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Immunology 13,18-19
Immunology chapters 13, 18, 19
| Question | Answer |
|---|---|
| selectins | family of CAMS that has a lectin-like domain, binds to specific sugars, and is expressed on vascular endothelial cells during an inflammatory response; is responsible for initial transient adherence of leukocytes to vascular endothelium |
| Mucins | family of CAMs that is heavily glycosylated and make great binding sites for lectins & selectins |
| Integrins | family of CAMs that are heterodimeric proteins, bind to ECM molecules and CAMs. |
| Ig-Superfamily | family of CAMs that are expressed on vascular endothelial cells and bind to integrins |
| chemokines | These are a superfamily of small polypeptides that control adhesion, chemotaxis, and activation of many leukocytes |
| CCR, CXCR; 7-pass G-protein-linked receptors | 2 chemokine receptors with brief description |
| 4 | number of cysteine residues possessed by chemokines |
| rolling, activation by chemoattractant stimulus, arrest & adhesion, and extravasation | Four basic steps of leukocyte extravasation |
| rolling | this extravasation step is mediated by E-selectins & P-selectins, which bind loosely to mucin-like CAMs or other sugars on leukocytes |
| Activation by chemoattractant stimulus | This extravasation step involves chemokines from endothelial cells binding to receptors on leukocytes, changing conformation/clustering of integrins |
| Arrest & adhesion | this extravasation step is mediated by integrins binding to Ig-superfamily CAMs |
| extravasation (transendothelial migration) | this fourth step in leukocyte extravasation involves WBCs actively diapedesing out in-between endothelial cells |
| monocyte | this type of extravasation is activated later because endothelial ligands needed for monocyte binding take longer to be expressed |
| lymphocyte recirculation | this increases the likelihood that antigen will be encountered by the right T or B cell |
| HEVs (high endothelial venules) | These are found in various lymphoid organs (poast-capillary venules, secondary lymphoid organs) and are the site of lymphocyte extravasation |
| tissue type where they first encountered Ag, thus returns to where it is most likely to meet up with the same Ag again | region where memorcy cells 'home' selectively |
| regions of infection, recognizing inflamed vascular endothelium & localized chemokines | region where effector cells 'home' |
| Hageman | This factor is activated in order to activate kallikrein in the kinin system |
| bradykinin | kallikrein cleaves kininogen to produce this |
| increase of vascular permeability, vasodilation, pain, & smooth muscle contraction | effects of bradykinin |
| kallikrein | other than kininogen, this also cleaves C5 into C5a and C5b (C5 convertase) |
| thrombin | damage to blood vessels leads to an increase in this |
| insoluble fibrin and fibrinopeptides | these are produced by thrombin being acted on by soluble fibrinogen to begin clot formation |
| fibrinolytic sytem | this system's purpose is to remove fibrin clots after they've done their job |
| anaphylatoxins | C3a and C5a are considered this, and part of their effect is to induce degranulation of mast cells |
| IL-1, IL-6, TNF-alpha | These cytokines are especially pyrogenic, increase vascular permeability, and activate T and B lymphocytes |
| arachidonic acid; PAF (platelet activating factor) | certain phospholipids in the membrane can be degraded into either this or this |
| prostaglandins and thromboxanes | arachidonic acid is converted into these via cyclooxygenase pathways |
| leukotrienes | arachidonic acid is conveted into this by the lipooxygenase pathway |
| COX inhibitors | These block the cyclooxygenase enzymes to prevent inflammation and pain |
| NSAIDS (non-steroidal anti-inflammatory drugs) | these inhibit cyclooxygenase enzymes (ex. aspirin, ibuprofen, tylenol) |
| swelling, heat, pain, vasodilation, increase of vascular permeability, accumulation of fluid in tissues | characteristics of localized inflammatory response due largely to tohistamine, prostaglandins, bradykinin, and fibrinopeptides |
| fever, increased production of hormones (ACTH, hydrocortisone), increase WBC production, production of APR proteins like CRP in liver | characteristics of systemic acute-phase response |
| Ag is not cleared from tissues, involve cytokines such as INF-gamma and TNF-alpha | characteristics of chronic inflammation |
| corticosteroids (SAIDS) | these are derived from cholesterol and mimic the action of hydrocortisone made by the adrenal glands (ex. predisone, prednisolone, methylprednisolone) |
| COX-1 | The inhibition of this COX causes gastritis and renal toxicity |
| celecoxib (celebrex) | drug that is preferential Cox-2 inhibitor |
| Influenza | This virus can transfer cross-species, and is enveloped with 2 specific glycoproteins |
| Hemagluttinin | This helps attack virus to host cell in Influenza |
| Neuraminidase | This helps viral budding from host cells in Influenza |
| nucleocapsid | this has 8 different ssRNA linear strands, and is associated with protein & RNA pol |
| Ag drift | series of spontaneous point mutations that occurr gradually to HA, NA; minor changes |
| Ag shift | sudden emergence of a new subtype with very different HA and NA; can readily occur via re-assortment when a cell is co-infected with two different viruses |
| IL-1, TNF-alpha | overproduction of these cytokines can lead to septic shock |
| Diphtheria | this disease is caused by a secreted exotoxin that causes formation of a tough fibrous pseudomembrane in the nasopharynx, which can lead to suffocation |
| diphtherotoxin | name for binding chain +toxin chain in disease caused by Corynebacterium diphtheriae. |
| toxoid | vaccine made by treating diphtherotoxin with formaldehyde |
| Tuberculosis | leading cause of death via a single infection agent; emergence of antibiotic-resistance strains |
| tubercle | in 90% of patients, this if formed to contain tuberculosis infection |
| BCG vaccine (Bacille Calmette-Guerin) | vaccine that is an attenuated strain of M. bovis, but is not 100% effective against tuberculosis |
| Lyme Disease | disease caused by Borrelia burgdorferi that is carried by a tick, and leaves a characteristic bull's-eye rash |
| rash, joint inflammation, neurological symptoms | after Lyme disease infection, anti-flagellar Ab are detected, resulting in a Type III hypersensitivity reaction, contributing to these symptoms |
| active immunity | one's own immune system is activated |
| passive immunity | one's own immune system is not activated, but is given Igs |
| Natural Active | This type of active immunity results from an infection |
| Artificial active | this type of active immunity results from vaccinations |
| IgG (placenta, and IgA (milk) | Natural Passive Immunity comes from Mom's: |
| vaccinia virus | live natural vaccine against smallpox |
| polio | Sabine vaccine orally administered against this virus |
| measles, mumps, rubella (german measles) | MMR vaccine against these 3 viruses |
| varicella zoster | vaccine against chicken pox virus |
| reversion | danger of life whole organism vaccines |
| polio | Inactivated Salk vaccine used against this virus |
| typhoid | Inactivated vaccine against Salmonella typhi |
| plague | Inactivated vaccine against Yersinia pestis |
| cholera | Inactivated vaccine against Vibrio cholerae |
| diphtheria, pertussis, tetanus | DPT vaccine against these 3 diseases |
| gas gangrene | subunit vaccine against clostridium perfringens |
| toxoids | subunit vaccine among the most successful bacterial vaccines |
| Bacterial polysaccharide capsules | subunit vaccine that causes formation of opsonizing Abs |
| Multivalent subunit vaccines | subunit vaccines that have multiple epitopes and contain immunodominant epitopes for both T & B cells |
| recombinant vector vaccines | subunit vaccines that use attenuated viruses or bacteria as vectors for Ag of other pathogens |
Created by:
charsany
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