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2011-01-18 14:35:57

step1 UW
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  1. H1 receptors blockade
    • loratadine, fexofenadine, cetirizine;
    • less sedating, do not cross BBB
  2. class MHC 1
    cytotoxic T cells require MHC class 1 molecules on the surface of the tumor cells in order to eliminate them
  3. Immature T-lymphocytes
    express both the CD4 and CD8 cell surface antigens in addition to a complete TCR or a pro TCR. These lymphocytes exist in the thymic cortex where they undergo positive selection and in the thymic medulla where they undergo negative selection.
  4. Immunologic abnormalities in sarcoidosis
    include intraalveolar and interstitial accumulation of CD4 + T cells, resulting in high CD4:CD8 T-cell ratios in bronchoalveolar lavage (BAL) fluid.
  5. Anti-Rh immunoglobulin (RhoGAM)
    consists of lgG anti-Rh(D) antibodies. lgG antibody isotypes are thought to be most effective in both blocking and clearing “foreign” fetal Rh(D) antigens after fetomaternal transfusion.
  6. Poison ivy dermatitis
    is one form of contact dermatitis, a type IV hypersensitivity reaction. Type IV hypersensitivity reactions are mediated primarily by T lymphocytes. The cutaneous lesions in poison ivy dermatitis are typically linear erythematous papules, vesicles or bullae that are pruritic.
  7. MHC Class II
    is expressed on the surface of antigen presenting cells (APC) and functions by presenting antigen that is foreign to the body. This antigen is taken into the APC by phagocytosis or endocytosis and is loaded onto MHC Class II within acidified endosomes, and the MHC Class II protein-antigen complex is then expressed on the cell surface for subsequent interaction with T-lymphocytes. Failure to acidify lysosomes would lead to deficient expression of MHC Class II bound to foreign antigen and subsequent lack of interaction between APCs and T-cells.
  8. Serum sickness
    is a Type III hypersensitivity reaction characterized by deposition of circulating, complement-fixing immune complexes and resulting vasculitis. Associated findings include fever, urticaria, arthralgias, glomerulonephritis, lymphadenopathy, and a low serum CS level 5-10 days after intravascular exposure to antigen.
  9. The acute hemolytic transfusion reaction
    is an antibody-mediated (Type II) hypersensitivity reaction wherein host antibody binds antigen on transfused donor red blood cells, activating complement. The complement membrane attack complex causes erythrocyte lysis, and anaphylatoxins mediate vasodilatation and symptoms of shock.
  10. IL-4
    is produced by the T2 subset of T-helper cells. It facilitates growth of B-cells andTH2 lymphocytes, and stimulates antibody isotype switching, particularly to IgE.
  11. IL-12
    stimulates differentiation of “naive” I-helper cells into the TH1 subpopulation. Patients with IL-12 receptor deficiency suffer from severe mycobacterial infections due to the inability to mount a strong cell-mediated granulomatous immune response. They are treated with IFN-y.
  12. Granuloma formation
    • is a manifestation of cell-mediated immunity driven byproducts of TH1 type CD4+ helper T cells parlicularlylL-2 and interferon-y (lNF-y) which stimulate TH1 type cell proliferation and macrophage activation, respectively.
    • TH2 type CD4+ helper T cells predominantly drive humoral immune responses. Their products include IL-4, which promotes IgE antibody production by B-cells, and IL-5, which promotes the production and activation of eosinophils and B-cell synthesis of IgA.
  13. SLE
    Antibodies against double-stranded DNA (anti-d5DNA) are specific for systemic lupus erythematosus. However they are only present in 60% of cases so absence of anti-dsDNA does not rule out the diagnosis. Anti-Smith antibodies are also specific for SLE.
  14. The staphylococcal scalded skin syndrome
    occurs in infants and children due to the production of the exotoxin exfoliatin by Staphylococcus species. It causes widespread epidermal sloughing, especially with gentle pressure (Nikolsky’s sign).
  15. Immunity to M. pneumoniae
    develops due to production of IgA and lgG antibodies. 1gM antibodies produced during an infection by M. pneumoniae are known as cold agglutinins.
  16. Chédiak-Higashi syndrome
    is an autosomal recessive disorder of neutrophil phagosome lysosome fusion that results in neurologic abnormalities, partial albinism and an immunodeficiency caused by defective neutrophil function.
  17. Contact dermatitis, granulomatous inflammation, the tuberculin skin test and the Candida extract skin reaction
    are all examples of delayed-type hypersensitivity reactions (DTH). The cells that mediate DTH reactions are TH1- lymphocytes that release interferon-g to cause recruitment and stimulation of macrophages. DTH reactions take days to reach their peak activity; this is in contrast to the other hypersensitivity reactions which cause clinical effects within minutes of antigen exposure.
  18. When a live attenuated vaccine
    (eg, the Sabin oral polio vaccine) is applied to mucosal surfaces, it appears to promote more prolonged synthesis and secretion of local mucosal IgA than does a killed vaccine (eg, the Salk inactivated polio vaccine). This increase in mucosal IgA offers immune protection at the normal site of viral entry.
  19. Secretory form of IgA
    consists of two immunoglobulin monomers, J chain and secretory component. This immunoglobulin is abundant in tears, saliva, mucus and colostrum. It is particularly important as a component of the colostrum, or the first breast milk fed to an infant after birth, where is functions to provide the infant with passive mucosal immunity.
  20. During the primary response to a new antigen,
    plasma cells produce 1gM only. Switching to other classes (isotypes) of immunoglobulins occurs later in the germinal centers of lymph nodes. lgG is the main immunoglobulin of the secondary response.
  21. Ataxia-telangiectasia
    is an autosomal-recessive disorder resulting from a defect in DNA-repair genes. The DNA of these patients is hypersensitive to ionizing radiation. Manifestations include cerebellar ataxia, oculocutaneous telangiectasias, repeated sinopulmonary infections, and an increased incidence of malignancy.
  22. Hyper-lgM syndrome
    results from an inability of B-lymphocytes to undergo isotype switching from 1gM to other immunoglobulin isotypes such as lgD, lgG, IgE and IgA. Clinically, hyper-lgM syndrome most commonly results in lymphoid hyperplasia and recurrent sinopulmonary infections. The syndrome results most commonly from a genetic absence of the CD-40 ligand on B-lymphocytes or from a genetic deficiency in the enzymes responsible for the DNA modification that takes place during isotype switching.
  23. Leukocyte adhesion deficiency
    results from the autosomal recessive genetic absence of CD18. This leads to the inability to synthesize integrins. Integrins are necessary for leukocytes to exit the bloodstream, and sequelae of this illness include recurrent skin infections WITHOUT pus formation, delayed detachment of the umbilical cord and poor wound healing.
  24. Langerhans cell
    s are dendritic cells found in the skin that act as professional antigen presenting cells. These cells are derived from the myeloid cell line and they possess characteristic racquet-shaped intracytoplasmic granules known as Birbeck granules.
  25. The process of negative selection
    in T cell maturation is essential for eliminating T cells that bind to self MHC or self antigens with high affinity. If these cells were permitted to survive they would likely induce immune and inflammatory reactions against self antigens leading to autoimmune disease.
  26. Major adaptive immune mechanisms that prevent reinfection with the influenza virus
    include anti-hemagglutinin lgG antibodies in circulation and mucosal anti-hemagglutinin IgA antibodies in the nasopharynx.
  27. C. tetani
    produces the protein exotoxin tetanospasmin that blocks release of inhibitory neurotransmitters from inhibitory motor interneurons in the CNS. Tetanus is prevented by immunization with toxoid that triggers the production of antitoxin antibodies (active immunity).
  28. In silicosis
    , there may be disruption of macrophage phagolysosomes by internalized silica particles. Macrophage killing of intracellular mycobacteria may be impaired as a result, causing increased susceptibility of patients with silicosis to pulmonary tuberculosis.
  29. Killed or viral component vaccines
    predominantly generate a humoral immune response instead of a strong cell mediated immune response.
  30. Di George syndrome
    is a T-lymphocyte immunodeficiency that results from maldevelopment of the third and fourth branchial (pharyngeal) pouches due to a deletion on chromosome 22. Clinical associations with this syndrome include absence of athymic shadow on neonatal X-ray, hypocalcemic tetany from absence of the parathyroids, cleft palate, mandibular deformity, low-set ears, and aortic arch abnormalities.
  31. The chemokine receptor CCR5
    acts as a coreceptor that enables the HIV virus to enter cells. Deletion of both of the genes that code for this receptor results in resistance to HIV infection. Deletion of one allele leads to delayed manifestations of the disease in infected individuals.
  32. Hyperacute rejection
    is a process that is mediated by preformed recipient antibodies against antigens on the host organ (Type II hypersensitivity). Examples of such mismatches include ABO blood group antibodies and anti-HLA antibodies. This form of rejection occurs immediately upon perfusion of the transplanted organ by recipient blood and is often diagnosed intraoperatively due to immediate mottling of the organ.
  33. Erythroblastosis fetalis and hemolytic disease of the newborn
    are diseases resulting from maternal anti-fetal erythrocyte antigen IgG antibodies. The mother is sensitized to antigens present on fetal blood and mounts a humoral immune response to these antigens causing hemolysis in the fetus in utero due to the capability of lgG to cross the placenta and enter the fetal circulation. This is one form of Type II (antibody mediated) hypersensitivity.
  34. Mutation of the FAS protein
    is thought to prevent apoptosis of auto-reactive lymphocytes, there by disposing the individual to develop autoimmune disorders such as systemic lupus erythematosus.
  35. Local defense against Candida
    is performed by T-cells whereas systemic infection is prevented by neutrophils. For this reason localized candidiasis is common in HIV (+) patients while neutropenic individuals are more likely to have systemic disease.
  36. Severe combined immunodeficiency (SCID)
    most commonly results from an autosomal recessive deficiency of adenosine deaminase, an enzyme necessary for the elimination of excess adenosine within cells. Toxic levels of adenosine accumulate within lymphocytes in this condition, leading to lymphocyte cell death and resultant cellular and humoral immune deficiency. Treatment is presently being researched using retroviral vectors to “infect” patient stem cells with the gene coding for adenosine deaminase.
  37. Chronic renal allograft rejection
    can manifest months to years after transplantation. It is mediated by recipient antibodies to graft endothelium formed after engraftment and causes an obliterative intimal smooth muscle hypertrophy and fibrosis of cortical arteries. Hyperacute rejection involves pre-formed recipient anti-donor endothelial antibodies which immediately cause vascular fibrinoid necrosis, neutrophil infiltration, and infarction of the graft. Acute rejection may be cellular and/or humoral, causing, respectively, an interstitial mononuclear infiltrate and/or a graft vasculitis intermediate in severity between hyperacute thrombosis and chronic intimal thickening.
  38. Rheumatoid arthritis
    is an autoimmune disease triggered by an unknown antigen. Cartilage components serve as autoantigens that activate CD4T-cells, which in turn stimulate B-cells to secrete 1gM against the Fc component of lgG (rheumatoid factor).
  39. Sensitized TH2 cells
    secrete IL-4 and IL-β which together promote B-lymphocyte class switching for IgE synthesis. They also secrete IL-5, which activates eosinophils and promotes IgA synthesis. An excess of these TH2- produced lymphokines may contribute to the pathogenesis of extrinsic allergic asthma. IL-i is secreted by macrophages to stimulate helper T-cells. IL-3 from helper T-cells recruits bone marrow stem cells. y-interferon from helper T-cells functions mainly to activate macrophages. TGF-β is growth factor involved in tissue regeneration and repair.