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exam 8

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 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 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 lesions
systemic lupus erythermatosus type 3 reaction clinical signs 1.glomerulonephritis 2.arthritis +/- 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
Created by: ejohnson17



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