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consists of central and peripheral lymphoid tissues and
antigens are individual components of substances that
enter or contact the body; the immune system recognizes these substances as being foreign interaction between components of the immune system and antigens is the immune response
Non-specific Immunity .distinguishes self from non-self (unresponsiveness to body’s own tissues. but doesn’t differentiate between specific pathogens a) first line of non-specific defense – includes skin and mucous membranes . preventing immune response to own cells).A.
natural killer cells – lymphocytes which are functionally and structurally different from other lymphocytes – nonspecific (attack anything that is considered foreign) and are capable of destroying tumor cells and virus-infected cells.b) second line of non-specific defense – includes chemical signals molecules. they do not need to be activated by other cells. anti-microbial substances. they are inhibited by molecules present on normal host cells . phagocytic and natural killer cells and fever associated with the inflammatory response (we will have a look at the Inflammatory Response later in the slide show) .
act against very specific antigens) .B. distinguishes between self and non-self and responds to specific foreign materials and pathogens lymphocytes (specific class of white blood cells) include: i) T cells (participate in cell-mediated immunity – destroy antigen-bearing cells) ii) B cells (participate in humoral immunity – B cells are transformed into plasma cells which produce and secrete antibodies. Specific Immunity develops over lifetime (it is acquired).
a heightened immune response is quickly produced response to commonly encountered microorganisms often goes unnoticed self-limitation – ability of lymphocytes to perform a function for a brief period (destruction of pathogen) and then die or differentiate into non-active memory cells . memory response exists where specific immunity is concerned – with subsequent exposure to the same antigen.
Antigens also known as immunogens – substances that enter the body and are recognized as being foreign to the host and stimulate an immune response. antigens are also found in transfused blood or transplanted organs (foreign protein molecules) antigenic molecules have a specific shape/configuration which is recognized by and bind to specific receptors on antibodies . poison ivy). fungi. recognized by receptors on immune cells and proteins antibodies (AKA – immunoglobulins) antibodies are generated in response to antigens microbial antigens include bacteria. plant resins (ex. protozoa and parasites antigens may also be other agents like pollen. insect venoms.
creating both effector cells (those responsible for destroying the antigen) and memory cells (for future use) .Immune Cells 1. lymphocytes are primary cells for specific immunity. additional accessory cells (non-lymphoid) are required for recognition and activation of specific immune responses by T and B cells. lymphocytes are generated in bone marrow and mature in central lymphoid tissues (what are some examples of these?) 2. dendritic cells and antigen-presenting cells (APC’s) a) APC’s and macrophages (phagocytes) present the antigen to T cells. cytokines (signaling molecules) stimulate T cells and B cells to divide multiple times. accessory cells include mononuclear phagocytes.
they also break down large antigen molecules and present them to T cells for initiation of the immune response. producing fever and priming and attracting T and B cells c) dendritic cells – also present antigen to T lymphocytes – found in lymphoid tissue and other areas where antigens enter the body. migrate to many tissues for maturity into macrophages large cells with numerous vacuoles (ex. macrophages engulf/trap infectious agents until specific immunity agents and cells can be activated. alveolar macrophages and those residing in lymph nodes). present in abundance on skin d) immunoglobulins – antibodies – proteins which are produced by activated B cells: .b) monocytes – produced and released by bone marrow. macrophages also secrete cytokines.
5 classes of antibodies: IgG – 75% of antibodies – anti-viral. sputum) and protects mucous membranes IgM – involved in early immune response and activates complement system IgD – found in B cells. antibacterial. binds to macrophages and activates complement system (group of proteins which are activated during inflammatory response) IgA . aids in their maturation IgE – binds to mast cells and basophils (see Inflammatory Response later in slide show). anti-toxin. involved in allergic reactions and hypersensitivity reactions responsible for histamine release .found in secretions (saliva.
Cytokines and the Immune Response Cytokines . mobilizing neutrophils.regulatory proteins produced in all phases of the immune response made by and act upon immune cells act as signaling molecules which regulate mobilization. proliferation and division of leukocytes from bone marrow(white blood cells . cytokines are produced by T cells and macrophages cytokines include interleukins 1-18 interleukin – 1 stimulates acute phase of immune response.see Inflammatory Response later in slide show). produces fever and activates the vascular epithelial response to injury and invading substances (see Inflammatory Response later in slide show) .
Passive Immunity passed from mother to infant before birth or via injection with high concentrations of antibodies for specific disease (ex.Mechanisms of the Immune Response 1. gamma globulin – used sometimes to treat immune deficiency disorders or hepatitis A postexposure to it) . Active Immunity (AKA – Acquired Immunity) immunization or having had contact previously with a specific antigen takes a few days to weeks after first exposure to the specific invader to become fully developed 2.
Humoral Immunity relies on presence of antibodies produced by B cells in blood combination of antibody with antigen may result in: a) clumping of cells b) neutralization of bacterial toxins and viruses c) destruction of pathogens d) complement system activation (see Inflammatory Response later in slide show) e) facilitation of phagocytosis .3.
intracellular bacteria and cancer cells T cells and macrophages dominate .4. Cell Mediated Immunity protects against viruses.
inappropriate immune responses) immune process is usually limited because destruction of pathogen ends response (foreign material no longer exists to stimulate response) and chemicals involved in the response (ex. cytokines) have short life span and are only secreted for short period. additionally.Regulation of the Immune Response lack of self-regulation leads to allergic reactions or autoimmune disorders (so. tolerance to own tissues (not recognized as foreign) prevents response to chemicals involved in the immune process .
if response is more generalized life threatening the suffix itis is added to the injured organ in naming the inflammatory condition – ex. also accompanies specific immune responses ** normally limited to local response.THE INFLAMMATORY RESPONSE Definition: body’s reaction to vascularized tissue injury. pericarditis means inflammation of pericardium or bronchitis means inflammation of bronchi . necessary for healing process to begin.
b) ischemic injury: decreased blood supply to tissue with subsequent decreased oxygen supply c) chemical injury: strong acids. etc. venom. allergic reactions d) biological invasion and any toxins they may secret to produce injury: viruses. bacteria. strong bases. but the degree of severity and its magnitude definitely varies . any type of tissue injury or invasion will trigger the inflammatory response: a) physical/mechanical injury: impact. temperature extremes. etc. the basic process of the inflammatory response is the always the same regardless of cause. distortion. fungi.
pain may be the only apparent sign. localized heat may also not be immediately obvious with inflammation of internal organs because temperature of deep organs is already core temperature less localized sign of inflammation (systemic manifestation) is fever – chemical mediators of inflammatory response (pyrogens) enter circulatory system causing increased body temperature and metabolic rate by affecting the hypothalamic control centres for body temperature . for deeper organs. aimed at removing and limiting the activity of injurious agents and at limiting the quantity of injured tissue signs of acute inflammation: localized redness swelling (edema) heat pain these signs are only obvious for superficial injury. ACUTE INFLAMMATION – immediate response to injury. non-specific in nature.A.
one of the first mediators of inflammatory response. basophils and mast cells (see Cells Involved in Inflammatory Response). Chemical Mediators of the Inflammatory Response inflammation is precipitated by injury. also causes bronchial smooth muscle contraction (short. causes increased permeability of capillary membranes and dilation of vasculature. found in high concentrations in platelets. but signs and symptoms are caused by chemical mediators: a) Histamine – widely distributed throughout the body.A. transient effect) .
bradykinin . increased capillary permeability and pain. ex. blood clotting system also contributes to vascular phase of inflammation (as stated above) .causes vasodilation. activated complement proteins (see below) and clotting factors.b) Plasma Proteases – consist of kinins.
c) Complement System – consists of plasma proteins. enhance inflammatory and immune responses in a cascade by exerting several different influences: i) guiding mast cells and basophils to site of injury or invasion ii) activating the above cells. causing release of other inflammatory mediators iii) causing cell membrane lysis of invading organism iv) presenting antigen-antibody complex to macrophages for phagocytosis .
ASA (AKA – Aspirin) or other NSAID’s (non-steroidal anti-inflammatory drugs) reduce inflammation and pain by inhibiting prostaglandin synthesis . pain and fever .several types of prostaglandins exist (including one called thromboxane). others promote platelet aggregation (clumping) and vasoconstriction .d) Prostaglandins – lipid soluble molecules (fatty acids) produced secondary to the release of arachidonic acid from phospholipid (endothelial cell) membranes in response to injury. contribute to vasodilation. increased capillary permeability. also released by mast cells and neutrophils .some prostaglandins also potentiate the effects of histamine.
etc.increased capillary permeability. released by leukocytes and mast cells and produced secondary to release of arachidonic acid from phospholipid membranes . like histamine. leukotrienes are also important mediators in asthma and anaphylaxis .).they are complimentary to histamine (have similar functions . these cause slow and sustained contraction of bronchial smooth muscle.e) Leukotrienes – also lipid soluble molecules.
also causes bronchospasm (again.f ) Platelet Activating Factor – produced by endothelial cell membrane lipids – causes platelet aggregation (clumping/gathering). acts to initiate inflammatory response (we’ll see this later in the slide show). asthma) g) Nitric Oxide – gas released by injured endothelial cells – vasodilator . activates neutrophils and attracts eosinophils.
neutrophil count in blood increases greatly during early phase of inflammation (particularly with bacterial infection) – mobilized from bone marrow . also generate oxygen free radicals and nitric oxide (NO causes vasodilation). neutrophils have divided nuclei (several lobes) and are often referred to as polymorphonuclear cells. Granulocytes (leukocytes covered in granules filled with inflammatory mediators) a) neutrophils . White Blood Cells (Leukocytes) and Others Involved In the Inflammatory Response 1.B.primary phagocytes that arrive at injury site first – contain enzymes and anti-bacterial substances which destroy or degrade engulfed materials.
mast cells reside within tissues (basophils are a type of white blood cell released into circulation by bone marrow) .b) eosinophils – increase in number in the blood during allergic reactions – responsible for controlling release of chemical mediators from mast cells and other leukocytes c) basophils – contain histamine and other inflammatory mediators. also involved in allergic responses d) mast cells are similar in function to basophils in that they also participate in inflammatory response. mast cells carry IgE immunoglobulins (antibodies) which play a large role in allergic responses and chronic inflammatory responses .
responsible for actual destruction of antigen.monocytes migrate to injured site within a day or two of the initial insult or invasion . signaling specific immunity processes and resolving inflammatory process (once antigen is gone.2.play major role in chronic inflammation by walling off foreign material that can not be broken down and eliminated from the region (usually inorganic molecules) – we’ll deal with chronic inflammation later in the slide show . response normally ends) . longer lifespan than granulocytes .capable of engulfing a significant quantity of foreign material . but only make up about 5% of total leukocytes. Mononuclear Phagocytes (monocytes) – largest of white blood cells.
fibrin (insoluble plasma protein) forms clot to prevent further red blood cell loss 4. vasoconstriction occurs 2 release of platelet activating factor and thromboxane (one type of prostaglandin) from platelets and injured endothelial cell membranes ***#2. small-diametered vascular structures are damaged (endothelial cells) 2. platelets in circulation adhere to and gather at site of damage (aggregation) 3.A/ Initial Response to Injury (how the acute inflammatory response begins) 1.3 and 4 above occur in aid of limiting blood loss and in walling off injured area .
leukocytes and antibodies (exudate) from vascular space to site of injury localized edema. basophils. furthering blood clotting – helps to keep any infectious organism from spreading to adjacent regions or beyond 3. blood flow in capillaries slows down (blood becomes more viscous). with fluid shift. clotting factors. pain also occurs as result of exudate applying pressure to surrounding sensory nerve fibres . lymphocytes. phagocytes.B/ Acute Vascular Response (follows initial response to injury) — initiated and controlled by chemical mediators released from cells or activated plasma proteins (mast cells. injured epithelial cells. leading to hyperemia (increased blood flow. therefore increased nutrients and oxygen) and escape of fluid. causing redness and heat 2. flooding of the injured region with fluid causes dilution of any toxic agents present. complement proteins) 1.vasodilation and increased capillary permeability.
C/Cellular Response .sequence of events is as follows: Pavementing Increased blood viscosity 2 fluid leaving vascular space (increased capillary permeability) caused by histamine. leukotriene and kinin release. periphery of blood vessels in the injured region Emigration Leukocytes pass through capillary walls into tissue spaces Chemotaxis Leukocytes are guided to site of injury via cytokines (signaling cells). cellular debris and complement fragments Phagocytosis Neutrophils (first) and macrophages engulf and degrade bacteria and cellular debris (if dead leukocytes remain at injury site – pus formation) . leukocytes are attracted to. and start to move along.
causing scarring and tissue deformity . may develop from recurrent or progressive acute inflammatory process or from low grade responses that fail to bring on a significant acute inflammatory response . infiltration of monocytes and lymphocytes occurs.rather than an influx of neutrophils initially. additionally. fibroblasts (new connective tissue cells) may proliferate.B. CHRONIC INFLAMMATION – may last for weeks. months or years.
. cystic fibrosis. AKA pneumoconiosis (a form of INTRAPULMONARY PARENCHYMAL DISORDER – you’ll deal with these in patho!) . so organic irritants (when inhaled.examples of irritants resulting in this type of response in terms of lung tissue are talc.may also be caused by long term exposure to bacteria or fungi.patients with recurrent pulmonary infection are also prone to this process (ex. bronchiectasis – again. patho) . silica (sand particles – if inhaled causes silicosis – pulmonary disease) and asbestos (asbestosis if inhaled) – inhalation of inorganic particulate causes inorganic alveolitis. lead to a different class of INTRAPULMONARY PARENCHYMAL DISORDERS – Hypersensitivity Pneumonitis – you’ll cover these in patho as well!) .
these materials are not easily digested/broken down by phagocytes. or different types of fungi. associated with foreign matter such as silica and asbestos (inorganic material) or micro-organisms such as those causing tuberculosis (Mycobacterium tuberculosis).i) non-specific chronic inflammation – diffuse (generalized) accumulation of macrophages and lymphocytes at site of injury. the invading substance becomes encapsulated by connective tissue and is isolated . patho!) ii) granulomatous inflammation – granuloma is a small lesion formed by monocytes and lymphocytes. leads to fibroblast proliferation with subsequent scar formation which may replace normal connective and functional tissues (ex: idiopathic pulmonary fibrosis – once again. and are not well controlled by other inflammatory mechanisms. the granulomas may become multinucleated giant cells that attempt to surround the foreign matter.
fever and inflammatory response occurring in other tissues/organs distal to initial site of injury or invasion → systemic inflammatory response – AKA SIRS. occasionally systemic manifestations occur 2° release of chemical mediators of inflammation into circulation increase in white blood cell count. may occur secondary to mediator release from a single severely injured organ. affecting other organ systems or by massive vascular invasion of pathogens (sepsis – AKA bacteremia) .Systemic Manifestations of Inflammatory Response inflammation normally remains localized. ARDS is a fantastic example of this particular process! a more widespread inflammatory response may result with increased capillary permeability throughout the body and global vascular smooth muscle dilation (what do you suppose happens to systemic blood pressure here?).