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MUST TO KNOW - IMMUNOSEROLOGY
Medical Technology (BSMT1)
Emilio Aguinaldo College
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MUST TO KNOW IN IMMUNOLOGY AND SEROLOGY
IMMUNOLOGY
Emil von Behring Serum antitoxins Robert Koch TB Elie Metchnikoff Phagocytosis Paul Ehrlich Immunity Charles Richet Anaphylaxis Jules Bordet Complement Karl Landsteiner ABO blood group SSR Gerald Edelman Rodney Porter
Structure of antibodies
Rosalyn Yallow RIA Snell Dausset Benaceraf
MHC
Niels Jerne Immunoregulation Kohler Milstein
Monoclonal antibody
Susumu Tonegawa Antibody diversity Deéjavu Thomas Murray
Transplantation
Peter Doherty Rolf Zinkernagel
Dual recognition
Barreé-Sinoussi Luc Montagner
HIV
Pope Innocent VII 1 st: blood transfusion Christopher Columbus Old world New world = smallpox New world Old world = syphilis 1984 Year of discovery of T cell receptor gene 1979 (-) Small pox US Russia
Pure culture of smallpox
Lysozyme Attacks bacterial cell wall Ineffective against Mycoplasma and Ureaplasma (no cell wall) LAK cells NK cells + IL- Against cancer NK/Null/3rd population lymphocyte
(-) Markers on T/B cells Kills virus and tumor cells CD 16, CD 56 Complement Major humoral immunity (natural) Phagocytosis “ICED”: Initiation, Chemotaxis, Engulfment, Digestion Direct phagocytosis Primitive pattern recognition receptor Indirect phagocytosis Via opsonins Initiation CR3 (3rd C’ component) Laminin receptor Leucyl-formyl-methionyl-phenylalanine receptor Chemotaxis C5a (potent chemotaxin) Job’s syndrome = N-RA/Abn-CA Lazy leukocyte syndrome = Abn-RA and CA Boyden Chamber assay = test for chemotaxis
Engulfment C3b (opsonin) Histamine From eosinophils and mast cells Vasodilation IL-1 Lymphokine activating factor Secreted by monocytes and macrophages Mediates fever, APR’s CRP Serum amyloid A
APR’s 20-1,000x Fibroblasts Young cells Stabilize the wound area IFN-α Leukocyte IFN (Type 1) Produced by viral-induced leukocyte culture Major producer: NK cell IFN-β Fibroepithelial IFN (Type 1) Produced by dsRNA fibroblast cells IFN-γ Immune interferon (Type 2) Produced by immunologically-stimulated lymphocytes TNF-α Cachectin Produced by macrophages TNF-β Lymphotoxin Produced by CD4+ and CD8+ lymphocytes H. influenzae N. meningitidis S. pneumoniae
Large capsule Cause meningitis
CGD (-) NADPH oxidase NBT dye test Test for CGD Granulocyte concentrate Appropriate blood component for CGD patients Hypothalamus Regulates body temperature (fever) Chronic inflammation γ-globulins (plasma cells) Heterophile antigens Antigen in unrelated plants and animals but are closely linked that they cross react with one another Order of activation (C’) C 142356789 Properdin Serum protein Bactericidal and viricidal Needs C3 and Mg2+ Betalysin Released by platelets Against Gram (+) except Streptococcus Active immunity Antibody production is done by the body Advantage: Long term Disadvantage: slow response Active natural Infection (Ag) Active artificial Vaccination (Ag) Vaccines: 1. Live = smallpox 2. Attenuated = BCG ( M. bovis ) 3. Dead = cholera, typhoid 4. Toxoid = C. tetani 5. Modified virus = poliovirus Passive immunity Antibody production is not done by the body Advantage: Immediate Disadvantage: short term Passive natural Transfer in vivo (Ab)
Cell flow cytometry Light scatter Forward LS = cell size Side/90O LS = cell granularity/complexity Fluorescence microscopy Labeled monoclonal antibodies Rosette test E-rosette assay = T cells (CD2) EAC (Erythrocyte Ab Complement rosette) = B cells Differentiate T cells and B cells T cell B cell Function CMI HI Organ Thymus BM (1st: Bursa of Fabricius – birds) Concentration 60-80% 20-35% (10-20%) Lifespan Longer Shorter Soluble substances Lymphokines Antibodies ID E-rosette Surface immunoglobulins Mitogen Concanavalin A Phytohemagglutinin Pokeweed mitogen
Lipopolysaccharide Pokeweed mitogen
Mitogen Substances that cause cells to divide Lymphocyte capping B cells HLA Chromosome 6 (short arm) Class I MHC Endogenous antigen Locus/Ag = HLA - A, B, C Chain structure = α-chain + β 2 microglobulin Cell distribution = all nucleated cells Presents antigen to CD8+ cells Class II MHC For antigen found on surface of the cell Locus/Ag = HLA - DP, DQ, DR Chain structure = α-chain + β-chain Cell distribution = B cells and macrophages Presents antigen to CD4+ cells Class III MHC “CCTB” Locus/Ag = C2, C4, TNF, Factor B Dendritic cells Most efficient APC Langerhans cells DC in skin IL-2 T cell growth factor Stimulates lymphocyte proliferation IL-3 Growth of stem cells and differentiation of blood cells IL- IL-
B cell growth factor 1 B cell growth factor 2 Differentiates B cell plasma cell IL-5: eosinophil differentiation IL-6 Enhance antibody production of plasma cell IL-12 NK stimulating factor Activates NK cells and cytotoxic T lymphocytes Heteroantigen Antigenic Graft rejection 1. Hyperacute = w/in mins 2. Accelerated = 2-5 days 3. Acute = 7-21 days 4. Chronic = >3 months Potent antigen >10 kDa Albumin 40 kDa Good immunogen
Hemocyanin 1M Da Excellent immunogen Proteins Most immunogenic (complex) Haptens Substance that is non-immunogenic but which can react w/ the products of a specific immune response Agglutinoids Agglutinins that are modified by heat Adjuvants Added to vaccines to enhance immune response 1. CFA = H 2 O in oil emulsion of M. butyricum or B. pertussis (MTB), stimulates T cells 2. LPS = stimulates B cells 3. Synthetic MDP (muranyldipeptide) = stimulates T cells 4. Alum adjuvant = stimulates phagocytic cells 5. Squaline = from shark’s oil, for HIV vaccine (MF59) Allograft Ex. Fetus on mother’s womb BM Most immunogenic graft Cornea Least immunogenic graft Avascular, privilege site Lymphocytotoxicity testing Determines class I and II Ag’s Ficolle-Hypaque solution: separates T and B cells from other cells Rgts: Trypan blue and C’ (from Guinea pig cells), antisera of known HLA spec. (+) Blue (-) Unstained Polyspecific reagents ID by elimination Nylon Wool technique For class II Mixture of T/B cells ---(Straw w/ nylon wool)---> B cells adhere to nylon wool B cells + antiserum of known HLA spec. ---(C’ + trypan blue)---> (+) Blue (-) Unstained MLR: Mixed Lymphocyte Reaction
For D-related antigens = Class II One way = one is inactivated Pt. lympho. + Donor lympho. (inactivated: irradiated/treated w/mitomycin) If incompatible proliferation of patient lymphocytes Tritiated hydrogen = radioactivity Antibodies Glycoproteins Ehrlich’s side chain theory Certain cells had specific receptor for antigen Antigen will select the cell w/ proper receptor Template theory (by Felix Haurowitz)
Antibody-producing cells produce generalized type of antibody Antigen serves as a mold/template Clonal Selection (by Neils Jerne & Macfarlane Burnet)
Most acceptable theory Individual lymphocyte produces 1 type of Ig Antigen finds cells capable of responding to that Ig proliferate Reduction of a polymer Ex. IgM
- 2-mercaptoethanol (2-ME)
- Dithiothreitol (DTT) Fab Ag binding 1 LC + ½ HC Fc Confer biologic activities of C’ fixation Skin fixation Placental transfer Papain 3 fragments = 2 Fab + 1 Fc Above the hinge region Pepsin 2 fragments = 1 F(ab) 2 + 1 Fc’ Below the hinge region
Produced by the liver except:
- C1 = intestinal epithelial cell
- Factor D = adipose cell Anaphylatoxin Release of vasoactive amines smooth muscle contractions vascular permeability Classical pathway Activated by Ag-Ab complexes C3 convertase: C4b2a/C4b2b C5 convertase: C4b2a3b/C4b2a3b C1q, 1r, 1s = bound by Ca2+ C1q = 6 globular structures (at least 2 globes must attach to Fc of CH2 of IgG/ CH3 of IgM) Alternative pathway Initiated by:
- Aggregates of IgA
- Yeast cell wall or zymosan
- LPS
- Cobra venom factor C3 convertase: C3bBb (stabilized by Properdin and Mg2+) C5 convertase: C3bBb3b Lectin pathway Initiated by microorganisms w/ mannose in their cell wall Lectins: proteins that attach to CHO MASP-1 & 2: MBL associated serine proteases 1 and 2 MBL = C1q MASP-1 = C1r MASP-2 = C1s C8 Starts pore formation (cell lysis) C9 cell lysis C1 INH Dissociates C1r and C1s from C1q Factor I Cleaves C3b and C4b Factor H Inactivates C3b Prevents binding of B to C3b C4-binding protein Inactivates C4b Vitronectin/S protein Prevents attachment of C5b67 complex to cell membrane DAF Dissociates C3 convertase HRF & MIRL (CD59) Inhibit MAC C1, C4, C2 deficiency LE-like syndrome C3 deficiency Severe and recurrent infections (most severe) C2 deficiency Most common C’ deficiency C56789 deficiency Neisserial infections (gonococcemia/meningococcemia) C1 INH deficiency HANE DAF/HRF deficiency PNH Hypersensitivity Reactions Type I Type II Type III Type IV Other name Immediate Anaphylactic
Cytotoxic Immune-complex Delayed Cell-mediated Immune mediator IgE IgG and IgM IgG and IgM T cells Complement involvement
No Yes Yes No
Effector cells Basophils Mast cells
RBCs WBCs Platelets
Host tissue cells T cells Macrophages
Type I Type II Type III Type IV Mechanism Release of mediators
Cytolysis due to Ab and C’
Deposits of Ag-Ab complexes
Release of lymphokines Examples Anaphylaxis Hay fever Food allergies Asthma Bee sting
HTRs AIHA HDN
Serum sickness Arthus reaction SLE RA
Low MW compounds (ex. Ni) Cosmetics Rubber Poison ivy/oak Myasthenia gravis Acetylcholine receptor blocking antibody Multiple sclerosis Anti-myelin antibody Pernicious anemia Anti-intrinsic factor antibody Anti-parietal cell antibody Goodpasture’s syndrome Anti-glomerular basement membrane antibody Primary biliary cirrhosis Anti-mitochondrial antibody Chronic active hepatitis Anti-smooth muscle antibody Hashimoto’s thyroiditis Anti-microsomal antibody Anti-thyroglobulin antibody Graves’ disease Anti-TSH receptor antibody Bence-Jones protein Multiple myeloma AFP Hepatocellular carcinoma hCG Choriocarcinoma Calcitonin Familial medullary thyroid carcinoma PSA Prostate cancer CEA Colorectal cancer CA 19-9 Pancreatic and colonic adenocarcinoma CA 15-3 Breast cancer CA 125 Ovarian cancer SEROLOGY 1’ immune response Long lag period Ab IgM 2’ immune response (anamnestic/booster)
Short lag period Ab IgG Affinity Attraction between 1 Fab and 1 epitope Weak bonds Dissociation can easily occur
- ionic bond
- hydrogen bond
- hydrophobic bond
- Van der Waals forces Avidity Sum of all attractive forces between multivalent Ag and multivalent Ab avidity = tendency of complex to dissociate Precipitation Soluble antigen == soluble antibody Noted by Kraus Zone of equivalence Max precipitation occurs (Ag = Ab) Prozone Antibody excess False (-) Remedy: Serum dilution Postzone Antigen excess False (-) Remedy: repeat the test after a week to give time for antibody production Passive immunodiffusion Passive: no electrical current is used
-HDN
-HTR
-AIHA
-DIHA
IgG Nonagglutinating Ab Can sensitize cells w/o causing visible agglutination AHG reagent Spans the distance between 2 IgG’s Mechanisms of DIHA 1. Drug absorption = Penicillin 2. Membrane modification = Cephalosporin 3. Immune complex formation = Stibophen, Phenacetin, Rifampin 4. Autoantibody formation (Gen. to Rh) = Methyldopa (Aldomet: Ab to Kidd), Mefenamic acid (Ponstel) HTR (+) DAT (-) DAT (mf) DAT = some are lysed and some are not lysed by C’ IAT In vitro sensitization Specimen: Patient serum (common) Uses: -Cross-matching -Ab detection -Ab identification -RBC Ag phenotyping (weak D) = Specimen: RBC Wash 3x To remove unbound globulins Inadequate washing False (-) antiglobulin test Unbound globulins can neutralize AHG reagent If (-) AHG Confirm by adding Check or Coomb’s cells (O+ RBCs sensitized w/ IgG) -Valid: Agglutination -To ensure AHG was added or not neutralized Types of AHG reagent 1. Polyspecific AHG = contain anti-IgG and anti-C3d (C’ degradation products) 2. Monospecific AHG = contain anti-IgG or anti-C3d Radioimmunoassay (RIA) Uses radioactive substances as label -Tritiated Hydrogen - 125 I Scintillation counter Measure radioactivity β = liquid scintillation counter γ = crystal scintillation counter Competitive binding assays (RIA)
Bound radiolabeled Ag is 1/α to patient Ag present
Noncompetitive immunoradiometric assays (IRMA)
Bound radiolabeled Ab is α to patient Ag present in supernatant fluid
RIST Measure total IgE RAST Measure Allergen-specific IgE Wastes container (DOH) 1. Red = sharps, needles 2. Yellow = infectious 3. Yellow w/ black band = chemical wastes 4. Green = non-infectious wet waste 5. Black = infectious dry waste 6. Orange = radioactive waste Enzyme immunoassay (EIA)
Similar to IRMA except that it uses enzymes
Horseradish peroxidase = most common
ALP
β-galactosidase
Glucose oxidase
G-6-PD Capture/Sandwich EIA Ab == Ag == enzyme labeled Ab Enzyme activity is α to the amount of Ag Fluorescent immunoassay Uses fluorophores/fluorochromes
Fluorescein Isothiocyanate (FITC) = Green
Tetramethylrhodamine Isothiocyanate (TRITC) = Red Direct immunofluorescent assay
Histopathology Unknown Ag + FITC/TRITC labeled Ab = (+) Fluorescence Indirect immunofluorescent assay
Serology (Ex. FANA, FTA-ABS) Known Ag + unknown Ab + FITC/TRITC labeled AHG = (+) Fluorescence Fluorescence polarization immunoassay (FPIA)
Change in polarization of fluorescent light emitted from a labeled molecule
PACIA Measures the number of nonagglutinating particles left Syphilis A.k. Great pox/Evil Pox/French/Italian/Spanish disease Caused by T. pallidum subsp. pallidum = RIP: Refrigerate blood for 3 days Congenital syphilis Hutchinsonian triad: Keratitis, Notched teeth, Deafness Treatment 1 st: Heavy metals (Ex. Arsenic: Arsphenamine, Salvarsan, 606) Penicillin: Drug of choice (crosses the placenta – Tx: Neurosyphilis) 1’ syphilis Lesion: Hard chancre Lab: Darkfield microscopy = (+) coiled organisms w/ corkscrew motility 2’ syphilis Highly infectious Systemic dissemination of organisms Wart-like lesions: Condylomata lata Lab: Darkfield microscopy, serologic tests Latent syphilis (-) Signs and symptoms (+) Serologic tests 3’ syphilis Granulomatous lesions: Gummas (Dead treponemes) CSF: Neurosyphilis Lab: Serologic tests Jarisch-Herxheimer phenomenon
Large quantities of toxins are released as the bacterial dies during treatment
Serologic Tests for Syphilis (STS)
♫ 1 st: Wasserman test = Principle: C’ fixation ♫ Nontreponemal serologic tests = nonspecific = Subjected to biologic false (+) = Principle: Flocculation (special type of precipitation involving fine particles) = Detects Reagin (Ab to cardiolipin) = Ex. VDRL, RPR, TRUST, USR, RST ♫ Treponemal Serologic tests = specific = Detect Treponemal antibodies = Ex. TPI, FTA-ABS, HATTS, TPHA, MHA-TP Biologic False (+) - Syphilis “TRIPLSM 2 ” TB RA IM Pregnancy Leprosy SLE Measles Malaria
e. Syphilis ASO Tube test Titer: reported as Todd unit Neutralization of the hemolytic activity of Streptolysin O (+) No hemolysis (-) Hemolysis Serum preparation Serum ÷ TV Titer Reciprocal of the highest dilution in w/c a positive reaction occurs RBC control No hemolysis SLO reagent control Complete hemolysis ASO Titer NV = 0-166 Todd (Tube test) Significant = >200 IU/mL (Slide test) DNase B Ab testing Anti-DNase B sometimes appear earlier than ASO Sensitivity for detection of glomerulonephritis Measured by neutralization DNA == methyl green Green DNase == DNA ≠≠ methyl green (-) Colorless Anti-DNase == DNase ≠≠ DNA == methyl green (+) Green [no color change] Streptozyme Slide agglutination screening test for detection of Ab’s to several Streptococcal Ag’s 1’ Hepatitis viruses Hepatitis A, B, C, D, E 2’ Hepatitis viruses EBV, CMV, etc. Hepatitis A Infectious hepatitis PicoRNAviridae (RNA) MOT: fecal-oral Short incubation period = 15-40 days Hepatitis B Serum hepatitis HepaDNAviridae (DNA) MOT: sexual, parenteral, perinatal Dane particle = infectious Hepatitis C Non-A, non-B hepatitis Flaviviridae (RNA) MOT: sexual, parenteral, perinatal Major cause of post-transfusion hepatitis (80% HCV || <10% HBV) Hepatitis D Viroid like (RNA) Require infection w/ HBV (coinfection or superinfection) Hepatitis E Caliciviridae/HepEviridae (RNA) MOT: fecal-oral, contaminated H 2 O fatality: pregnant HBsAg A.k. Australia antigen 1 st marker to appear in HBV infection Screen blood donors Acute or chronic infection HBeAg High vertical transmission risk (Mother Child) High degree of infectivity HBcAg NOT a serologic marker Detected only by liver biopsy IgM anti-HBc 1 st antibody to be produced Only marker detectable during “core window” period Acute infection Total anti-HBc Acute or chronic IgG: lifelong marker of HBV Anti-HBs Marker of past infection and immune state
Tested for vaccination and follow up Anti-HBe Marker of convalescence (recovery) HBsAg Anti-HBc Anti-HBs No HBV infection - - - Early infection + - - Acute HBV + + - Window period - + - Past infection - + + Immunization - - + HCV Surrogate test: ALT, (+) anti-HBc Specific test: (+) Anti-HCV = ELISA, RIBA IgM anti-HDV Detected by ELISA IgM anti-HEV Detected by ELISA, WB, Fluorescent antibody blocking assay HEV RNA ID by PCR PCR D>A>E: Denaturation > Annealing > Extension 1 st generation test (HBsAg) Ouchterlony double diffusion 2 nd generation test (HBsAg) Counterelectrophoresis Rheophoresis Complement fixation 3 rd generation test (HBsAg) RIA ELISA RPHA RPLA HIV-1 A.k. HTLV-III, LAV, ARV RNA virus (ssRNA, icosahedral, enveloped) Retroviridae (Lentiviridae) AIDS in US, Europe HIV-2 West Africa Less pathogenic, transmission HIV Retains infectivity for: 3 days (dried specimen) >A week (aqueous environment) Main structural genes (HIV) Env Gag Pol Env (envelope) gene gp = gp120: knobs/spikes = gp41: spans the inner and outer membrane Attachment and fusion to CD4+ cells Gag (Group Ag) gene p = p = p = p Located in nucleocapsid Pol (polymerase) gene Located in the core near the nucleic acid = Reverse transcriptase: transcribes RNA DNA = Integrase: inserts viral DNA to host DNA Ab to p24 1 st Ab to appear in HIV infection Screening tests (HIV) 1. ELISA = standard screening test 2. Agglutination tests = gel/latex particles 3. Dot-Blot testing Confirmatory tests (HIV) 1. Western Blot = standard confirmatory test
Amboceptor (hemolysin) Indicator Sheep RBCs coated w/ anti-sRBC IM Caused by EBV = Target cells: B cells (CD21) Hema: Lymphocytosis Atypical lymphocytes = T cells reacting to B cells infected w/ EBV Paul-Bunnell screening test General/screening test for heterophile Ab’s Reagent: sheep RBC (+) Agglutination Davidsohn differential test (Tube)
- Adsorption (removal of Ab in serum) w/ Guinea pig kidney cells and beef/ox erythrocytes
- Addition of indicator cells (sRBCs)
- Agglutination Antibodies to IM (+) Adsorption w/ beef/ox erythrocytes (+) Agglutination after adsorption w/ GPK cells Antibodies to Forssman Ag (+) Adsorption w/ GPK cells (+) Agglutination after adsorption w/ beef/ox erythrocytes Antibodies to Serum sickness
(+) Adsorption w/ beef/ox erythrocytes and GPK cells (-) Agglutination after adsorption w/ beef/ox erythrocytes and GPK cells EBV Ag’s 1. VCA = Viral Capsid Ag (cytoplasm) 2. EA = Early Ag a. EA-D = Diffuse early Ag (nucleus and cytoplasm) b. EA-R = Restricted early Ag (cytoplasm) 3. EBNA = Epstein-Barr nuclear Ag (nucleus) Monospot/Spot/Rapid differential slide test
Horse RBCs (indicator cells) = more sensitive indicators of Ab’s found in IM
Additional Topics H. capsulatum Cross reacts w/ B. dermatitidis SREHP Serine-rich E. histolytica protein Optimal pLDH (parasitic LDH) Malarial organisms Malaquick HRP-2/HRP II Ag: Histidine Rich Protein Ag P. falciparum Streptococcus MG Primary atypical pneumonia OspC Outer membrane associated protein Lyme disease Latex agglutination Cryptococcal Ag in CSF Seroconversion (+) specific Ab previously undetectable Transient Hypogammaglobulinemia of infancy
5-6 months of age IgG = most affected
Selective IgA deficiency Most common congenital immunodeficiency Severe combined immunodeficiency
Most serious congenital immunodeficiency Affects T and B cells Children Enclosed in a plastic bubble (“Bubble boy”) DiGeorge’s syndrome Congenital thymic aplasia X-linked hypogammaglobulinemia
Bruton’s agammaglobulinemia All Ig (-) B cells Common variable immunodeficiency
Recurrent bacterial infection and sinusitis Selective IgG deficiency may occur PNP deficiency Metabolism of purines is affected
WAS Triad of immunodeficiency, eczema and thrombocytopenia Inability to mount IgM response to the capsular polysaccharide of bacteria A-T IgG 2 , IgA, IgE Uncoordinated muscle movements (ataxia) Dilatation of blood vessels (telangiectasia) Waldenstroöm’s macroglobulinemia
IgM other antibodies Leukocyte adhesion deficiency syndrome
Defective adhesion protein (CD18) on the surface of phagocytes
S. typhi (Widal) Titer of >1:160 (clinically significant) R. rickettsii (Weil-Felix) Titer of >1:320 (clinically significant) Tolerance Refers to the specific immunological non-reactivity to an antigen resulting from a previous exposure to the same antigen Tolerogen Antigens that induce tolerance Self-tolerance No immune response against self-antigens Clonal detection Involves killing of T cells (negative selection) that reacts against antigens present in the fetus at that time Central tolerance Tolerance to self acquired w/in the thymus Peripheral tolerance Tolerance acquired outside the thymus Clonal anergy Functional inactivation of certain T cells Clonal ignorance State in which certain autoantigens are undetected by the immune system under normal circumstances Autoimmunity Result of breakdown of mechanisms responsible for tolerance Induction of immune response against components of the self Molecular mimicry Invading pathogen expresses antigens that resemble “self”. These activate T and B cells. When the infection is under control, these cells may now turn against self-antigens Ex. Rheumatic heart disease Sjoögren’s syndrome Chronic inflammatory disease that affects the exocrine glands (lacrimal and salivary glands) Reiter syndrome Triad of arthritis, conjunctivitis and urethritis HLA-DR3 SLE Addison’s disease Graves’ disease IDDM Myasthenia gravis Sjogren’s syndrome Atrophic thyroiditis HLA-DR4 RA (HLA-Dw4) IDDM HLA-B27 Ankylosing spondylitis Reiter syndrome HLA-Dw5 Pernicious anemia HLA-DR5 Goitrous thyroiditis
MUST TO KNOW - IMMUNOSEROLOGY
Course: Medical Technology (BSMT1)
University: Emilio Aguinaldo College
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