Term
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Definition
| occurs when the natural barriers have been compromised and inflammation is activated. Also called the third line of defense. Comprised of T (from thymus) and B (from bone marrow) cells |
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Definition
| substances the body recognizes as foreign or "non-self." Reacts with antibodies or antigen receptors on B and T cells. Most antigens are immunogenic. |
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Definition
| Will induce an immune response resulting in the producton of antibodies or functional T cells. |
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Term
| Criteria influencing the degree to which an antigen is immunogenic |
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Definition
1. Foreign-ness to the host
2. Appropriateness in size (larger = more immunogenic)
3. Having an adequate chemical complexity
4. Being present in a sufficient quantity |
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Term
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Definition
an arm of the immune response consisting of B lymphocytes which produce antibodies (aka: immunoglobulins)which circulate in the blood and bind to antigens on infectious agents. Binding causes either a direct inactivation of the microorganism or activation of inflammatory mediators. Primarily responsible for protection against many bacteria and viruses.
Produce memory cells. |
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Term
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Definition
T-Cells undergo differentiation during an immune response and develop into several subpopulations of cells that react directly with antigen on the surface of infectious agents. They can stimulate the activities of other leukocytes or they can attack and kill targets directly. Targets include a variety of viruses and also cells that become cancerous.
Produce memory cells. |
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Term
| Antigen Presenting Cells (APCs) |
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Definition
| are highly specialized cells that express both MHC-I and MHC-II moleculesand serve two major functions during adaptive immunity: 1)They capture and process antigens for presentation to T-lymphocytes and 2) they produce signals required for the proliferation and differentiation of lymphocytes. |
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Term
| Major Histocombatibility Complex (MHC) |
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Definition
| Glycoproteins that are found on the surface of every cell in the body except red blood cells. Antigen presentation and distinguishing self from non-self is the primary role. There are 2 types: MHC I, MHCII |
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Term
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Definition
| on all nucleated cells and platelets in the body. They bind peptide epitopes from endogenous antigens dervied from intracellular proteins to enable immune recognition by T-cells and T8-lymphocytes. They have a single transmembrane chain and microglobulin. |
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Term
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Definition
| found on B cells, APCs and some epithelial cells. Molecules bind peptide epitopes from exogenous antigens from extracellular organisms to enable immune recognition by T4-lymphocytes and TH cells. MHC II have 2 transmembrane chains. |
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Term
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Definition
Smallest and most abundant class of immunoglobulins. Accounts for most of the PROTECTIVE activity against infections. Found in extracellular fluid and blood. Main immunoglobulin in secondary response (subsequent exposures to same antigen).
ONLY ONE THAT CROSSES PLACENTA |
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Definition
IgA1 is found predominantly in blood. IgA2 is found in bodily secretions. May function to protect immunoglobulins against degradation by enzymes also found in secretions; plays a critical role in mucosal immunity.
Secreted in breastmilk |
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Term
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Definition
| Largest of the immunoglobulins. It is the first antibody produced during the initial, or primary, response to antigen. Found in serum 7-10d after eposure. Synthesized early in neonatal life, and its synthesis may be increases as a response to infection in utero. |
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Term
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Definition
| Information on its role is limited. It is found in very low concentrations (least abundant) in the blood, where they do not appear to have a known function. Located primarily on surface of developing B lymphocytes where they function as one type of B-cell antigen receptor |
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Definition
| The least concentrated immunoglobulin. Appears to have very specialized functions as a mediator of many common allergic responses and in the defense against parasitic infections. |
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Definition
| (aka active acquired immunity) is produced by an individual after either natural exposure to an antigen or after immunization. It is long-lived. |
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Definition
Does not involve the host’s immune response. Occurs when preformed antibodies or T lymphocytes are transferred from a donor to the recipient. Can occur Naturally or Artificially. It is only temporary because the donor’s antibodies or T cells are eventually destroyed.
Naturally—passage of maternal antibodies across the placenta to the fetus
Artificially—a clinic using immunotherapy for a specific disease |
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Term
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Definition
| Antigens that are too small to be immunogens by themselves but become immunogenic in combination with larger molecules that function as carriers for the hapten.(example: PCN and poison ivy, they initiate allergic responses only after binding to large-molecular-weight proteins in the allergic individual’s blood or skin) |
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Term
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Definition
| Created by both humoral and cell mediated immunity. Remember specific antigens to induce a secondary response on subsequent exposures. DO NOT require further differientation so they are available quickly. |
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Term
| Lymphokine producing cells |
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Definition
Secrete cytokines that activate other cells such as macrophages.
Part of the cell mediated response |
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Term
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Definition
| Attack antigens directly and destroy cells with foreigh antigens on cell membrane. |
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Definition
| AKA CD4. Regularoty cells that control both cell mediated and humoral response. Particularly important in protecting against viruses, tumors, and pathogens resistnt to killing by neutrophills and macrophages. |
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Term
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Definition
are molecules produced by infectious agents that can bind to the T-helper cell’s TCR (T-cell receptor) and MHC (major histocompatibility complex) outside of the normal binding sites resulting in activation of large populations of Th cells and inflammatory cytokines regardless of antigen specificity. Overproduction of pro-inflammatory cytokines results in symptoms of a systemic inflammatory reaction including fever, low blood pressure, and potentially, fatal shock.
EX: bacterial toxins produced by Staphylococcus aureus and Streptococcus pyogenes, including the SAGs that cause toxic shock syndrome and food poisoning. |
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Term
| Primary humoral immune response |
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Definition
| – Initial exposure to most antigens is followed by a latent period of approximately 5-7 days during which B cell differentiation and proliferation occur (clonal selection). Typically, IgM is produced first, followed by IgG in equal or lesser amounts. If no further exposure occurs, circulating antibody is catabolized and measurable quantities fall. |
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Term
| Secondary(Anamnestic) humoral immune response |
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Definition
| Subsequent exposure to a specific antigen is characterized by a more rapid production of a larger amount of antibody than the primary response. This is a result of memory cells that do not require further differentiation. IgM may be transiently produced in about the same quantity as with primary exposure. IgG production is increased considerably and may remain elevated for an extended period of time, making it the predominant antibody class of the secondary response and the explanation for protective secondary immunity. |
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Term
| Aging (over 60yo) and Immune function |
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Definition
Immune function decreases with age.
T cell function decreases (not #), delayed hypersensitivity decreases, decreased T cell mediated response to infection, Circulating autoantibodies and immune complexes increase. |
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Term
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Definition
| Recognizes antigen and communicates that information to the cell nucleus. |
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Term
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Definition
| lymphoid cells similar to T cells but lack antigen specific receptor. |
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Term
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Definition
| hypersensitivity to environmental antigens. A sensitization process involving multiple exposures to the allergen occurs before adequate amounts of antibody or T cells are available to elicit allergic response. |
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Term
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Definition
altered immunologic response to an antigen that results in disease or damage to an individual.
4 Types: Type I- Type IV |
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Term
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Definition
AKA: Isoimmunity. When the immune system of one individual produces an immunologic reaction against tissues of another individual.
Ex: transfusion reactions, hemolytic disease of the newborn, and transplant rejection. |
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Term
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Definition
disturbance in immunologic tolerance to self-antigens.
More often seen in women d/t cyclic estrogen/progesterone of menstural cycle. |
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Term
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Definition
| rapid and severe immediate hypersensitivity reaction |
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Term
| Type I IgE-Mediated Hypersensitivity Reactions |
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Definition
Most common allergies (example, pollen) are type I reactions. Most occur against environmental antigens and are therefore allergic. . Repeated exposure usually is required to become “sensitized”.
Examples: asthma, atopic dermatitis/rhinitis, allergic anaphylaxis. |
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Term
| Type II: Tissue-Specific Hypersensitivity Reactions |
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Definition
A specific type of cell or tissue that has a tissue-specific antigen on their surface, such as on the plasma membrane (example, platelets). Symptoms are determined by tissue type.
Ex: myasthenia gravis, graft rejection, transfusion rxns.
Five general mechanisms by which these reactions affect cells. |
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Term
| 5 Mechanisms of type II hypersensitivity reactions |
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Definition
1. The cell can be destroyed by antibody (IgG or IgM) and activation of the complement cascade through the classical pathway.
Ex: autoimmune hemolytic anemia.
2. Antibody may cause cell destruction through phagocytosis by macrophages.
3. Antibody and complement may attract neutrophils…which release their granules…and destroy the tissues.
4. Antibody-dependent cell-mediated cytotoxicity (ADCC) involves a subpopulation of cytotoxic natural killer (NK) cells which release toxic substances.
5. Cell malfunction, not death, is caused by the antibody interfering with cell surface receptor, inappropriately stimulating or destroying them. Example, Graves’ disease. |
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Term
| Type III: Immune Complex-Mediated Hypersensitivity Reactions |
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Definition
Most are caused by antigen-antibody complexes that are formed in the circulation and deposited later in vessel walls or extravascular tissues.
Not organ/tissue specific, harmful effects caused by compliment activation through the generation of factors for neutrophils. Lysosomal enzymes are released into inflammatory site causing tissue damage.
Ex: glomerulonephritis, vasculitis, arthritis, degenerative joint disease, rheumatic heart disease, reynauds syndrome, SLE, serum sickness, arthus reaction |
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Term
| Type IV: Cell-Mediated Hypersensitivity Reactions |
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Definition
Only one NOT mediated by antibody, mediated by T lymphocytes.either Tc cells (attack directly) or lymphokine-producing Th1 cells (produce cytokines that activate phagocytic cells esp. macrophages which release lysosomal enzymes).
Ex: PPD skin test for TB
graft rejection, allergic reactions from poison ivy and metals, and many autoimmune diseases such as rheumatoid arthritis, Hashimoto disease, and Type I insulin dependent DM.
DELAYED, takes about 3d to manifest. |
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Term
| Typical allergens, by type, that cause hypersensitivity |
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Definition
Type I: pollens, molds, foods, animals, house dust.
Type II: penicillin or sulfonamides
Type III: hepatitis B. RARE
Type IV: usually plant resins (ex: poison ivy), metals (ex: nickel), chemicals (ex. detergents), and topical antibiotics (ex. neomycin). |
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Term
| Clinical symptoms of Type I hypersensitivity |
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Definition
are mostly due to the biologic effects of histamine.
Respiratory: include conjunctivitis, rhinitis, and asthma
GI: N/V/D, cramps, pain, malabsorption. Usually caused by food/meds.
Skin: hives(uticaria) may develop. Wheal and flare reaction has white fluid-filled blisters (wheals) and red surrounding areas (flares). Itching is present. |
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Term
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Definition
| genetic predisposition to develop allergies, particularly Type I. Atopic individuals tend to produce higher quantities of IgE. |
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Term
| Systemic Lupus Erythmatosus |
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Definition
chronic, multisystem, inflammatory disease and is one of the most common, complex, and serious of the autoimmune diseases. SLE occurs more often in women, occurs more often in blacks,has a genetic predisposition, Affects almost every body system. Develops slowly and is difficult to diagnose.
Clinical manifestations include:
•arthralgias or arthritis (90%)
•vasculitis and rash (70-80%)
•renal disease (40-50%)
•hematologic abnormalities (50%, esp. anemia)
•cardiovascular diseases (30-50%) |
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Term
| SLE diagnosis requires presence serially or simultaneousely of 4 of these |
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Definition
1.Facial rash confined to cheeks (malar)
2.Discoid rash (raised patches, scaling)
3.Photosensitivity (avoid light esp ultraviolet)
4.arthritis
5.Renal disorder
6.Neurologic disorders (seizures or psychosis)
7.Hematologic disorders (hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia)
8.Immunologic disorders |
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Term
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Definition
Most important trans rxn is the ABO system. consists of two major carbohydrate antigens, labeled A and B. Codominant, meaning that both A and B can be expressed. Blood type A has the A carbohydrate antigen and antibodies to B. They cannot accept blood types B or AB.
Type B has the B antigen, and antibodies to A. They cannot accept blood types A or AB.
Type AB has both the A & B antigen, and no antibodies. They can accept any blood type (universal recipients).
Type O has neither the A or B antigen, and antibodies to A & B. They can only accept blood type O (universal donors). |
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Term
| Hemolytic disease of the newborn |
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Definition
The RhD protein is dominant, and determines whether the pt is Rh-positive or Rh-negative.
If D antigen is expressed on RhD protein = Rh-positive.
If the D antigen is not expressed = Rh-negative.
Rh-negative mothers can make IgG anti-D if exposed to Rh-positive RBCs of fetus. |
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Term
| Transplant rejection types |
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Definition
1. Hyperacute rejection: Immediate and rare. Called a “white graft” since tissue turns white due to lack of circulation upon placement. Usually occurs in recipient with preexisting antibody to antigens in graft, such as previous graft or prior blood transfusion.
2. Acute rejection: Occurs within days or months, primarily a Type IV cell-mediated response against unmatched HLAs. Sensitization is initiated by recipient’s lymphocytes interacting with donor’s dendritic cells, resulting in recipient Th1 and Tc cells against donor’s antigens.
3. Chronic rejection: (p. 275.) Occurs months or years after placement; slow, progressive organ failure. May be caused by inflammatory damage to endothelial cells lining blood vessels as a result of a weak cell-mediated reaction against minor histocompatibility antigens on graft. |
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Term
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Definition
1.Attachment: to the target cell determines host range and tropism.
2.Penetration: by endocytosis or membrane fusion.
3.Uncoating: the release of viral nucleic acid from the viral capsid by viral or host enzymes.
5.Assembly: the formation of new virions.
6. Release: by cell lysis, budding. New virions are released from the cell for transmission of the viral infection to neighboring uninfected cells. |
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Term
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Definition
Replicate in cytoplasm of invaded cell
Ex: polio and parainfluenza |
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Definition
Require DNA of cell to replicate. Virus enters nucleus and uses DNA polymerase.
Ex: Hep B, herpes, herpes zoster |
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Term
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Definition
Converts RNA genetic info to DNA using reverse transcriptase within T-helper cell of host.
Ex: HIV/AIDS |
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Term
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Definition
| Most common of human diseases. Viruses are simple microorganisms, have no metabolism and are incapable of independent repoduction. They are obligitory intracellular parasites, meaning they have to invade a permissive cell and use it to replicate. Therefore, viral genes can become part of the genetic information of a cell and its protegy. |
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Term
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Definition
Many pathogenic bacteria reside in humans without causing disease. This local colonization can still spread the disease even if the person does not have the symptoms- that person is then in a carrier state
Transmitted through human to human contact.
Invasion results in direct confrontation with the individual’s primary defense mechanisms. Survival and growth of the bacteria depend on the body’s defenses and the bacteria’s capacity to resist.
Pathogens produce exotoxins, they also elicit production of antitoxins.
Bacterial infections damage tissue directly, by bacterial products, or indirectly as a result of inflammation |
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Term
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Definition
1.Capsulation- coating with self protein. Ex: pneumococcal, TB, Strep
2.Exotoxins- release proteins to hurt cell membrane. Immunogenic causing antitoxins to form. Vaccines fro antitoxins- Tetanus, diptheria, pertussis.
3.Endotoxins- In cell walls of many gram neg bacteria. Released when cell destroyed. Pyrogenic, causing fever adn activating inflammaroty response. Ex: syphillis tx with pcn causes destruction of spirochete = release of endotoxin. causes high fever with in 24hrs. Called Jarisch-Herxheimer rxn. |
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Term
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Definition
Unicellular microorganism that establishes a symbiotic relationship with host- parasite benefits at the expense of the host.
Ex: Giardia Lamblia (diarrhea), Trichomoniasis. |
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Term
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Definition
Fungus are large microorganisms with thick rigid wall. Grow as single celled yeast or multicelled molds, and reproduces by simple diffusion or budding. Fungus are opportunistic. Mycosis (fungal infection) usually occurs in immune compromised people. low wbc or decreased immune response promotes fungal infection. fungus normally live in GI tract/vagina. dec immune system, change in pH, or antibiotics that kill normal flora allows overgrowth.
Superficial mycosis causes tineas (tinea capitus/corporus)
deep mycosis involves internal organs and can be life threatening. |
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Term
| Clinical manifestation of infection |
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Definition
| fatigue, malaise, weakness, loss of concentration, generalized aching, loss of appetite |
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Term
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Definition
Exogenous pyrogens-derived from outside the host. Ex: endotoxin release
o Endogenous pyrogens- produced by the individual. ( EX: interleukin 1, 6, Interferon, tumor necrosis factor…)- raise the thermoregulatory set point through stimulation of prostaglandin synthesis. |
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Term
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Definition
induce active immunologic protection before exposure to the infection. An initial immunization protocol produces large numbers of memory cells and a sustained protective secondary immune response. Vaccine induced protection does not last as long as infection induced immunity, so booster shots are needed.
o Vaccination against toxins is achieved using toxoids- purified toxins that have been chemically detoxified without loss of immunogenitcity.
Vaccines are usually attenuated (weakened).
Hep B vaccine is recombinant viral protein. Initiates antibody response
Hep A and pneumonia vaccines are an inactivated (killed). Uses antigens on cell. |
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