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  1. Definitions:
    Immune System
    Immunity: response to foreign substance

    Antigen: substance that stimulates immune response; foreign

    Immune system: all of the cells, chemicals and actions which are involved in responding to a foreign substance (antigen)

    Epitope: portion of an antigen recognized by antibodies or T Cells.
    I. Serum: Fluid portion of blood (no anticoagulants in collection); contains plasma: platelets + anticoagulants & Complement: group of proteins help fight infections

    • II. Hematopoietic stem cells (from bone marrow-stem cells)
    • 1. Erythrocytes- RBC
    • 2. Platelets
    • 3. LEUKOCYTES OR WHITE BLOOD CELLS: in blood & tissues of myeloid/lymphoid origins; part of immune system in 2nd & 3rd line of defense
  3. Granulocytes
    • Myeloid Lineage; help the body fight bacterial infections: lobed nucleus w/ granular cytoplasm
    • Basophils: Fight infections

    Eosionophils: fight parasitic infections

    Neutrophils: Fights bacterial infection; phagocytic; produces inflammatory cytokines: chem messengers that leave cell and produce redness
  4. Macrophages
    • -Leukocyte; Myeloid lineage;
    • -in blood matures as macrophages in tissues *NOT IN BLOOD*
  5. Mast cells
    • -Leukocyte; Myeloid lineage;
    • -responsible for allergies & histamine release; fights parasitic/helminthes infections in tissues)
  6. Natural Killer Cells & Lymphocytes:
    -Lymphoid Origin: in the blood until differentiated into effector cells.

    Natural Killer Cells: kill some virus infected cells and cancer cells

    • Lymphocytes: SPECIFIC immunity (two kinds:
    • -->B Lymphocytes: provide humoral immunity; develop in bone marrowplasma cells. Produces antibodies:  proteins fight infection when activated by specifically recognizing antigens.
    • -->T Lympocytes: provide cellular immunity; made in thymus (above <3); “tolerance” to self-antigens occurs during development immunity
  7. Dendritic Cells (DC)
    Leukocyte;important link b/w innate & cellular immunity; some have myeloid immunity
  8. First line of defense:
    • -chemical/Physical barriers
    • A. Skin: mucus membranes
    • B. Lysozyme: works against peptidoglycan
    • C. Stomach acid low pH
    • D. Respiratory tract cillia
  9. Second line of defense:
    -complement, opsonization, interferons, phagocytosis
    • -complement:   proteins in  serum; work with or w/o antibodies to destroy cells to get rid of cellular microbes & opsonization
    • -Interferons: made by virally infected cells; help protect other cells from infection by making warning proteins (non-specific; for any virus)
    • -Phagocytosis by Macrophages (myeloid mononuclear) & Neutrophils (polymorpho granulocyte): engulfment & digestion of something by a cell; produce cytokines/chemokines
  10. Complement & Opsonizaton:
    -Two pathways: Alt & Classical
    • a. Opsonization: microbe is coated for recognization by complement proteins -->Lysis of pathogen: poking holes in membrane “Membrane Attack Complex”
    • b. Two pathways: Alternative & Classical

    • Alternative pathway: active all the time; doesn’t require antibodies. C3B (activated protein) binds to ANY cells and assembles another complement proteins (C35,etc): host cells inactivate this BUT  in “foreign” cells it leads to Opsonization & MAC formation
    • Classical pathway: requires antibodies in specific immunity
  11. Cytokines & Chemokines
    ---> 4 signs of inflamation:
    -Chemokine IL-8:
    -Cytokines IL-1, IL-6 &TNF-alpha:
    • Produce by neutrophils and macrophages;chemical signals used by immune cells; combined actions lead to inflammation at infection site
    • --> 4 signs of inflamation: Heat & Redness (increased blood flow), pain, and swelling (increased permeability of blood vessels).
    • a. Chemokine IL-8: recruits more phagocytes.
    • b. Cytokines IL-1, IL-6 &TNF-alpha: cause fever (WBC work better since bacteria dislike heat) and allow immune cells to work better.
  12. How Macrophages phagocytose microbes (innate)
    -TLR4 Receptor
    -Phagosome & Lysosomes
    -MHC2 antigen
    -what microbes adapted to evade this step?
    complement proteins (C3B-activated) are on the antigens; recognized by macrophages/neutrophils that have "complement receptors" that bind C3B--> then CD14 proteins on macrophages then bind to LPS cells (gram neg) --> works with TLR4 receptor on macrophage (to start transcription/translation of genes to start making inflammatory cytokine).

    Then macrophage performs phagocytosis by joining a phagosome (vesicle/vehicle for antigen) and a lysosome (digestive enzymes) to make a phaglosome.Remaining bits become MHC2 peptide used on surface of APC cells. MHC2 antigen (a peptide from original gram neg cell) which later communicate with specific immunity

    **Note: Listeria monocytogenes: escape the phagosome  & Mycobacterium tuberculosis adapted to evade this step**
  13. Third Line of Defense:
    • -SPECIFIC DEFENSE: cells/chemicals of immune system; specific acquired immunity: antigen only activated when the specific antigen is encountered; WBC: B & T lymphocytes
    • - APC's & MHC's
    • - B Lympocytes Antibodies
    • - T Lymphocytes
  14. Antigen Presenting Cells
    -Three APC's?
    -First T helper cell to be alerted?
    • -have MHC 2 presented on surface for T Helper cells..
    • APC's include:
    • Macrophages (phagocytosis)
    • Dendritic cells (phagocytosis)
    • B cells: have Immunoglobulin /BCR/antibody on surface to specifically bind viruses or bacteria or other antigen

    -MHC 2: surface of APC ONLY; displays peptides from phagocytosed pathogens like bacteria; Recognized by T Helper Cell (CD4+  T cells= first to be alerted)
  15. MHC cells:
    -how many complexes?
    -MHC 1
    • "Major histocompatibility complex": proteins located on surface of host cells and present antigenic peptides to T Cells; two types w/ 6 diff complexes: half are MHC 1 and rest are MHC 2.
    • -Polymorphisms :MHC vary in alleles, reason why blood transfusions trigger immune responses.
    • -->MHC 1: displays intracellular pathogen peptides on all host cells; recognized by cytotoxic T Lymphocytes ( CTL/ CD8+ T cells); HLA-A,B&C

    -->MHC 2: surface of APC ONLY; displays peptides from phagocytosed pathogens like bacteria; Recognized by T Helper Cell (CD4+  T cells= first to be alerted)
  16. B Lymphocytes:
    -immunity type:
    -structure: Progression of one infection vs. Diff infections
    -constant & variable regions
    • -humoral immunity: humoral response is mediated by B-cells (that produce plasma cells that produce antibodies)
    • -develop in the bone marrow
    • -antibodies/Immunoglobulins: proteins made by B cells during a specific immune response.

    -Structure: two light & heavy polypeptide covalent chains with a constant region: determines class of antibodies; 5 diff constant & variable regions

    -variable regions: binds to conformational epitope of antigen—allows for specificity (“Ig” part)  ; millions of variable.

    -->During progression of one infection: Cells can change constant region and keep variable region the same as infection progresses. With different infections: certain constant region and variable region specific to that
  17. Diversity in variable regions of antibodies
    -when does it cocur
    -Gene rearrangement & Somatic Hypermuation
    • -occurs BEFORE encountering the antigen.  B & T cells have less genes;
    • -Gene Rearrangements at DNA level w/ different combinations of light and heavy chains
    • -mistakes in joining gene segments occurs;
    • -“somatic hypermutation”: mutations in variable region occur AFTER encountering the antigen (during proliferation of genes that code for the variable region)
  18. Antibody Classes:
    -based on what structural region
    -how do isotypes swtich
    -five classes
    • -based on the constant region;
    • -these isotypes can switch (retain same specificity but use a diff constant region thru alterations in DNA by editing cutting/splicing out variable region genes in RNA)

    a. IgM: membrane bound; 1st antibody secreted; works w/ classical complement pathway (specific); works in agglutination

    b. IgG: Blood/tissues; most common in blood; type 2& 3 Hypersensitive reaction (see later notes)

    c. IgA: mucosa/secretions (breastmilk)

    d. IgD: membrane bound

    e. IgE: works w/ mast cells to respond to allergies & parasitic functions; involved in Type I Hypersens. Reaction
  19. How do B Lymphocytes specifically respond to infection:
    -Membrane bound antibody ?
    -monoclonal antibodies secreted

    -THREE examples of how antibodies specifically fight infections:
    • Naïve B cells has membrane bound antibody which encounters antigen==> differentiate into plasma cell and secretes antibody which binds to antigen.
    • a. Naïve B cell have membrane bound antibody which allows to recognize antigen (IgM or IgD)
    • b. Secreted antibody: after activation and differentiation, naïve B cells become plasma cells (clones)-secrete same/monoclonal antibodies into plasma

    • THREE examples of how antibodies specifically fight infections:
    • i. Bind & neutralize exotoxins/viruses by surrounding membrane so that virus can’t use surface proteins to activate at target site after traveling in blood stream.
    • ii. Opsonization: bind to bacteria and help phagocytose small cellular pathogens.
    • iii. Activate complement (innate immunity)classical pathway to poke holes in pathogen cells; example  of how innate and specific defense work together.
  20. Clonal Deletion:
    Removal of B Cells which react too strongly with self-antigens to prevent production of antibodies that attach self-antigens.
  21. T Lymphocytes:
    -->On  surface:
    • --cellular immunity; lymphocytes; part of specific immunity
    • -migrate out of marrow & mature in Thymus; undergo selection process to make sure they can recognize MHC and won’t react against self-antigens.

    • -->On  surface:
    • a.T-Cell Receptors (recognize MHC & peptide from antigens)
    • b.CD4 or CD8 (T Helper Cells)
    • c.other proteins
  22. CD4+  T cell Receptors:
    -“BOSS”; has CD4 & T Cell Receptor; has two roles:

    i. antigen recognition: “Sounds alarm”, APC stimulates T Helper cell (CD4+) by 2 signals including MHC2/peptide; occurs in lymph nodes, spleen, tonsils, salivary glands, etc

    • ii. activating other WBC’s:  Naïve T helper cell produces cytokines (chem messengers) so that:
    • (1)CD8+ cytotoxic T Cells are ready to kill infected host cells
    • (2) B cell-->plasma cells which secrete antibodies
    • (3) activate macrophages (phagocytosis); one of the cytokines is IL-2 (a cell growth factor; stimulates proliferation) *know it*
  23. CD8+ Cytotoxic T lymphocytes (CTL):
    -activated by?
    -perforins & granzymes
    -Apostosis vs Necrosis
    • -has CD8 and T Helper Cell
    • -activated by CD4+ cells; divide and kill infected cells: Apoptosis (cell suicide)
    • -CTL’s recognize MHC 1/antigen complex on host cells; perforins (pokes holes in cell membrane) and granzymes (proteases) allow programmed cell death/suicide; neat death so viruses are stuck inside
    • -BETTER than necrosis: water balloon pops-->messy.
  24. CD4+  T Cell Subsets:
    helps w/ cellular and humoral immunity and maintain tolerance (CD25)
    1. Antigen Recognition
    2. Activation: clonal expansion, differentiation, gene rearrangement
    3. Effector Phase
    1. ANTIGEN RECOGNITION (“Sounding the Alarm”):  Antigen Presenting cells stimulate CD4+ (helper T cells) w/ at least 2 signals such as MHCII/Peptide which interacts with T-Cell Receptor on the T Helper cell. Once activated,  CD4+/T Helper Cell produces IL-2 cytokine (growth factor) so that T-Cells can divide and proliferate.

    • 2. ACTIVATION (“Prepare to Fight”): Activated CD4+ makes cytokines that will activate other T-Cells such as CTL’s to become ready to kill infected host cells, B Cells to become plasma cells and macrophages activated.
    • -->B & T cells undergo Clonal expansion (division  and duplication of many identical daughter cells) and Differentiation (cytokines produce development changes in the cells to express new genes when encountering the antigen)
    • -->Note: “Clonal Selection hypothesis”: T & B cells already have receptor specificity before exposure to the antigen; so clonal expansion and differentiation is choosing from one of these “pre-made” cells (one billion variations in receptor specificity) and cloning it.
    • -->“Gene Rearrangement”:  The molecular reason for the diversity of receptor specificity; DNA of T/B Cells is shorter due to rearrangement or changes during cell development. Occurs by splicing DNA segments and ligating remaining pieces (and mistakes just add to diversity)

    3. EFFECTOR PHASE:  Pathogens/infected host cells are destroyed; B Cells make antibodies; Macrophages phagocytose & kill pathogens BETTER; CTLs kills infected cells (apoptosis)
  26. Primary & Secondary Immune Responses:
    -antibody titer
    A. Primary: Response to a NEW antigen; takes time to develop specific immune response to it (undergo the three specific immune response phases where IgM & IgG made mostly) but B & T cells can become memory cells that remain in body along with antibodies; “Antibody titer”: The amount of antibodies against a particular antigen; measure in serum of blood sample.

    B. Secondary: Much quicker response due to previous exposure to antigen and memory B/T cells (why vaccinations work well—secondary
  27. Lymphatic System:
    -Lymph Role in infection
    Pathway: Lymph fluid (was once blood that loses fluid into capillaries and tissues) and WBC’s which patrol tissues move to the nearest lymph node--> returned to heart--> join blood again.

     Lymph Organs: Nodes (armpit, neck, groin), spleen, tonsils, salivary glands, etc.

    • 3. Lymph role in infection: APC’s/macrophages after phagocytosis move to nearest lymph node where and naïve lymphocytes specific for the antigen meet them…
    • “swollen glands”: sign body is seriously fighting an infection
  28. Tolerance
    ability of immune system to recognize/tolerate self antigens w/o triggering immune response; developed by T/B cells during development by destroying autoreactive lymphocytes
  29. Autoimmunity & examples:
    when host immune system sees self antigens as foreign & attacks it.

    • 1. Multiple Sclerosis: attacks myelin
    • 2. Lupus: attacks nuclear antigens
    • 3. Rheumatoid arthritis: attacks joins; swollen painful joints
    • 4. Type I diabetes: attacks insuling producing cells in pancreas.
  30. Four Types of Hypersensitivity Reactions
    -Type 1: systemic and Local symptons
    -mast cells
    • Type I ( IgE mediated, soluble antigen): response to harmless antigen so that Mast Cells (in tissues; release cytokines, histamine, leukotrienes which cause the symptoms) bind to IgE  and IgE antbodies bind antigen when it is encountered again.
    • --> Systemic symptoms: reacts to ingest/injected allergens and release of mast cell chemicals-->drop in BP and anaphylactic shock.
    • --> Local symptoms: caused by asthma, hay fever symptoms & hives; very sensitive to small amts of antigen.

    Type II (IgG): penicillin allergies & RH incompatibility

    Type III (IgG): Immune complexes like Lupus; antibodies grab onto each other and stick to an antigen to create clumps where large clumps are phagocytosed but intermediate sized get stuck in tissue and cause pain.

    Type IV (delayed): Based on T Cell reactions; memory T cells respond quickly to macrophage that present antigen and active macrophages to cause inflammation; TB skin test
Card Set:
2013-05-28 17:56:01
Microbio Final

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