Micro Lecture Ch16/17
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Differentiate between innate and adaptive immunity.
- Innate immunity: what we're born with; Defenses against any pathogen.
- - invariant (generalized)-provides protection against a wide variety of pathogens
- - early, limited specificity (reacts same way to everything)
- - the first line of defense
- -found in all multicellular organisms (adaptive is only in vertebrates)
- -uses receptors and effectors that are ancient in their linage
- -distinguishes self from non-self perfectly
- -defects in innate immunity are very rare and almost always lethal
Innate immunity consists of:
- -mucosal surfaces
- -chemical barriers
- -normal microbiota (competes with pathogens)
- II.Cellular response
- –inflammatory reaction
- –natural killer and mast cells
- III.Soluble factors (tags foreign things)
- Adaptive immunity: allowed to adapt or change; Immunity, resistance to a specific pathogen.
- -variable (custom)
- -involves antibodies
- - later, highly specific
- ‘‘remembers’’ infection
- -Naturally acquired active immunity (resulting from infection)
- -naturally acquired passive immunity (transplacental-from mother or via colostrum-from breast milk)
- -artifically acquired active immunity (injection of Ag vaccination)
- -artifically aquired passive immunity (injection of Ab)
- Key difference is that adaptive immunity has memory cells:
- Immunological memory = protection of host against a second infection by the same pathogen. Lasts for a very long time, in some cases for life.
•Sensitized memory cells respond within hours
•Antibody levels peak in 2 to 3 days at much higher levels than in the primary response
•Antibodies bind with greater affinity, and their levels in the blood can remain high for weeks to months
Describe the role of the skin and mucous membranes in innate immunity.
The body's first line of defense against infections is a phyical barrier and the nonspecific chemicals of the skin and mocous membranes.
- Skin (epidermis): tightly packed cells that contain keratin, a protective protein
- Wounds, burns, insect bites
- Mucosal surfaces
- Respiratory, GI, Reproductive
- (described in next card)
Differentiate physical from chemical factors, and list examples of each.
- Physical barriers:
- •Intact skin: the structure of intact skin and the waterproof protein keratin provide resistance to microbial invasion
- •Mucous membrane protection-mucous traps many microorganisms that enter the respiratory and gastrointestinal tracts; in the lower respiratory tract, the ciliary escalator moves mucus up and out
- •Ciliary escalator: Microbes trapped in mucus are transported away from the lungs.
- •Lacrimal apparatus: Washes eye.
- •Saliva: Washes microbes off from gums and teeth.
- •Urine: Flows out.
- •Vaginal secretions: Flows out.
- Chemical Barriers:
- •Fungistatic fatty acid in sebum (skin oils).- sebum contains unsaturated fatty acids, which inhibit the growth of pathogenic bacteria. Some bacteria commonly found on the skin can metabolize sebum and cause the inflammatory response associated to acne
- •Low pH (3-5) of skin. (most microbes prefer pH6-5)
- •Perspiration washes microbes off skin
- •Lysozyme in perspiration, tears, saliva, and tissue fluids.
- •Low pH (1.2-3.0) of gastric juice.
- •Transferrins in blood finds and binds iron (a component that bacteria look for to steal).
- •Nitrous oxide inhibits ATP production.
Describe the role of normal microbiota in innate resistance.
changes the environment, a process that can prevent the growth of pathogens
Classify phagocytic cells, and describe the roles of granulocytes and monocytes.
- macrophages, neutrophils, natural killer cells, and mast cells
- A soluble factor, complement, is also involved
- •Neutrophils: granular White Blood Cell (WBC); phagocytic (most important and most abundant phagocyte)
- very short lifetime-t1/2=6 hrs
- 55% of bone marrow weight devoted to neutrophil production
•Eosinophils: granular WBC, toxic to parasites
•Basophils (aka mast cells): granular WBC, produce histamine
- phagocytic, like macrophages
- •Neutrophils also release toxic chemicals that destroy everything in the area, including the neutrophils themselves
- •Monocytes: agranular WBC, phagocytic as mature
•Natural Killer Cells (agranular)
•Mast Cells (agranular)
- •Macrophages: mature monocytes (agranular)
- Phagocitiize bacteria, viruses, dead cells, dust
- most circulate in theblood, lymph and extracellular fluid
- they are attracted to the site of infection by chemicals given off by dying cells
- after ingesting a foreign invader, they “wear” pieces of it called antigens on their cell membrane receptors – this tells other types of immune system cells what to look for
Granulocytes predominate during the early stages of infection, whereas monocytes predominate as the infection subsides
Define phagocyte and phagocytosis.
- •Phago: from Greek, meaning eat
- •Cyte: from Greek, meaning cell
•Ingestion of microbes or particles by a cell, performed by neutrophils and macrophages
Describe the process of phagocytosis, and include the stages of adherence and ingestion.
- Chemotaxis is the process by which phagocytes are attracted to microbes
- toll-like receptors on a phygocyte adhere to the microbial cells; adherence may be facilitated by opsonization-coating the microbe with serum proteins
- pseudopods of phagocytes engulf the microbe and enclose it in a phagosome to complete ingestion
- many phagocytized microbes are killed by lysosomal enzymes and oxidizing agents
Identify methods of avoiding destruction by phagocytes.
Evasion mechanisms include M protein, capsules, leukocidins, membrane attack complexes, and prevention of phagolysosome formation
- Inhibit adherence: M protein, capsules
- Streptococcus pyogenes, S.pneumoniae
- Kill phagocytes: Leukocidins
- Staphylococcus aureus
- Lyse phagocytes: Membrane attack complex
- Listeria monocytogenes
- Escape phagosome
- Shigella and Rickettsia
- Prevent phagosome-lysosome fusion
- Survive in phagolysosome
- Coxiella burnetti
List the stages of inflammation.
- Swelling (edema)
- Stage 1: Acute-phase proteins activated (complement, cytokine, and kinins)
- Stage 2: Vasodilation (histamine, kinins, prostaglandins, and leukotrienes-other compounds in the blood lead to vasodilation)
- Stage 3: Margination (when WBCs line up and form a barrior around the invasion) and emigration (taking the infection out of the blood) of WBCs
- Stage 4: Tissue repair
Acute Phase proteins
- Vasodilation, increased permeability of blood vessels
Vasodilation, increased permeability of blood vessels
Intensify histamine and kinin effect
Increased permeability of blood vessels, phagocytic attachment
Describe the cause and effects of fever.
- caused by recognition of gram neg in the body
- •Hypothalamus normally set at 37°C.
- •Gram-negative endotoxin cause phagocytes to release interleukin–1 (IL–1).
- •Hypothalamus releases prostaglandins that reset the hypothalamus to a high temperature.
- •Body increases rate of metabolism and shivering which raise temperature.
- •When IL–1 is eliminated, body temperature falls (crisis).
- Fever is an abnormally high body temp produced in response to bacterial or viral infection
- bacterial endotoxins, interleukin-1 and tumer necrosis factor alpha can induce fever
- a chill indicates a rising body temp; crisis (sweating) indicates that the body's temp is falling
- A substance (part) that causes the body to produce specific antibodies or sensitized T cells.
the foreign object that trigger immune response
- •Body does not direct immune response against whole bacteria, fungi, protozoa or viruses.
- •Molecules on foreignobjects are what trigger a specific immune response
- •Include components of bacterial cell walls, capsules, pili,and flagella, as well as proteins of viruses, fungi, and protozoa
- •Food and dust can also contain antigenic particles
Explain the function of antibodies and describe their structural and chemical characteristics.
- •Antibody (Ab): Proteins made in
- response to an Ag; can combine with that Ag.
- •Also called immunoglobulin or antitoxin
•Proteinaceous molecules that bind antigens at the antigen-binding site (unique location to the specific receptor).
•Each is made of two heavy
and two light chains
of amino acids, held together by disulfide bonds
- Made up of variable (meaning they change..the difference has to do with the shapes of the arms)and constant regions (the constant Y shape).
- -parts of the antibody (Ab) are constant, i.e., the same for every antibody
- -parts are variable - the arms of the “Y” have different amino acid sequences that cause specific binding to antigen
•the fact that there are many different variable regions results in antibodies that react with almost any antigen you could possibly encounter!
- How they work:
- •Some act as opsonins, and adhere to microbes to identify antigens for phagocytes and stimulate phagocytosis.
•Some work by neutralization
(i.e. they neutralize toxins for e.g. those causing diphtheria and tetanus) by binding to the toxin to neutralize it so it cant work
•Some cause agglutination
(clumping together) of bacteria making them less likely to spread
Differentiate between plasma cell and memory cell.
- plasma cell- a cell that an activated B cell differentiates into; plasma cells that stay in the blood plasma that manufactures specific antibodies; makes antibodies to a pathogen
- memory cell- A long-lived B or T cell responsible for the memory, or secondary, response; remember the same pathogen for faster antibody production in future infection
Describe clonal selection.
- B cells can recognize an almost infinite number of antigens, but each particular cell recognizes only one type of antigen. an encounter with a particular antigen triggers the proliferation of a cell that is specific for that antigen into a clone of cells with the same specificity, hence ther term colonal selection
- 1. stem cells differentiate into mature B cells, each bearing surface immunoglobulins against a specific antigen
- 2. B cell III complexes with its specific antigen and proliferates
- 3. some B cells proliferate into long-lived memory cells, which at a later date can be stimulated to becomin antibody-producing plasma cells
- 4. other B cells proliferate into antibody-producing plasma cells
- 5. plasma cells secrete antibodies into circulation
Describe how a human can produce different antibodies.
during development, the genes in embryonic B cells recombine so that mature B cells each have different genes for the V region of their antibodies
- The diversity of antibodies:
- •During embryonic development, variable region genes combine with constant region genes to produce > 1015 different antibodies.
- •Affinity: Strength of bond between Ag and Ag.(how much of a good fit it is)
- •Specificity: Ab recognizes a specific epitope (antigenic shape).
Differentiate between helper T, cytotoxic T, and regulatory T cells.
- •helper T cells – start the immune response (help B cells)
- Helper T cells (TH) are the first to interact with antigen-presenting cells or APCs. They have a variety of functions, including causing the activation of the antibody-producing B cells (which engage in “chemical warfare” by producing antibodies that react with antigen) and also activation of cytotoxic cells (which engage in “hand-to-hand combat” by producing chemicals which kill other cells). Usually these are CD4+ and recognize antigen presented on Class II MHC molecules.
- •cytotoxic T cells – kill the body’s abnormal cells, like virus-infected cells and cancer cells
- •Activated into Cytotoxic T
- Lymphocytes (CTLs) or Killer T Cells.
- •Directly kill cells of the body that are infected with viruses and other intracellular pathogens by inducing apoptosis.
- Apoptosis-programmed cell death
- Cytotoxic T cells (TC) aka Killer T cells are the body’s main defense against virus-infected cells and against cancer cells. When TC cells encounter a cell that presents foreign antigen, they may kill by literally punching holes in the membrane of the APC using perforin, a protein that inserts itself into the membrane of the APC and forms an open pore. TC cells may also produce proteins that act at the surface of the APC, but trigger internal biochemical changes that result in apoptosis of the APC. TC are CD8+ and recognize antigen presented on Class I MHC molecules.
- •suppressor T cells – suppress the activities of other T cells, helping to end the immune response
- T cells (TS) are antigen-specific and suppress the functions of other types of T cells. The mechanisms by which TS cells downregulate the other cells are not well understood, but they include secretion of chemical signals (cytokines) that cause the other T cells to produce fewer of the surface markers that are involved in their activation. Suppression function is important when an infection has been contained and an immune response is no longer appropriate.
Define antigen-presenting cell.
- aka APCs
- APCs include B cells, dendritic cells, and macrophages
- dendritic cells are the primary APCs
- Activated macrophages are effective phygocytes and APCs
- APCs carry antigens to lymphoid tissues where T cells that recognize the antigen are located
Describe the function of natural killer cells.
- aka NK
- lyse virus-infected cells, tumor cells, and parasites
- they kill cells that do not express MHC class I antigens
destroy cells which don’t express “self” proteins.
Identify at least one function of each of the following: cytokines, interleukins, interferons
Cytokines- cells of the immune system communicate with each other by these chemicals
Interleukins-cytokines that serve as communicators between leukocytes
Interferons-a chemical (cytokine) produced by virus infected cells that contributes to their death by apoptosis
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