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Test 3

Immune

QuestionAnswer
Innate Immunity (non specific) Body's FIRST natural defense to any intruder Primary goal: prevent intruder from entering the body & kills if intruder does get inside Does NOT differentiate between one pathogen and another
Innate Immunity components Skin (physical barrier) Mucous membranes (traps pathogens trying to get inside the body; physical barrier) - no keratin Lysozyme in eyes (chemical barrier) Stomach acid (chemical barrier)
Mast cells Cause inflammation by histamine signals being released when the mast cells find a pathogen
How inflammation response works Mast cells send out a histamine signal which alerts the body and causes blood to go to the area where signal was released. This brings wbcs to the site This can also cause an allergic reaction because pathogen found can turn out to be dust
Phagocytes (innate) Neutrophils - Produces peroxide and releases granules Eosinophils - Phagocytizes invaders and antibody coated phagocytes Monocytes/macrophage - Phagocytizes anything that comes into the tissue after rupture. Seen as initial line of defense
Phagocyte function Patrols the body Destroys foreign substances, pathogens, and cellular debris First line of cellular defense - can attack and remove microorganisms before lymphocytes know they're there
Natural Killer (NK) cells - non phagocytic Detects when our self cells "went rogue" or are infected with a virus When a normal cell stops producing the Major Histocompatibility Complex (MHC), NK cells bind to them and releases a chemical to destroy it Can't recognize specific antigens
Dendritic cells Ingests pathogens and carry info about that pathogen to the adaptive immunity cells Link between innate and adaptive systems Activates b and t cells Gives information to our t cells
Adaptive/acquired immune system Can differentiate between different pathogens Has 2 main parts: t lymphocytes and b lymphocytes Protects against infectious agents and abnormal body cells Amplifies inflammatory response Activates complement
T lymphocytes There when there's already an infection, so the cell mediated immune response occurs B cells come in when pathogens come in but don't cause any disease
T helper cells (TH or CD4 cells) Take signals from dendritic cells or macrophages Form effector t cells which circle body and call wbcs Form memory t cells which keeps a record of antigens for future records
Cytotoxic t cells (TC or CD8 cells) Brought out when some cells of the body become infected with pathogens that have antigens bound to class MHC 1 molecules (essentially kills infected and dying cells) Needs IL-2 from TH cells to activate fully;this prevents abnormal TC cell activation
TH and TC cell functions These cells respond primarily to cells infected with intracellular pathogens: Viruses Intracellular bacteria Cancer cells Foreign cells such as those from a transplanted organ
B cells Produce antibodies that fit on the antigens of the pathogen which signals macrophages to come and kill the pathogen Produces memory b cells when an antigen is encountered
B & T memory cells Work together to keep a record of all encountered infections which strengthen body's response to these in the future
Innate and Adaptive Innate response is QUICKER and nonspecific; works within hrs If innate needs help, it signals the adaptive system which is slower and takes days to respond
Thymus function Makes sure we are immunocompetent Only a few cells of each clone exist in body at any given time Recognizes and responds to pathogens, Screens these cells & destroys clones that cannot recognize as antigens
Thymus pt 2 T cells bind to cells that display foreign antigen fragments as a part of MHC MHC class II — on macrophages, B lymphocytes, and dendritic cells Recognized by TH cells Naive t cells are put into circulation when they survive thymus maturation
Classes of MHC MHC class I — on all nucleated human cells, recognized by cytotoxic t cells MHC class II — on macrophages, B lymphocytes, and dendritic cells, recognized by t helper cells
Complement pathway Classical pathway, lectin and alternative pathway
Complement pathway pt 2 Classical pathway: inactive complement proteins bind to antibodies bound to antigen Lectin: produced by innate system to recognize foreign invaders Alternative pathway - when inactive complement proteins encounter foreign cells (bacteria)
Types of cytokines Interleukin, interferon, and tumor necrosis factor
Tumor necrosis factor Secreted by active macrophages Increases activity Stimulates phagocytes to release additional cytokines
Interleukin Produced by leukocytes Stimulates production of neutrophils by bone marrow Stimulate NK cells, triggers production of interferons Activates t cells
Interferon Produced by macrophages, dendritic cells, NK cells, and cells of adaptive immunity Produced in response to infection with intracellular agents Primary action is inhibit viral replication in host cells
Interferon pt 2 Interferon alpha and beta cells will kill the whole cell and introduce neighboring cells to be resistant against infection Gamma inhibit viral replication
Fever (febrile) Body temp is above 99 degrees F Warning sign that there's an inflammatory process going on When pyrogens are released from damage cells or bacteria, our temp rises Increased metabolic rate means faster repair
Chemotaxis Ability to migrate to the tissue
Marginalization Ability to adhere to the cell
Components of inflammatory response Margination, diapedesis, chemotaxis, and phagocytosis
Corticosteroids Stop formation of prostaglandins and leukotrienes Ex: cortisone and prednisone
NSAIDs Stops cyclooxygenase and prevents prostaglandins Ex: ibuprofen
Types of grafts Autografts involve tissue transplanted from one site to another in the SAME person Isograft involves organs and tissues transplanted between two identical individuals
Types of grafts pt 2 Allografts are the most common types of grafts Xenografts are rare and involves organs and tissues transplanted between two individuals of different species
Hypersensitivity disorders Allergens are exposed to immune cells which results in rash, hives, alterations, etc. Allergen binds to b cell, which goes into cells that secrete IgE antibodies
Immunodeficiency disorders and autoimmune disorders Immunodeficiency disorders happen when one or more parts of the immune system fail Autoimmune disorders is when the immune system can treat self antigens as foreign and attack body’s own tissues
Hypersensitivity disorders Asthma Anaphylactic shock (drastic) * There is a: 1. systemic release of histamine 2. systemic vasodilation (bp drops) 3. increased permeability VERY FATAL
Hypersensitivity type 2 (antibody mediated) Antibodies produced by the immune response to foreign antigens binds to self antigens Happens when foreign antigens bind to normal self antigens EX: donor erythrocytes infused into another individual are mismatched
Hypersensitivity type 3 (immune complex mediated) Reactions are mediated by immune complexes or clusters of soluble antigens bound to antibodies Cleared by phagocytes, some can't be ingested by macrophages
Hypersensitivity type 3 pt 2 They are deposited in capillary beds in kidneys, bv walls, synovial joints, and choroid plexuses When deposited they start an inflammatory reaction which attracts neutrophils that cause damage
Hypersensitivity type 4 Mediated by T cells rather than antibodies TH cells recognize antigens bound to MHC molecules as foreign and mediate their destruction by activating and recruiting macrophages and in some cases TC cells Reaction generally takes 2–3 days to manifest
Hypersensitivity type 4 pt 2 TH cells must be sensitized by an initial exposure, and reaction occurs with subsequent exposures EX: contact dermatitis
Immunodeficiency disorders Caused by a decrease in function in one or more components of the immune system Two types: primary and secondary
Primary immunodeficiency disorders most common dysfunctions of innate immunity involve deficient complement proteins or abnormalities in phagocytes Higher risk for bacterial infections and parasitic infections Common dysfunctions of adaptive immunity include
Hypogammaglobulinemia Characterized by a decrease in one or more types of antibodies
Severe Combined Immunodeficiency (SCID) A cluster of immune disorders Caused by failures of lymphoid cell lines in bone marrow; affect B cells, NK cells, and T cells Features: low circulating levels of lymphocytes, failure of thymus to develop, and failure of cell-mediated immunity
Secondary Immunodeficiency disorders Many forms, many are induced artificially to fight cancers originating in bone marrow or to prevent transplant rejection: Cancers of immune cells and lymphoid organs that depress immune response also cause secondary disorders
AIDS Most common cause of secondary immunodeficiency disorders Spreads through infected blood, semen, vaginal fluid, or breast milk HIV-1 binds and interacts with cells displaying CD4 molecules Virus liked CD4 molecules, allows for entry into host cell
HIV 1 (retrovirus) Enzyme catalyzes transcription of viral RNA into DNA DNA copy of viral genome is then inserted into host DNA, where it triggers production of viral RNA and proteins
HIV 1 phases Acute phase lasts about three months: characterized by a sharp decline in TH cells and a sharp rise in HIV-1 virions Patients may exhibit flu-like symptoms during this phase, although condition often goes unnoticed
HIV 1 phases pt 2 Chronic phase begins with production of antibodies to HIV-1 virions, an initial slight recovery in number of TH cells, and a decline in number of HIV-1 virions May last eight or more years in untreated individuals Final phase: when you get AIDS
HIV 1 s/s Adaptive immune system fails Purple skin lesions (Kaposi sarcoma; a cancer) Recurrent infections
Autoimmune disorders Occurs when populations of self-reactive T cells or B cells that secrete antibodies bind to self antigens (called autoantibodies)
Created by: fmenelas1
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