination |
| Immunocompetence | The body's ability to react to foreign substances |
| Immunocompetence | Development of B and T LYMPHOCYTES |
| Two Characterizing features of the third line of defense | specificity and memory |
| What does Specificity and Memory do in the third line of defense? | Only recognize certain (specific) pathogens |
| Antigen | anything foreign that activate B-cells and T-cells |
| Immunogen | Any substance that induces a state of sensitivity or resistance after processing by the immune system of the body. |
| Major Histocompatibility Complex (MHC) | series of glycoproteins (MHC molecules) found on the surface of all cells EXCEPT red blood cells |
| Red Blood Cells and MCH | Red blood cells have its own markers |
| If MCH is ABSENT, what will happen to the cell? | The cell will be destroyed by the immune system |
| MHC | mark Self verses Self |
| MHC | present antigens |
| Development of the Dual Lymphocyte System | B-cells and T-cells work together |
| Development of the Dual Lymphocyte System | High level of communication between the two cell types |
| Development of the Dual Lymphocyte System | When antigens are presented, both B-cells and T-cells are activated |
| Steps of the Development of the Dual Lymphocyte System | Step 1: Lymphocyte Development Step 2: Presentation of Antigens Step 3 and 4: T-cell Response |
| Step 1: Lymphocyte Development | All lymphocytes arise from the same basic stem cell type |
| Where do Lymphocytes come from? | come from pluripotential |
| What is Pluripotential? | Stem cells having the developmental plasticity to give rise to more than one type. Example: undifferentiated blood cells in the bone marrow. |
| Step 1: Lymphocyte Development- Final Maturation for B-cells | Occurs in specialized Bone Marrow sites |
| Step 1: Lymphocyte Development- Final Maturation for T-cells | Occurs in the Thymus |
| Step 1: Lymphocyte Development- After maturation of B-cells and T-cells | Both cell types migrate to separate areas in the lymphoid organs "going to the dump to shop" |
| Specific Events in B-cell Maturation | Bone marrow sites harbor stromal cells Stromal cells nuture the lymphocytes stem cells and provide chemocal signals that initiate B-cell development B-cells circulate through the blood, "homing" to specific sites in lymph nodes, spleen, and GALT |
| Specific Events in B-cell Maturation | Adhere to specific binding molecules where they come into contact with antigens |
| B-Cell Receptor | Immunoglobulim receptors (Igs) Y-shaped arrangement Ends of forks (of y shape) contain pockets called the antigen binding sites Can be highly variable in shape to fit a wide range of antigens Variable regions (V)-folk Constant regions (C)-handle |
| Specific Events in T-Cell Maturation | Directed by the thymus gland and its hormones Circulate between the lymphatic and circulatory system, migrating to specific T-cell areas of the lymph nodes and spleen Mature T lymphocytes express T-cell receptor and co-receptors (CD-4 or CD-8) |
| T-Cell Receptor | Constant Region Variable Region Antigen binding site Co-Receptor Never Secreted; always attached |
| Immunological Diversity | 500 gene segments that can be rearranged t produce diverse receptor types |
| Immunological Diversity | *Different B and T cells are made which leads to specificity *By the time B and T cells reach the lymphoid tissue they are equipped to respond to a single, unique antigen *Each line of lymphocytes is termed a clone |
| Step 2: Presenttation of Antigens | Perceived as foreign Antigenic Molecule |
| Antigenic Molecule: Proteins and polypeptides | Enzymes, cell surface structure, hormones, exotoxins |
| Antigenic Molecule: Lipoproteins | Cell membrane |
| Antigenic Molecule: Nucleoproteins | DNA complexes to proteins but not pure DNA |
| Antigenic Molecule: Polysacchararides | Certain bacterial capsules |
| Antigenic Molecule: Haptens | small foreign molecules that are too small to elicit an immune response on their own *if linked yo a larger carrier molecule, them the combination develops IMMUNOGENICITY |
| Role of antigen processing and presentation | *Produce APCs *Engulf the antigen and modify it so it is more immunogenic and recognizable - Epitope *After processing, the antigen is bound to the MHC receptor and moved to the surface of the APC so it is accessible to T lymphocytes |
| What is APC? | APC (Antigen-presenting cells): cells that act upon and formally present antigens to lymphocytes *Macrophages *Dendritic cells (related to macrophages) *B cells |
| Step 3 & 4: B-Cell Response | Activation of B Lymhocytes |
| Activation of B Lymhocytes | *Clonal section and binding of antigen *Antigen processing and presentation *B-cell/ T-cell recognition and copperation (T- Helper) *B-cell activation *Clonal expansion (copies) *Antibody production and secretion *Plasma cells and memory cells |
| What are Memory Cells? | Long term B-cells |
| What are Plasma Cells? | Antibody producer factors that is fighting right now |
| Classes of Immunoglobulins (Igs) | B cell receptors (weight and arrangement) IgM- 1st one made during an infection IgA- important in mucosal defense IgD- acts as a receptor IgG- most prevalent AB IgE- Allergies |
| Antigen- Antibody Interactions | Principal activity of antibody: unite with , immobilize, call attention to, or neutralize the antigen for which it was formed |
| Antigen- Antibody Interactions : Opsonization | plasma cells- antibody marks to kills |
| Antigen- Antibody Interactions: Neutralization | not allowing microorganisms to attach |
| Antigen- Antibody Interactions: Agglutination | accumulate; stick together which prevents it from doing what its suppose to do |
| Antigen- Antibody Interactions: Complement fixation | antibodies cause complement and produce MACs (donuts) which cause them to die |
| Antigen- Antibody Interactions: Antitoxin | Antibodies going totoxin don't allow it to find its target and it dies |
| Monitoring Ab Production: Primary Response | *First exposure *Latent period- lack of antibodies synthesis *Synthesis of antibodies -first IgM, second IgG, then some IgM ad IgA *Titers (In immunochemistry, a measure of antibody level in a patient, determined by agglutination methods.) |
| Monitoring Ab Production: Secondary Response | *Re-expossre to the same immunogens *Antibody synthesis, titer, and length of antibody persistence is rapid and amplified *primary due to memory cells |
| Step 3 & 4: T- Cell Response | Cell-Mediated Immunity (CMI) |
| Cell-Mediated Immunity (CMI) | *require the direct involvement of T lymphocytes throughout the course of the reaction *T cells require some type of MHC recognition before they can be activated *T cells stimulate other T cells, B cells, and phagocytes *Cytokine production |
| What is Cytokine production? | production of chemicals produced by T- cells |
| T cell Activation and Differentiation | *Recognize an antigen only with an MHC carrier *T cell is sensitized when an antigen/ MHC complex is bound to its receptors *The activated T cells then transform in preparation for mitotic divisions and differentiate into one of the subsets |
| T Helper Cells (T H) | *Play a central role in regulating immune reactions to antigens *Involved in activating Macrophages -directly by receptor contact -indirect y by releasing cytokines |
| T Helper Cells (T H) | *Secrete interleukin-2 (type of cytokine) *some secrete interleukin- 4,5, and 6 (help activate B-cells) |
| T Helper Cells (T H): Secrete interleukin-2 | stimulates the primary growth and activation of many types of T cells |
| T Helper Cells (Th): secrete interleukin- 4,5, and 6 | stimulate various activities of B-cells |
| Regulatory T Cells (Tr) | *T-cells regualte *Maintain "Happy Medium" *Carry CD4 markers *Control Inflammation *Prevent Autoimmunity *Prevent immune response against normal flora |
| Cytotoxic T Cells (Tc) | *Cytotoxicity *Target cells that Tc cells can destroy include: Virally infected cells, cancer cells, and cells from other animals and humans *After activation the Tc cell severely injures the target cell- secrerion of perforins and granzymes |
| What is Cytotoxicity? | the capacity to kill a specific target cell |
| What are Perforins? | Proteins released by cytotoxic T cells that produce pores in target cells |
| What is Granzymes? | Enzymes secreted by cytotoxic T cells that damage proteins of target cells. |
| Natural Killer Cells (NKC) | *Related to T- cells *Lack specificity for antigens *Circulate through the spleen, blood, and lungs *Probably the first killer cells to attack cancer cells and virus-infected cells |
| Vaccines | Whole bacterial cell or virus -Killer cells or inactive viruses- dead -Live, attenuated cells or viruses- softened Antigenic molecules derived from bacterial cells or viruses |
| Whole bacterial cells or virus: Dead | dead organisms are safest less effective immunogens wrong POE (portal of entry) |
| Whole bacterial cells or virus: Live | live organisms offer better response mimic actual infection mutate back to virulent form |
Created by:
Jervetteg
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