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1st Aid: Immunology

QuestionAnswer
3 area of Lymph node Follicle; medulla; paracortex
Functions of lymph node nonspecific filtration by macrophages, storage and activation of B and T cells, antibody production
Describe the lymph node area: follicle site of B cell localization and proliferation. Located in outer cortex.
Differentiate the primary and secondary follicles of the lymph nodes Primary: dense and dormant; Secondary: pale central germinal centers and active
Describe the lymph node area: Medulla Has medullary cords (pakced lymphocytes and plasma cells) and medullary sinuses. Sinuses communicate with efferent lympjhatics and contain reticular cells and macrophages
Describe the lymph node area: paracortex houses T cells. between follicles and medulla.
What part of lymph node enlarges in an exremem cellular immune response? Paracortex
What area of the lymph node is not well developed in patients with DiGeorge Syndrome? Paracortex
Drains upper limb and lateral breast axillary lymph nodes
Lymph node draining stomach Celiac
Lymph node draining duodenum/jejunum Superior Mesenteric
Lymph node draining sigmoid colon colic--inferior mesenteric
Lymph node draining rectum and anal canal internal iliac
Lymph node draining anal canal below pectinate line Superificial inguinal
lymph node draining testes superficial and deep plexuses--para aortic
Lymph node draining scrotum superficial inguinal
Lymph node draining thigh superficially Superficial inguinal
Lymph node draining the lateral side of the dorsum of the foot popliteal
Right lymphtic duct drains? Thoracic duct drains? Right arm/chest/half of head; everything else
Where are T cells found within the spleen? Within the periarterial lymphatic sheath (PALS) within the white pulp of the spllen
Where are B cells found in the spleen? In follicles within the white pulp of the spleen (inner layers)
How does splenic dysfunction lead to increases suspetibility to encapsulated organisms? Decreased IGM---Dec complement activation--- dec C3b opsonization--inc susceptibility
What organisms are you more suseptible to with splenic dysfunction? Encapsulated organsims (SHiN SKiS): Strep, H. influenza type B, Neisseria meningitidis, Salmonella, Klebsiella pneumoniae, group B Streptococci
What is the site of T cell differentiation? Thymus
From what is the thymus developmentally derived? epithelium of the 3rd branchial pouch
What is in the cortex of the thymus? Medulla? Cortes: dense immature T cells; Medulla: pale with mature T cells and epithelial reticular cells containing Hassall's corpuscles
Where does positive (MHC restriction) and negative selections (nonreactive to self) occur respectivley for T cells Positive: Cortex of thymus; Negative: medulla or thymus
components of innate immunity? neutrophils, macrophages, dendritic cells, natural killer cells (lymphoid origin), Complement
Components of Adaptive Immunity? T cells, B cells, Circulating Antibody
What encodes major histocompatibility complexes? HLA (human leukocyte antigen)
HLA for MHC I HLA-A; HLA-B; HLA-C
MHC I binds? TCR and CD8
MHC I is expressed by? all nucleated cells (not RBCs)
MHC I mediates? How? Viral immunity; antigen loading in the RER with intracellular peptides
What does MHC I pair with to be expressed on the cell surface? B2 microglobulin
HLA for MHC II HLA-DR, HLA-DP, HLA-DQ
MHC II binds? TCR and CD4
MHC II expressed on? only on APCs
How is antigen loaded on MHC II? Does it bind large or small peptides? antigen loaded following release of invariant chain in an acidified endosome; Large peptides (hot dog shaped groove)
HLA-A3 disease? Hemochromatosis
HLA-B27 diseases? (4) PAIR: psoriasis, Ankylosing spondylitis, Inflammatory bowel disease, Reiter's Syndrome
HLA DQ2/DQ8 disease? Celiac Dz
HLA DR2 diseases? MS, hay fever, SLE, Goodpastures
HLA DR3 diseases? Diabetes mellitus type I, Grave's disease
HLA DR4 diseases? RA; diabetes mellitus type 1
HLA DR5 diseases? Pernicious Anemia--B12 deficiency, Hashimoto's Thyroiditis
Describe teh action of Natural Killer Cells? Use perforin and granzymes to induce apoptosis of virally infected cells and tumor cells
What cell's activity is enhanced by IL2, IL1, IFNB, and IFN a? Natural Killer cells
What triggers the action of Natural Killer cells? when exposed to nonspecific activation sinal on target cell and/or absence of class I MHC on target cell surface
Antibody associated with Type I hypersensitivty? Allergy: IgE
Ab associated with Type II and Type III hypersensitivity reactions? Cytotoxic and Immune Complex: IgG
Activites of Antibodies? Opsonization, neutralization (IgG), activate compliment (IgM, IgG), sensitize mast cells (IgE)
What mediates Type IV hypersensitivity rxns? Delayed cell-mediated: T cells
What mediates Hyperacute organ rejections? Antibodies (B cells0
What action ensures survival of T cells during positive selection in the thymic cortex? T cells expressing TCR bind surface self MHC molecules
How does negative selection of T cells occur in the medulla of the thymus? T cell expressing TCRs with high affinity for self antigens undergo apoptosis
Describe naive T cell activation foreign body phagocytosed by dendritic cell--presented on MHC II to Th cell and MHC I to Tc cell (signal 1); Costimulatory signal with B7 and CD28 (signal 2); cytokines and cell killing action
Describe B cell activation and class switching Th cell activated--B cell receptor mediated endocytosis and MHC II presentation to TCR on Th (Signal 1); CD40 receptor on B cell binds CD40 ligand on Th cell (Signal 2)--cytokines determine Ig class switching, activation-switching, afinity maturation, Abs
Th1 cells secrete? IFN y
Th2 cells secrete? IL4,5,10,13
Th1 cells do? activate Macrophages (IFN-y)
Th2 cells do? recruit eosinophils for parasite defense and promote IgE proudction by B cells
Th1 cells inhibited by? IL4,10
Th2 cells inhibited by? IFNy
Function of Regulatory T cells? Suppress CD4 and CD8 Tcells by producing IL10 and TGF-B antiinflammatory cytokines
CD3 , CD4, and CD25 are expressed on? T reg cells
What potion of Ab fixes complement? Fc portion of IgM and IgG
Do heavy chains contribute to Fc or Fab fractions of Ab? both
What poriton of the Ab determines its idiotype? Fab
4 C's of Fc fragment? Constant, Carboxy terminal, Complement binding (IgM and IgG), Carbohydrate side chains
What portion of b determines its iso type? Fc
How is diversity granted to Ab's? Random recombination of VJ (light) and VDJ (heavy) genes; random combos of heavy chains with light chains; somatic hypermutation (follows antigen stimulation); addition of nucleotides to DNA during recombination by terminal deoxynucleotidyl transferase
What isotypes do mature lymphocytes express? IgM and IgD on surface
Most abundant Ab isotype? function? IgG; fixes complement, crosses placental barrier (passive immunity), opsonizes bacteria, neutralizes bacterial toxins and viruses
IgA functions? prevents attachement of pathogens to mucous membranes; secreted as dimer and crosses via trancytosis
IgA acquires secretory component where? from epithelial cells before secrteion
Ab in primary response to antigen? Secondary? IgM; IgG
Does IgM cross placenta? no; IgG does
IgM shape? pentamer (helps with trapping)
IgE function? hypersensitivity rxN? Binds mast cells and basophils with crosslinking when exposed to allergen; Type I (allergy) released of histamine and other mediators
Thymus independent antigens lack what? peptide component, cannot be presented by MHC (LPS from gram neg bacteria and polysaccharide capsular antigne)
Immunological memory results from Thymus Independant or Dependent antigens? Dependent
What mediates the classical Complement pathway? Alternative path? Lectin Pathway? IgG or IgM; microbe surface molecules; mannose or other sugars on microbe surface
C3b function? opsonization and clearing of immune complexes
What complement components function in anaphylaxis? C3a, C5a
C5a functions? anaphylaxis and neutrophil chemotaxis
C5b-9 function? cytolysis by MAC
two primary opsonins in bacterial defense? C3b and IgG
Dz where C1 esterase inhibitor is deficient? What meds are contraindicated? Hereditary Angioedema; ACE inhibitors
C3 deficiency can result in two diseases/conditions Sever, recurrent pyogenic sinus/resp tract infections; increase suspetibility to type III hypersensitivity reactions
Recurrent Neisseria bactermia can result from what specific immune deficiency? C5-C9 def
Decay accelerating Factor (DAF) deficiency can result in? complement mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria (PNH); DAF is complement inhibitor
Important cytokines secreted during inflammation (acute) Hot T-Bone stEAk: IL1 (hot), IL2 (stimulates T cells), IL3 (stimulates bone marrow), IL4 (stimulates IgE production), IL5 (IgA production)
IL-1? endogenous pyrogen; activates endothlial adhesion molecules; recruit leukocytes (macrophages)
IL-6? Endogenous pyrogen; causes fever and stimulates Acute Phase Proteins (macrophages and Th2 cells)
IL-8? Major chemotactic factor for neutrophils (macrophages)
IL-12? Induces differentiation of T cells into Th1 cells; activates NK cells (macrophages and B cells)
TNF-a? mediates septic shock; activates endothelium; causes leukocyte recruitment and vascular leak (Macrophages)
IL-2? Stimulates growth of helper, Cytotoxic, and T reg cells (ALL T cells)
IL-3? Supports the growth and differentiation of bone marrow stem cells. Like GM-CSF (ALL T cells)
IFN-y activates macrophages and Th1 cells. Antiviral/antitumor properties? (Th1 cells)
IL-4? induces differentiation of Th2 cells; promotes B cell growth; enhances class switching to IgE and IgG (Th2 Cells)
IL-5? Promotes differentiation of B cells; enhances class switching to IgA; Stimulates growth of eosinophils (Th2 cells)
IL-10? Modulates inflammatory response; inhibits actions of activated T cells and Th1. (Th2 and Tregs)
What do IFNs do in general? place uninfected cells in antiviral state by inducing production of a ribonuclease that inhibits viral protein synthesis by degrading viral mRNA
IFN a nd B have what antiviral effect? inhibit viral protein synthesis
IFN y have what antiviral effect? Increase MHC I and II expression and antigen presentation in all cells
Cell surface proteins of T cells TCR (MHC-antigen), CD3 (TCR signal transduction), CD28 (B7 on APC)
Cell surface proteins of Th cells CD4; CD40
Cell surface proteins of Tc cells CD8
Cell surface proteins of B cells Ig; CD19; CD20; CD 21 (EBV receptors); CD40; MHC II, B7
Cell surface proteins of Macrophages CD14, CD40, MHC II, B7; Fc and C3b receptors (enhanced phagocytosis
Cell surface proteins of NK Cells CD16 (Fc or IgG), CD56 (unique)
Describe the action of superantigen toxins from S. pyogenes and S. aureus? Crosslink B region of TCR to MHC II causing massive release of cytokines following from continous stimulation
How do endotoxins/LPS affect immune system? directly stimulate macrophages by binding endotoxin receptor CD14
Antigenic Variation in Salmonella? Borrelia? N. gonorrhoeae? 2 flagellar variants, relapsing fever, pilus protein
Antigenic Variation in influenza? Antigenic shift (RNA/DNA reassortment) and Antigenic Drift (minor)
Antigenic variation in trypanosomes? programmed rearrangment
For what diseases are passive immunity preformed antibodies commonly given? (4) Tetanus Toxin; Botulinum Toxin; HBV; Rabies Virus
For what diseases are combined passive and active immunizations given? Hepatitis B and Rabies
Kinds and examples of vaccines? Live attenuated (measles/mumps/Sabin/rubella/varicella/yellow fever); Inactivate/Killed vaccine (Cholera/HepA/Salk/Rabies)
What type of immunity is conferred by Live attenuated vaccine? Inactivate/killed vaccine? Cellular response; Humoral Immunity
Describe Type I hypersensitivity and tests for it? Allergic/anaphylactic reaction after free antigen cross linking IgE on PRESENSITIZED mast cells or basophils which releases vasoactive amines; Skin test for specific IgE
Describe Type II Hypersensitivity Rxn and tests for it? Cytotoxic, Ab mediated destruction of a cell following binding of IgM or IgG (opsonization-phagocytosis, complement lysis, Ab-dep cell-mediated cytotoxicity from NK cell); direct and indirect Coombs
Describe Type III Hypersensitivity Rxn and tests for it? Immune complex-antigen-Ab (IgG) complexes activate complement which attracts neutrophils that release lysosomal enzymes; immunofluorescent staining
What is serum sickness? Type III rxn which Abs to foreing proteins are produced (5 days). Immune complexes form and deposit in membranes, where the fix complement
What is Arthus reaction? Local, subacute Type III reaction when intradermal injection of Ag induces Abs and forms immune complexes in the skin--edema, necrosis, activation of complement
Describe Type IV Hypersensitivity Rxn and tests for it? sensitized T lymphocytes encounter Ag and then release lymphokines (macrophage activation; NO Abs): 4 T's (T cells, Transplant rejection, TB skin tests, Touching (contact dermatitis); Patch Test, PPD
Quickly categorize Hypersensitivity rxn ACID: Anaphylactic (I), Cytotoxic-Ab mediated (II), Immune Complex (III), Delayed-cell mediated (IV)
Type of Hypersensitivity Disorder: Anaphylaxis from Bee sting I
Type of Hypersensitivity Disorder: allergy I
Type of Hypersensitivity Disorder: Autoimmune Hemolytic Anemia II
Type of Hypersensitivity Disorder:Pernicious Anemia II
Type of Hypersensitivity Disorder:Idiopathic Thrombocytopenic Purpura II
Type of Hypersensitivity Disorder:Erythroblastosis fetalis II
Type of Hypersensitivity Disorder: Acute Hemolytic Transfusion reaction II
Type of Hypersensitivity Disorder:Rheumatic Fever II
Type of Hypersensitivity Disorder: Goodpasture Syndrome II
Type of Hypersensitivity Disorder: Bullous Pemphigoid II
Type of Hypersensitivity Disorder: Pemphigus Vulgaris II
Type of Hypersensitivity Disorder: SLE III
Type of Hypersensitivity Disorder: Polyarteritis Nodosa III
Type of Hypersensitivity Disorder:Post Strep Glomerulonephritis III
Type of Hypersensitivity Disorder:Serum Sickness III
Type of Hypersensitivity Disorder:Arthus Reaction (swelling following tetanus vaccine) III
Type of Hypersensitivity Disorder: MS IV
Type of Hypersensitivity Disorder: Guillain-Barre Syndrome IV
Type of Hypersensitivity Disorder: Graft-Versus Host Disease IV
Type of Hypersensitivity Disorder: PPD (TB test) IV
Type of Hypersensitivity Disorder: Contact Dermatitis (poison ivy) IV
Blood transfusion results in Urticaria, pruritus, wheezing, and fever. What is going on and how do you treat? Type I allergic reaction against plasma proteins in transfused blood; Antihistamine
Blood Transfusion results in Dyspnea, bronchospasm, hypotension, respiratory arrest and shock. What is happening? Anaphylaxis following transfusion of IgA containing blood to an IgA deficient person
Blood transfusion is followed by fever, headache, chills and flushing. They are experincing a Type II hypersensitivity reaction. What condition and how did it happen? Febril nonhemolytic transfusion reaction where host Abs against donor HLA antigens and leukocytes
Blood Transfusion followed by fever, hypotension, tachypnea, tachycardia, flank pain, hemoglobinemia (intravascular), jaundice (extravascular hemolysis). This is a TYPE II rxn. What condition and why? Acute Hemolytic Transfusion reaction where intravascular hemolysis occurs from ABO blood goup incompatibility or extravascular hemolysis occurs from host Ab rxn against foreign Ag on Donor RBC
SLE AutoAbs? ANAs, Anti-dsDNA, Anti-Smith
Drug induced lupus AutoAs? Antihistone
RA autoantibody? Rheumatoid factor, Anti-CCP
CREST Scleroderma autoantibody? Anticentromere
Diffuse Scleroderma autoAb? Anti-Scl-70 (anti-DNA topoisomerase I)
Primary Biliary Cirrhosis AutoAb? Antimitochondrial
Celic Disease AutoAb? IgA antiendomysial, IA anti-tissue, Transglutaminase
Goodpasture's Syndrome AutoAb? Anti-Basement Membrane
Pemphigus Vulgaris AutoAb? Anti-Desmoglein
Hashimoto's Thyroiditis AutoAb? Antimicrossomal, Antithyroglobulin
Polymyositis and Dermatomyositis AutoAb? Anti-Jo-1, Anti-SRP, Anti-Mi2
Sjogren's syndrome AutoAbs? Anti-SSA (anti-Ro); Anti-SSB (Anti-La)
Autoimmune hepatitis AutoAb? Anti-Smooth Muscle
Type 1 diabetes mellitus AutoAb? Anti-glutamate decarboxylase
Granulomatosis with Polyangitis (Wegener's) AutoAb? C-ANCA
Churg-Strauss syndrome AutoAB? p-ANCA
With a T cell deficiency you would expect what bacterial effects? Viral? Fungi/parasites? Sepsis; CMV/EBV/VZV/Chronic Resp virus; Candida, PCP
With a B cell Deficiency you can expect what bacteria? Virus? Fungi/Parasites? Encapsulated bacteria (SHiN SKiS); Enteroviral, Encephalitis, poliovirus; GI giardiasis
With a granulocyte deficiency you expect what bacteria? Fungi/Parasites? Staph, Burkholderia cepacia, Serratia, Nocardia; Candida, Aspergillus
With Complement Deficiency you expect what bacterial infection? Neisseria (no MAC)
Recurrent bacterial infections after 6 months old as a result of opsonization defect. Normal Pro-B, dec maturation and number of B cells, dec Igs of all classes. Dz and defect X-linked (Bruton's) agammaglobulinemia; X-linked recessive with defect in BTK (tyrosine kinase gene= no B cell maturation)
IgA<7mg/dL with normal numbers of other isotypes; False positive B-HCG test due to presence of heterophile Ab; What Dz and what therapy is contraindicated in these people? Selective IgA deficiency; Blood transfusion containing IgA
Acquired in 20s-30s that grants increase risk of autoimmune disease, lymphoma and sinopulmonary infections. Normal number of B cells but decrease plasma cells and IgG Common Variable Immunodeficiency; defect in B cell maturation
Hyopcalcemia manifesting Tetany, recurrent viral/fungal infections, congenital heart and great vessel defects; Decreased PTH; absent thymic shadow on CxR Thymic aplasia (Digeorge syndrome); 22q11 deletion; failure to develop 3rd and 4th pharyngeal pouch
Disseminated mycobacterial infections with decreased IFN-y IL-12 receptor deficiency; Decreased Th1 response
Coarse Facies, cold (noninflamed), staphylococcal Abscesses, retained primary Teeth, increased IgE, Dermatologic problems (eczema); Increased IgE (FATED): Hyper-IgE syndrome (Job's Syndrome); Th1 cells do not produce IFN-y neutrophils do not respond to chemotactic stimuli
Failure to thrive, chronic diarrhea, thrush. Recurrent infections, absence of thymic shadow, germinal centers SCI
Triad of cerebellar defects (ataxia), spider angiomas, IgA deficiency; Increased AFP Ataxia-telangiectasia; defects in ATM gene, codes DNA repair enzymes
Severe pyogenic infections early in life with increased IgM; Decreased IgG, IgA and IgE Myper-IgM syndrome; Most commonly defective CD40L on helper T cells=inability to class switch
Triad of Thrombocytopenic purpura, INfections, and Eczema; Increased IgE, IgA; Decreased IgM Wiskott-Aldrich Syndrome; X-linked, WAS gene on X chromosome with T cells unable to reorganize actin cytoseleton
Defect in LFA-1 integrin (CD18) protein on phagocytes Leukocyte adhesion deficiency (type 1)
Recurrent pyogenic infections by staphylococci and streptococci; partial albinism, peripheral neuropathy; Giant Granules in neutrophils Chediak_Higashi Syndrome (defect in lysosomal trafficking regulator gene (LYST); microtubule dysfunction in phagosome-lysosome fusion)
What mediates Hyperacute transplant rejection Ab (type II Rxn) from preformed donor antibodies
What mediates Acute transplant rejection Cell-mediated due to CTLs reacting against foreign MHCs
What mediates Chronic Transplant rejection Class I MHC (nonself) perceived by CTLS as class MHC I (self) presenting nonself antigen
Cyclosporide MoA? binds cyclophilins. This complex blocks the differentiation and activation of T cells by inhibiting calcineurin, thus preventing production of IL2 and its receptors
Clinical indication for Cyclosporine? selected autoimmune disorders and for supression of organ rejection
Tacrolimus (FK-506) MoA binds FK binding protein inhibiting calcineurin and secretions of IL2 and other cytokines
Cyclosporine Toxicity? nephrotoxic, HT, hyperlipidemia, Hyperglycemia, Gingival Hyperplasia, hirsutism
Tacrolimus (FK-506) indication potent immunosuppresant used in organ transplant recipients
Tacrolimus Toxicity? Nephrotoxic, HTN, hyperlipidemia, hyperglycemia, tremor
Sirolimus (rapamycin) MoA Inhibits mTOR. Inhibits T cell proliferation in response to IL-2
Sirolimus (rapamycin) indication? Immune suppresion after kidney transplantation in combination with cyclosporine and corticosteroirds
Sirolimus (rapamycin) Toxicity? Hyperlipidemia, Thrombocytopenia, leukopenia
Azathioprine MoA? Antimetabolite precursor of 6-mercaptopurine that interferes with the metabolism and synthesis of nucleic acids. Toxic to proliferating lymphocytes
Azathioprine CLINICAL USE Kidney transplantation, autoim mune disorders (including glomeru lonephritis and hemolytic anemia) .
Azathioprine Toxicity Bone marrow suppression. Active metabol ite mercaptopurine is metabol ized by xanth ine oxidase ; thus, toxic effects may be increased by allopurinol.
Muromonab-CD3 {OKT3) MoA Monoclonal antibody that binds to CD3 (epsilon chain) on the surface of T cel l s . Blocks cellular i nteraction with C D 3 protein responsible for T-cel l signal transduction.
Muromonab-CD3 {OKT3) Indication I mmunosuppression after k idney transplantation
Muromonab-CD3 {OKT3) toxicity Cytokine release syndrome, hypersensitivity reaction
Aldesleukin (interleukin-2 ) Indication Renal cell carcinoma, metastatic melanoma
Epoetin alfa (erythropoietin) Indication Anem ias (especially in renal fai lure)
Filgrastim (granulocyte colony-stimulating factor Indication Recovery of bone m arrow
Sargramostim (granulocyte-macrophage colonystimulating Indication factor) Recovery of bone marrow
a-interferon Indication Hepatitis B and C, Kapos i 's sarcoma, leuke m ias, mal ignant melanoma
beta-interferon Indication Multiple sclerosis
gamma interferon Indication Chron ic granulomatous d isease
Oprelvekin (IL-11) Indication Thrombocytopen i a
Thrombopoietin Indication Thrombocytopenia
Muromonab-CD3 Prevent acute transplant rejection
Digoxin I mmune Fab Antidote for digoxin intoxication
lnfliximab Crohn's d i sease, rheumatoid arthritis, psoriatic arthritis, ankylosing spondyl itis
Adalimumab Crohn's d isease, rheumatoid arthritis, psoriatic arthritis
Abciximab Prevent card iac ischem i a in unstable angina and i n patients treated with percutaneous coronary intervention
Trastuzumab HER2-overexpressing breast cancer
Rituximab CD 20; B -cell non-Hodgkin's lymphoma
O malizumab IgE; Additional line of treatment for severe asthma
Created by: gsei174