ch 15 and 16.txt

• Microorganisms found growing on the body surface of healthy individuals.
• Protects through: COMPETITIVE Exclusion
• Covers binding sites so pathogens CANNOT bind
• Competes for nutrients so pathogens DO NOT get them

• Normal flora(microbiota)
• Skin/Mucous membrane
• Saliva, tears: have antimicrobial activities (ie: lysozyme or perioxidase)
• Fever: due to pyrogens (fever inducing substances-can be EXOGENOUS or ENDOGENOUS) which respond to temp body changes
• Inflammation

• Barriers that shield the body from EXTERNAL surroundings:
• SKIN: composed of 2 main layers:
• DERMIS: tight fibrous connective tissue
• EPIDERMIS: many layers of epithelial cells – outermost keratinized, and they slough off as they shed
• MUCOUS membranes: line the digestive, respitory & genitourinary tract. Some have mechanisms to propel microorgs and viruses to areas where they can be ELIMINATED (have antimicrobial secretions)

• MONOCYTES and MACROPHAGES
• MONOCYTES: Circulating for few days and then end up in tissues (spleen).
• Involved in inflammatory response. These cells come from Stem cells. Precursor cells called MONOBLASTS.
• MACROPHAGES: WBC’s produced by Differentiation of monocytes. CIRCULATE in blood & Present in TISSUE Precursor is a LEUKOCYTE. Function with innate immunity and help initiate ADAPTIVE immunity as well.
• They stimulate lymphocytes

• White blood cells
• 1. Granulocytes
• a. Neutrophils: INNATE Response (most abundant) Circulating (most of circulating leukocytes). In tissue (only during inflammation)
• b. Basophils (involved in allergy): Circulating. Mast cells in tissue (release inflammatory inducing chems)
• c. Eosinophils(in allergy & rid of worms): Circulating?? Few in tissue (only during inflammation & allergies)
• Agraulocytes
• Mononuclear Phagocytes- MONOCYTES: circulate in the blood. Macrophages evolve from Monocytes: form of monocytes that are Present in MOST Tissue
• Dendritic cells: found in tissue – engulf cells & bring it to adaptive immune system.

• Adaptive immunity:
• 1. B cells: involved in HUMORAL immunity. Extracellular immune response via B lymphocytes
• 2. T cells: involved in Cell-Mediated immunity. Intracellular immune response via cytotoxic T cells
• *Also - Natural Killer cells (NK) that are involved in INNATE immunity
• T-helper cells involved in both types of lymphocytes

• Leukocytes are white blood cells…involved in INNATE immunity and CAN augment adaptive response
• Lymphocytes are involved in AQUIRED immunity. T lymphocytes and B lymphocytes

• ANTIMICROBIAL SUBSTANCES:
• Peroxidase: breaks down hydrogen peroxide into reactive oxygen
• Lysozyme: degrade peptidoglycan
• Lactoferrin: sequesters IRON for microorgs, which is essential for microbial growth
• Defensins: antimicrobial peptides in the microbial membrane

• Involves a series of proteins in the blood (in their inactive form)
• 1. Stimulate inactive proteins to INITIATE cascade of rxns
• 2. Augments activities of the adaptive immune response – lead to rapid ACTIVATION of components
• Can lead to:
• 1. inflammation: C3a and C5a can INDUCE changes in epithelial cells to initiate INFLAMMATORY response
• 2. opsonization: C3b can bind to foreign material to allow for phagocytosis (Phagocytes to recognize this as foreign)
• 3. Lysis of foreign cells by multiple C proteins attacking cells

• Alternate Pathway: ?Binding of C3b to cell surface to INITIATE activation of other proteins
• Lectin Pathway: ? Mannan Binding Lectins (MBLs) attach to surface to activate other complement proteins
• Classical Pathway ? ANTIBODIES interact complement C1 leading to activation of all complement proteins

• Cytokines (voice of cell)BIND To cell surface receptors and REGULATE cell function
• 1. CHEMOKINES: Fxn- chemotaxis: enhance cell ability to migrate to site
• 2. Colony Stimulating Factors: Fxn- multiplication and differentiation of leukocytes
• 3. INTERFERONS: fxn- control of viral infections (also assoc w/inflammatory response)
• 4. INTERLEUKINS: fxn- produced by leukocytes (imp in innate & adaptive immunity)
• 5. Tumor necrosis factor: fxn- kills tumors & initiates inflammation

• 1. CHEMOTAXIS: cells recruited to infection site
• 2. RECOG/Attachment: Receptors bind to invading microbes
• 3. ENGULFMENT: Phagocyte engulfs invading foreign phagosome
• 4. Phagosome/Lysosome Fusion: Phagosome binds to lysosome
• 5. Destruction & DIGESTION: Organism KILLED
• 6. EXOCYTOSIS: Phagocyte expels material out of the cell

• Initiated by tissue damage or microbial invasion
• BLOOD vessels undergo changes (DIALATE – results in INCREASED blood flow) to allow for certain IMMUNE particles to leak out (LEUKOCYTES and PHAGOCYTES)
• 1. Toll-like receptors triggered to release PRO-INFLAMMATORY cytokines
• 2. Enzymatic cascade can be triggered or if Tissue damage.
• 3. Microbial cell surface can trigger Complement cascade: results in production of C3a and C5a.

• Releases toxic products from phagocytic cells, which can cause TISSUE DAMAGE
• If it is areas around the brain or spinal cord, can cause MENINGITIS and serious INJURY

• 1. Viral infection, which leads to virus producing dsRNA. This activates the synthesis and secretion of INTERFERON from cells.
• 2. These INTERFERON molecules enter new cells and activate synthesis of iAVP (inactive ANTI-VIRAL proteins).
• 3. When Virus comes to these cells to infect, the iAVP recognizes the dsRNA and this TRIGGERS Inhibition of translation & mRNA destruction (APOPTOSIS).
• 4. Although the cell dies, it is actually working to help cells by PREVENTING viral spread.

• TISSUE DAMAGE: initiates Enzymatic cascade (leads to coagulation cascade
• MICROBIAL PRODUCTS (ie: bacterial DNA): trigger Toll-Like receptors of Macrophages-release cytokines
• MICROBIAL CELL SURFACES: trigger Complement cascade-produces C3a and C5a

Programmed cell death w/out inflammatory response. Involves cell changes to UNDERGO signaling of Macrophages. Cells DO NEED APOPTOSIS mechanism b/c sometimes inflammatory response will cause damage and death, so apoptosis is necessary.

Blood vessel dialation allows fluid to leak from vessels into the tissue. Pro-inflammatory cytokines act on phagocytes which move towards area of injury, followed by LEUKOCYTES

Complement protein C5a attracts phagocyte to organism to be engulfed. Protein C3b binds to foreign material . Opsonization allows phagocytes to EASILY grab pathogens

• ENDOGENOUS Pyrogens: Fever INDUCING cytokines (temp regulating center responds to these when fever occurs)
• EXOGENOUS pyrogens: the microbial products

• Is a Good indication of INFECTION
• Fever INHIBITS GROWTH of pathogens by:
• 1.ELEVATING temperature &
• 2. Activating & speeding up defenses

a molecule that reacts specifically with either an ANTIBODY or an antigen RECEPTOR on a lymphocyte

a part of the ANTIGEN that is RECOGNIZED by B-cells, T-cells or antibodies.

produced from lymphocytes, binds to antigens (specific antigen-antibody interaction)

antibodies obtained from DIFFERENT B-cell resources. Identify Multiple epitopes

a monospecific antibody that is made by IDENTICAL immune cells that all come from the same parent cell. Identifies ONE epitope

• 21. Describe the structure of IgG and what the different parts of the molecule do, especially the Fc region, heavy and light chains, variable regions.
• IgG: Structure= Monomer
• Fxn: provdes the LONGEST term of protection, it is the most abundant of total blood immunoglobulin,
• and is also the most abundant during the secondary response.
• Fc region: The constant region of the HEAVY chains (not the whole constant region, but 2 of the 3 subunits) recognized by receptors in the placenta, allowing it to cross the placenta and protect a developing fetus. (due to its long half-life it provides continued protection for 3-6mo post birth)
• HEAVY chain: contains part of the constant region, also has a variable region to it. In the constant region, the aa sequence is the same for all antibodies of a given class, and provides it with its functional framework
• LIGHT Chain: Contains a constant and variable region
• Variable Regions: This region contains the antigen binding sites, which are very precise. The differences in the variable region account for the specificity of the antibody molecule.

• IgG: Antibody of Memory (involved in secondary immune response)
• IgM: 1st Ab to respond to infection.
• IgA: Found in secretions (important in mucous membrane), found in saliva, tears, breast milk.
• IgD: Maturation of antibody response
• IgE: Barely in blood. Involved in allergic reaction

• B cells: Humoral Immunity-deals with antigens that have not entered a host, but are extracellular.
• Starts in bone marrow, where the B cells may be triggered to proliferate into PLASMA cells
• These PLASMA cells produce ANTIBODIES
• These antibodies are produced when antigens bind to the B cell receptors

• 1. Neutralization: PREVENTS toxin from interacting w/cell (ie: coats virus)
• 2. Immobilization and prevention of adherence: Binding of Abs to cellular structures to INTERFERE with their FXN. (ie: Abs attach to flagellum of bac)
• 3. Agglutination & precipitation: Clumping of bac cells by specific Ab
• 4. Opsinization: Bac coated with ANTIBODIES to enhance Phagocytosis
• 5. Complement Activation: Ab binding TRIGGERS Classical Pathway
• 6. Ab Dependent Cellular Cytotoxicity: Multiple Abs bind to cell, which becomes a Target for certain cells (ie NK cells attach to Fc region when Abs bound to cell)

• Only a specific antibody responds to an antigen when introduced. The MULTIPLICATION of this specific antigen is called CLONAL SELECTION.
• When the antigen is presented, the B-cell with the antibody that binds to this epitope of the antigen is activated (activated lymphocytes), they proliferate and eventually become plasma cells (effector lymphocytes), which generate Ab’s against this antigen. Memory (lymphocytes) B cells are also made to recognize this antigen in the future.

• B cells: BCR binds to the antigen, but many times Thelper cells are needed to confirm this is an antigen (works to activate B-cell to divide & proliferate)
• T-cells: Do NOT interact with the FREE antigen (it must be presented by the host cell). These host cells must have the MHC (major histocompatibility complex) receptors for it to bind to. T cells also do NOT produce antibodies

• EXOGENOUS: produced outside of the APCells. B cell engulfs Antigen and then presents part of the antigen on the cell surface, now called APCell. T helper cell is now activated thru release of substances from Ag. T helper binds to APcells Activate B cells to divide & proliferate (produce plasma & memory B cells). Th cells STIMULATE other T-cells.
• Rec. MHC class II

• ENDOGENOUS: produced within the target cell. Cytotoxic T cells proliferate & differentiate to destroy INFECTED or cancerous self cells. Induces these cells to undergo apoptosis
• Rec. MHC Class I

T helper cells activate B cells to proliferate and then eventually become plasma (antibody producing) cells.

• Humoral immunity involves B-cells using their protective immunity function outside of the cell, such as killing an antigen outside of the host cell. Production of Antibodies in serum, lymph, mucus & milk are examples, all produced by B-lymphocytes.
• This may involve the process of B cell activation and clonal selection????
• Cell mediated immunity involves Cytotoxic T cells or other immune resonses related to antigens acting inside a host cell. Kills virally infected cells, cancerous cells.
• Cytotoxic T cell activity is incluced in this????
• T-helper cells required for both

It allows T-cells to recognize APCells with the antigen present. Since T-cells do not bind to antigen, but they bind to the host cell, this is what the host cell has as its receptor to help T-cells identify that this cell has an antigen present.

They are able to recognize the specific antigen right when it comes back & produce antibodies rapidly. They do not have to go through the steps involved with clonal selection. IgG is produced for the Memory B cells.

• Naturally Aquired: antigens enter the body and body has to produce antibodies – either Actively (as done with lymphocytes) or Passively (as antibodies produced from mom passed to fetus or through breast milk).
• Artificially Aquired: ACTIVE: antigens are present in vaccines and body responds by making antibodies
• Passive: Antibodies are given to body through INJECTION

• IE: have a blood sample and use Anti-A antibodies against it. If a precipitate forms, you know that they have A antigens, so they have type A blood. If the Anti-B antibodies are added and there is NO precipitate, you know they do NOT have B antigens, so they are Just type A.
• If Rh antibodies are added and there is a precipitate formation, you know they have Rh factor, so they are A(Rh) +.