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immunology8
exam 8
| Question | Answer |
|---|---|
| role of activated CD4 T cells | MHC restricted 1.facilitate humoral response 2.facilitate CTL response 3,facilitate phagocytic response |
| role of activated CD8 T cells | cytotoxic T cells 1.kill infected or abnormal cells |
| transplantation | process of taking cells, tissues, or organs (graft) from one individual and placing them into a different individual. |
| donor | provides graft |
| recipient | receives the graft |
| atuologous | from one individual to the same individual |
| syngeneic | between two genetically identical individuals |
| allogenic | between genetically different individuals of the same sp. |
| xenogeneic | between individuals of different sp. |
| why are MHC proteins the most important alloantigen for transplant rejection/tolerance | 1.highly polymorphic 2.on all cells. Many of them on each cell 3.lymphocytes will react to foreign MHC |
| hyperacute reaction | 1.occur within minutes 2.directed against graft vasculature 3.due to presence of performed antibodies (classical complement) |
| how are hyperacute reactions prevented | blood typing |
| acute reaction | 1.occur within days-weeks 2.adaptive immune response 3.mediated by T cells and AB specific for alloantigens 4.CD8 T cells directly kill graft cells 5.CD4 cells secrete cytokines and induce inflammation |
| how are acute reactions prevented | immunosuppressive therapy |
| chronic reaction | 1.occur over months to years 2.adaptive immune response 3.mediated by T cells and AB specific for alloantigens 4.CD4 cells secrete cytokines and induce inflammation and fibrosis |
| graft vs host disease | 1.tissue from graft is attacking host tissue 2.caused by rxn of grafted mature T cells with alloantigens of host |
| immunogenic factors that cause graft vs host disease | 1.NK cells, CD8 CTL, cytokines |
| transplanting what generally causes graft vs host disease | marrow or organs with sig number of T cells |
| Prevention of transplantation rxn | 1.match MHC alleles 2.immuno suppression |
| what does general immunosuppression work | mainly inhibit T cell activation and effector function |
| basiliximab works against | IL-2 |
| cyclosporin works against | T cell phosphatase (calineurin). isolated from fungus |
| calieurin | required to activate trascription factor NFAT. required for transcription of cytokine genes in T cells. |
| tacrolimus works against | calcineurin |
| do RBCs have MHC | No. have glycosylated membrane proteins. |
| what species have AB naturally | Cats and humans |
| In cats what blood type is dominant | A is dominant over B |
| type A cats | most common. have low level AB against type B |
| type B cats | less common. have high level of AB against type A. Cross matching critical!! |
| what happens when type B cat receives type A blood | immediate anaphylactic rxn |
| what happens when type A cat recieves type B blood | first time maybe minor rxn. second time anaphylactic rxn |
| cross matching | detects presence of serum AB to RBC antigens |
| how is cross matching done | via saline agglutination assays |
| cross matching process | 1. donor serum mixed with recipient RBC 2.Donor RBC mixed with recipient serum |
| which blood type allele is most antigenic in dogs | DEA 1.1+. most common. primary lytic factor |
| what happens when a DEA1- dog is transfused with DEA1+ blood | the dog becomes sensitized |
| what blood type allele occurs on 98% of canine RBCs | DEA 4 and 6 |
| universal blood donor type in dogs | DEA 1.1- |
| Most common antigenic blood type variants in horses | Aa and Qa |
| fresh whole blood | collected immediately prior to transfusion |
| what factors do fresh whole blood supply | viable platelets, RBCs, WBCs, all clotting factor and plasma proteins |
| stored whole blood can be stored for how long | 28-35 days |
| stored whole blood contains what factors | RBCs, WBCs, plasma proteins. platelets are only viable for 2 hrs after refrigeration. labile clotting factors are only active for 24 hrs |
| Packed RBCs are prepared by | separating whole bood into red blood cells and plasma |
| Packed RBCs can be refrigerated for how long | 28-35days |
| Fresh frozen plasma | plasma separated from fresh whole blood and frozen at -20C to -30C within 6-8hr of collection from donor |
| what factors does fresh frozen plasma contain | all clotting factors, labile factors. viable for 1 yr |
| what happens to fresh frozen plasma after 1 yr | relabeled as frozen plasma to reflect loss of clotting factors |
| frozen stored plasma contains what factors | small amount of clotting factors, all Vit K dependent factors, plasma proteins. stored for 5 yr |
| what plasma type can be used to treat warfarin toxicity and why | Frozen stored plasma because contains all Vit K dependent factors |
| cryoprecipitate | prepared from fresh frozen plasma, thawed at 0-6C. resulting precipitate. |
| what factors does cryoprecipitate contain | clotting factors 8/11/13, von Willebrand's factor, fibrinogen 10 fold. can be stored for 1 yr at -20C. |
| what factors define cancer | 1.abnormal cell prolif 2.metastases 3.cell death 4.angiogenesis 5.avoid immune destruction |
| cancer and immune system | 1. more common in patients with defective immune systems 2.spontaneous resolution of cancer after severe infection 3.tumor with lymphoid infiltrates have better prognosis 4.vaccinations to prevent specific cancer types |
| tumor specific antigens | 1.CD antigens 2.C-kit 3.tyrosinase 4.PSA 5.FOCMA |
| CD antigens | differentiation antigens. proteins associated with specific stage of cell differentiation |
| C-kit | mutated proteins. altered forms of normal cellular proteins. important for stem cell maturation. promotes growth and diff. |
| tyrosinase | excessive amount of normal proteins, over-production of normal cell products |
| PSA | Cancer/tesitis antigens. proteins of unknown function |
| FOCMA | Viral coated proteins. products of genes of oncogenic viruses |
| C-kit in canine mast cell tumor | aberrant expression is associated with poor outcome. overexpression and mutations allow selective tumor targeting. small molecular inhibitors that block activation site in kinase |
| tyrosinase | melanosome associated glycoprotein that is critical for melanin production. expression limited to melanocytes. |
| tyrosinase regulation | up reg in dev melanocytes. turned off in quiescent melanocytes. overexpression in melanocytic tumors |
| most effective immune responses targeting tumors | are CTLs and NK cell responses |
| tumor developed mechanisms to evade immune recognition | 1. aberrant proteins weakly immunogenic 2. tumors dev resistance to immune recognition or destruction 3.immune dysfunction |
| mechanisms of tumor resistance | 1.reduced or absent expression of tumor antigens 2.reduced or absent MHC1 expression. no tumor specific CTL response. |
| TGF Beta and tumor cells | suppressive in early phase of tumor dev. promoter in later phase of tumor formation |
| immunosuppressive cytokines | TGF beta, IL-4, IL-6, IL-10 |
| tumor blocks the action of what co stimulator | CD28/B7 |
| CTLA-4 and cancer signaling | inhibitory signal to B7 costimulator. block in melanoma, lung cancer |
| PD-1 cell surface cancer signaling | found on T cells and Pro-B cells. activation promotes apoptosis, block in melanoma, and lung cancer |
| what T cells subsets are increased in circulating Tregs in tumor bearing dogs | CD4, FOXP3, |
| what is the CD8/Treg ratio prognostics for | survival chance |
| Three general strategies for cancer treatment | 1.non-specific immune stimulants 2.passive immunotherapy 3.active immunotherapy |
| cytokine therapy includes what factor | IFN-a, IFN-b, IFN-g, TNF-a, IL-2. |
| invitro primed T cell therapy | lyphokine activated killer cells. Adoptive T cell therapy improves outcome in canine lymphoma |
| monoclonal Ab therapy | target vascular stroma, tumor antigens, membrane death receptors. treat many solid and hematogenous cancer. |
| monoclonal Ab therapy uses what markers | CD52-pan-lymphoid marker CD20-B-cell marker |
| examples of vaccinations against oncogenic viruses | 1.FeLV-leukocell 2 vaccine (FOCMA antigen) 2.papilloma virus 3.marek's disease in avian |
| DNA vaccinations against tumor specific antigens | xenogenic tumor antigens to overcome self tolerance |
| Feline fibrosarcoma | most common SQ tumor of cats. strong association with FeLV/ rabies vaccination. high metastatic rate. IL-2 activity. USDA approval IL-2 therapy |
| equine sarcoids | most common skin tumor of horses. strong associated with bovine papilloma virus |
| canine osteosarcoma | most common bone malignancy in dogs. highly aggressive |
| use on what immune stimulants improve canine osteosarcoma outcome | 1.LMTP 2.local infection 3.cytokines |
| what are the USDA approved tumor directed immunotherapeutics | 1.Oncept IL-2 2.oncept melanoma 3.canine lymphoma AB |
| Oncept IL-2 | canary pox virus w/ DNA sequence for feline IL-2 insert. injected intralesionally. promote local IL-2 expression. |
| Oncept IL-2 used to treat | feline fibrosarcoma |
| oncept melanoma | pING plasmid w/DNA for human tyrosinase insert. injected IM. stim cross response against canine tyrosinase. |
| oncept melanoma used to treat | canine oral melanoma |
| canine lymphoma AB | CD52-pan-lymphoid (full AB). leads to ADCC, complement mediated lympholysis. CD20-B-cell specific (full AB). |
| Central self tolernce | immature self-reactive lymphocytes die or alter specificity so wont recognize self antigen. occurs in thymus and bone marrow |
| peripheral self tolerance | mature self reactive lymphocytes die, anergy, or suppressed by T reg cells. maintained in lymph nodes and circulation |
| mechanism of central tolerance in B cells | 1.clonal anergy 2.clonal deletion |
| clonal anergy B cells | soluble self-antigen leads to anergy of cell w/out cross-linking of lymphoid receptor |
| clonal deletion B cells | cross-linking of lymphoid receptor with MHC. leading to apoptosis. |
| mechanism of central tolerance in T-cells | 1.clonal deletion 2.positive selection 3.receptor editing changes in TCR |
| clonal deletion T cells | when react stongly with self antigen. negative selection |
| positive selection T cells | those react weakly |
| Absence of T cell co stim | Anergy |
| Fas | death receptor on all cells |
| Fas-Fas-L interaction | apoptosis |
| mutations in Fas and/or Fas ligand in humans results in | Auto immune lymphoproliferative syndrome |
| mechanisms of immune suppression of T reg cells | 1. activated by their TCR 2.Non-specific inhibitors 3.contact- inhibition 4.section of cytokines(TGF-B, IL-10) |
| non pathogenic autoimmunity | auto AB are found in normal healthy patients. ABs against proteins in aged RBCs for removeal |
| pathogenic Autoimmunity | associated w/ either normal or abnormal immune response |
| abnormal immune responses: mechanism | 1.cytokine dysregulation 2.loss of suppressor activity (cancer) 3.genetic defects (Fas) 4.Molecular mimicry (microbial cross resistance) |
| organ specific autoimmune disease | self antigen expressed on single organ or tissue. clinical signs referable to organ dysfunction |
| example of organ specific autoimmune disease | Myasthenia gravis |
| systemic autoimmune disease | autoantibody present for multiple self antigens affecting a wide variety of organs. |
| systemic autoimmune disease what causes organ damage | immune compelx deposition |
| example of systemic autoimmune disease | SLE |
| What is autoimmune hemolytic anemia | when erythrocytes bind anti-erythrocyte autoantibodies. Type 1 hypersensitivity |
| three mechanisms of autoimmune hemolytic anemia | 1.FcR+ cells in spleen 2.complement activation and CR1+ cells in spleen 3.complement activation and intravascular hemolysis |
| what is the result of autoimmune hemolytic anemia | 1.phagocytosis and erythrocyte destruction 2.lysis and erythrocyte destruction |
| systemic lupus erythermatosus type 2 reaction clinical signs | 1.anemia 2.skin lesions |
| systemic lupus erythermatosus type 3 reaction clinical signs | 1.glomerulonephritis 2.arthritis +/- 3.skin lesions |
| autoantigen in systemic lupus erythermatosus | nuclear proteins, DNA, RNA, histones |
| insulin dependent diabetes mellitus is what type of hypersensitivity reaction | type 4 |
| test to diagnose AIHA | Coombs test or Saline aggultination |
| test to diagnose systemic lupus | 1.ANA (antinuclear AB) test. AB directed against histones and riboproteins 2.LE prep |
| test to diagnose SLE or pemphigus | IFA on tissue sections |
| test to diagnose myasthenia gravis | acetylcholine receptor AB |
| mechanisms to target when treating auto immune disease | 1.reduce immune response 2.reduce inflammatory response 3.induce and maintain remission of clinical signs use a low drug dose |
| Medications to treat auto immune disease | 1.Corticosteroids 2.azathioprine 3.cyclosporine 4.cyclophosphamide |
| what type of hypersensitivity reaction is more easily treated | type 2. ok against type 3. |
| immunodeficiency | disease in which immune function is partially or totally absent. primary immunodeficiency |
| immunosuppression | inhibition of the immune system by an extraneous factor. secondary immunodeficiency |
| primary immunodeficiency | 1.inherited 2. classified according to branch of immune system |
| primary immunodeficiency can be classified how | 1.defects in mechanical barriers 2.defects in non specific defenses 3.defects in specific defenses |
| clinical symptoms that may lead to immuno deficient state | 1.unexplained neonatal illness affecting more than one animal in a litter 2.illness due to commensal or low pathogenic organism 3.recurrent illness 4.disease from MLV |
| Example of disease with defect in mechanical barrier | ciliary dyskinesia |
| ciliary dyskinesia genetic inheritance | autosomal recessive disorder |
| ciliary dyskinesia | dysplastic or immotile cilia due to abnormalities in microtubule organization |
| ciliary dyskinesia clinical signs | poor weight gain, coughing, nasal discharge, bronhopneumonia |
| example of disease with defects in non specific immunologic defenses | 1.cyclic hemayopoiesis of grey collies 2.chediak Highashi syndrome 3.pelger huet anamaly 4.canine granulocytopathy syndrome 5.leukocyte adhesion deficiency |
| cyclic hemayopoiesis of grey collies clinical signs | dilution of skin/hair pigment. cyclic fluctuation in WBC#. decreased number and function of neutrophils. recurrent infections |
| chediak Highashi syndrome genetic inheritance | autosomal recessive. mutation in CHS1 gene |
| chediak Highashi syndrome clinical signs | incomplete albinism, recurrent infections, enlarge granules w/in granulocytes, prolonged bleeding, photophobia |
| what is the CHS1 gene involved in | lysosomal trafficking. |
| how is chediak Highashi syndrome diagnosed | signs and blood smears (giant lysosomes) |
| pelger huet anamaly genetic inheritance | autosomal dominant disorder w/ incomplete penetrance |
| pelger huet anamaly | incomplete segmentation of granulocyte nuclei. PMNs look immature. PMNs have impaired ability to extravasate into infected tissue |
| canine granulocytopathy syndrome aka | canine leukocyte adhesion deficieny |
| canine granulocytopathy syndrome genetic inheritance | autosomal recessive trait |
| canine granulocytopathy syndrome | neutrophils have defective respiratory burst. |
| canine granulocytopathy syndrome clinical signs | severe skin infections. |
| leukocyte adhesion deficiency | mutation in integrin neutrophils (cant emigrate from blood vessels). unable to phagocytose bacteria coated with C3b |
| immunodeficiency of weimaraners clinical signs | recurrent fevers, diarrhea, pneumonia, pyoderma, osteomyelitis |
| leukocyte adhesion deficiency | low levels of IgG, IgA, IgM. defective neutrophil function. may have adverse response to vaccination |
| examples of defects in specific immunologic defenses | 1.RAG deficiency 2.MHC deficiency 3.Btk deficiency 4.TCR complex signaling |
| disease examples of defects in specific immunologic defenses | 1.severe combined immunodeficiency 2.SCIDS 3.Agammaglobulinemia 4.IgM deficiency 5.transient hypogammaglobulinemia 6.Trait A46 |
| severe combined immunodeficiency genetic factor | Defect in DNA dependent protein kinase. can't paste DNA strands after cutting. sends apoptosis signal |
| severe combined immunodeficiency | no functional V region of B and T cell receptors. no functional T or B cells |
| Canine SCID genetic inheritance | X linked. males only. |
| Canine SCID | normal B cell level but decreased Ig. decreased CD8. |
| Canine SCID clinical signs | LN and thymus small. often die from distemper MLV vaccine |
| Canine SCID genetic mutation | IL-2 receptor |
| Agammaglobulinemia | No B cells, AB |
| Agammaglobulinemia genetic inheritance | X linked disorder. seen in male foals |
| Agammaglobulinemia genetic mutation | Bruton tyrosine kinase. impairs B cell signaling. |
| transient hypogammaglobulinemia | delayed Ig synthesis. must distinguish from SCID. May need plasma AB. self limiting |
| Trait A46 genetic inheritance | autosomal recessive |
| Trait A46 | cant absorb zinc (needed for thymulin). T cell function impaired, decreased cell mediated immunity |
| examples of acquired/secondary immunodeficiency | 1.Failure of passive immunity transfer 2.Parvovirus 3.BVDV 4.FeLV 5.pasteurella |
| mechanism of immune suppression FIV | 1.loss of CD4 numbers 2.cytokine dysregulation 3.immunologic anergy and apoptosis |
| result of loss of CD4 numbers in immune suppression FIV | 1.Failure of cell mediated immunity (Th1) response 2.development of opportunistic infections |
| result of cytokine dysreguation in immune suppression FIV | inability to mount primary immune response against intracellular pathogens |
| systemic immune diseases preferentially affect what in the body | capillary beds |
| systemic immune disease results from | combination of genetic predisposition, environmental exposure, immune complex deposition |
| in systemic lupus erythematosus auto AB lead to damage through what mechanisms | 1. immune complex deposition through binding free antigen, glomerulonephritis 2.deposition in vascular walls and arteries 3.deposition in synovium and arthritis 4.aberrant activation of B cells 5.aberrant complement activation |
| systemic lupus erythematosus: musculoskeletal clinical signs | 1.non erosive polyarthritis 2.myositis |
| systemic lupus erythematosus; Hematologic clinical signs | 1.thrombocytopenia 2.anemia 3.leukopenia 4.splenomegaly |
| systemic lupus erythematosus:cardiovascular clinical signs | 1.vasculitis 2.myositis 3.arrhythmias |
| systemic lupus erythematosus:renal clinical signs | 1.glomerulonephritis |
| systemic lupus erythematosus: misc, clinical signs | 1.fever 2.opportunistic infections |
| LE preps | 1.blood clots, incubated 2.apoptotic cells phagocytosed 3.examine for neutrophils that have phagocytosed nuclear material |
| Antinuclear AB test | 1.use mouse liver cells (capture antigen) 2.patient anti-nuclear AB, if present, binds to antigen |
| systemic lupus erythematosus biopsy result | 1.fibrinoid necrosis and PAS+ precipitates along dermo-epidermal junction 2.mucin deposition in dermis 3.edema, hemorrhagem inflammation 4.fibrinoid material around cessels 5.bullous formation |
| systemic lupus erythematosus immunoflorescence results | 1.IgM+ 2.IgG+ 3.complement+ 4.ANA+ |
| discoid lupus erythematosus | mild variant of SLE where only facial/skin lesions are seen. affects basal layer of skin. |
| discoid lupus erythematosus clinical signs | 1.nasal dermatitis 2.depigmentation 3.erythema 4.erosion 5.ulceration 6.scaline 7.crusting |
| autoimmune polyarthritis | deposition of Ig or immune complexes w/in joints. |
| erosive polyarthritis aka | rheumatoid arthritis |
| erosive polyarthritis | erosion of joint cartilage, deformities, bony ankyloses, soft tissue swelling. generation of auto-AB |
| non erosive polyarthritis | most important variant in domestic species. no joint cartilage erosion, lesion confined to joint capsule and synovia |
| erosive polyarthritis diagnosis | 1.presence of RF AB 2.neg ANA |
| erosive polyarthritis treatment | 1.analgesics 2.steroid 3.anti-metabolites 4.monoclonal AB to TNF, CD4,IL-2 5.Joint fusion |
| three groups of non erosive polyarthritis | 1.arthritis associated w/ systemic lupus 2.arthritis associated w/ myositis 3.idiopathic polyarthritis |
| arthritis associated w/ systemic lupus diagnosis | symptom of SLE. positive ANA, multi organ disease |
| arthritis associated w/ myositis diagnosis | muscle atrophy and pain w/ non erosive arthritis. muscle biopsies show mononuclear inflammation. neg ANA |
| idiopathic polyarthritis type 1 | uncomplicated. cyclic fever, severe joint pain, neg ANA. RF |
| idiopathic polyarthritis type 2 | associated w/ infectious lesion outside joint. reactive process 2nd to respiratory, urinary, dental infection. cellulitis |
| idiopathic polyarthritis type 3 | associated w/GI disease. may be ID to type 2 |
| idiopathic polyarthritis type 4 | associated w/ neoplasia. seminomas, carcinomas |
| idiopathic polyarthritis symptoms | fever,lethargy,anorexia,lameness,muscle atrophy.stiffness after rest.soft tissue swelling and joint effusion |
| idiopathic polyarthritis typically affects what joints | stifle, elbow, carpus |
| dermatomyositis | clinical syndrome of dermatitis and myositis. normal at birth and dev skin lesion at 7-11wk. dev myositis at 12-23wks |
| dermatomyositis clinical signs | skin lesion.chronic hypopigmentation, alopecia, hyperpigmentation. typically starts on face |
| dermatomyositis caused by what Ig | rise in circulating IgG. normalize as disease resolves |
| dermatomyositis treatment | pred, Vit E, pentoxy |
| vasculitis clinical signs | episodic fever and cervical pain |
| vasculitis disease progress | lead to fibrosis. progress to amyloidosis |
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ejohnson17
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