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Step 1 - Immuno charts

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denniskwinn's version from 2015-04-25 16:04

Complement Cleavage

ACTIVITYMEDIATORSEFFECT
Opsonization of antigenC3b&C4b↑ phagocytosis by Mphages&nphils
ChemotaxisC3a&C5aAttraction of nphils&monocytes to inflamm site
DegranulationC3a&C5a (anaphylotoxins)Release of inflamm mediators from mast cells&bphils
Clearance of immune complexesC3b :Reduced buildup of potentially harmful antigen-Ab complexes
B cell activationC3dPromotion of humoral immune response
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Question Answer
C1, C2, or C4 deficiency (classical pathway)Immune complex diseases such as glomerulonephritis, SLE,&vasculitis Pyogenic staph&strep infections
C3, factor B, or factor D deficiency (alternate pathway)Disseminated pyogenic infections, vasculitis, nephritis
C5 through C9 deficiencyNeisseria species infections; some types of SLEIndividuals with C1 to C4 deficiencies are prone to pyogenic infections; those with C5 to C9 deficiencies are prone to neisserial infections.
C1 esterase inhibitor deficiency Hereditary angioedema - Marked by recurrent, acute attacks of skin&mucosal edema
DAF deficiency PNH - Complement-mediated intravascular hemolysis
ADCC Ab-dependent cellular cytotoxicity
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Phagocytic Disorders

DISEASEDEFECTCLINICAL
Chédiak-Higashi syndromeReduced ability of phagocytes to store materials in lysosomes and/or release their contentsRecurrent pyogenic infections (e.g., Staphylococcus&Streptococcusspecies)
Chronic granulomatous diseaseReduced production of H2O2&superoxide anion due to lack of NADPH oxidase (especially in nphils)↑ susceptibility to catalase-producing bact (e.g.,Staphylococcus species)&fungal infections
Job syndromeReduced chemotactic response by nphils&high immunoglobulin E levelsRecurrent cold staph abscesses; eczema; often associated with red hair&fair skin
Lazy leukocyte syndromeSevere impairment of nphil chemotaxis&migrationRecurrent low-grade infection
Leukocyte adhesion deficiencyDefect in adhesion proteins reducing leukocyte migration into tissues&adherence to target cellsRecurrent bact&fungal infections; poor wound healing; delayed separation of umbilical cord
Myeloperoxidase deficiency↓ production of HOCl&other reactive intermediatesDelayed killing of staphylococci&Candida albicans
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ACUTECHRONIC
CellsInfection: nphils, Mphages, Allergy: eosphils, mast cellsMphages, lymphocytes
MediatorsComplement, kinins, prostaglandins, leukotrienes, acute phase cytokines, chemokinesCytokines from Mphages&T cells
LesionRash, pus, abscessRash, fibrosis, granuloma
ExamplesResponse to infection, hypersensitivity responseAutoimmunity, response to intracellular bact infection
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Cytokines

RESPONSECYTOKINES
Acute phaseIL1, TNF-α, IL-6, IL-12
Th1IL-2, IFN-Ɣ, Lymphotoxin
Th2IL-4, IL-5, IL-10
Th17IL-17
TregTGF-β, IL-10
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Question Answer Column 3
CYTOKINESOURCEeffects, target
IL-1Mphage, dendritic cell, B cellActs on various nonimmune cells to initiate acute phase responses, fever, coactivates TH cells
IL-2TH1 cellPromotes growth&activation of T&B cells
IL-3TH cellStimulates hematopoiesis in bone marrow
IL-4TH2 cell, mast cellPromotes growth&differentiation of B cells, Enhances IgG&IgE synthesis, Stimulates TH2 response
IL-5TH2 cellPromotes growth&differentiation of B cells, Enhances IgA synthesis, stimulates growth&activation of eosphils
IL-6TH2 cell, Mphage, dendritic cellPromotes formation of plasma cells from B cells&Ab production, Induces synthesis of acute phase proteins by liver cells
IL-10TH2 cellReduces TH1 response by inhibiting IL-12 production by Mphages,Reduces class II MHC expression by APCs
IL-12Mphage, dendritic cell, B cellStimulates formation of TH1 cells, Acts with IL-2 to promote formation of CTLs, activates NK cells
IL-17TH17 cellPromotes nphil activation&inflamm responses
IL-23Dendritic cellPromotes TH17 responses
IFN-γTH1 cell, NK cellEnhances Mphage activity, Inhibits TH2 response, Mediates aspects of type IV hypersensitivity
TNF-αMphage&other cellsHas effects similar to IL-1, Promotes cachexia associated with chronic inflamm, Is cytotoxic for tumor cells
TNF-β (lymphotoxin)TH1 cell, TC cellEnhances phagocytic activity of Mphages&nphils, Is cytotoxic for tumor cells
TGF-βMphage, Treg cell, B cellGenerally limits inflamm response, enhances IgA synthesis
CXC-type chemokines (e.g., IL-8)Mphage, nphil, endothelium, fibroblastAttracts nphils&promotes their migration into tissues
CC-type chemokines (e.g., MIP, RANTES)Mphage, nphil, endothelium, T cellAttracts Mphages, eosphils, bphils,&lymphocytes
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TYPE OF RESPONSEACUTE PHASETH1TH17TH2TREG/SUP
InducerPAMPIL-12, IL-6TGF-β, IL-6, IL-23IL-6IL-10, TGF-β
MediatorIL-1, TNF-α, IL-6, IFN-α,IFN-β, IL-12IL-2, Lymphotoxin, IFN-ƔIL-17IL-4, IL-5, IL-10IL-10, TGF-β
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Question Answer
TERMDEFINITION
Adjuvantenhances immune response to antigen when administered with it →improved response to vaccines
AffinityBinding strength of a single variable region of an Ab
AntigenSubstance that binds to Abs&T cell receptors. most antigens are also immunogens, some are antigenic but not immunogenic.
AvidityCombined binding strength of the multiple interactions between a multivalent Ab molecule&all the corresponding epitopes on an antigen
Epitope (antigenic determinant)Region on an antigen molecule to which a single Ab molecule or T cell receptor binds. An antigen usually has multiple epitopes, can react with Abs of different specificities.
Fab fragmentPortion of Ab molecule, produced by papain digestion, that contains a single antigen-binding site.
Fc fragmentPortion of Ab molecule, produced by papain digestion, that fixes complement&binds to Fc receptors
Hinge regionFlexible portion of Ab heavy chains located between the Fab&Fc regions, containing intrachain disulfide bonds; present in IgG, IgA, andIgD
ImmunogenSubstance capable of eliciting a specific immune response
Monoclonal AbHomogeneous Ab that recognizes only one epitope; produced by a single clone of plasma cells
Polyclonal AbMixture of Abs that recognize different epitopes on an antigen; produced by multiple clones of plasma cells in response to an antigen containing different epitopes.
Thymus-dependent antigensAntigens that require helper T cells to induce Ab production = most protein antigens
Thymus-independent antigensAntigens possessing many repetitive structures that can induce Ab production without helper T cells
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Isotypes 

IgGIgMIgAIgDIgE
Heavy classγμαδΕ
Subclassesγ1, γ2, γ3, γ4 -α1, α2--
MW secreted Ab (kDa)*154900160-320185190
Maximal valence*210422
% of total serum75-855-105-15<1<1
T1/2 (days)23562-3 :2-3
action siteSerum, tissueSerumSecretionsB cell surfaceMast cells
effectAntigen clearance from host(secondary response)Antigen clearance from host(primary response)Prevention of antigen crossing membranesActivation of B cellsType I hypersensitivity (anaphylaxis)
Complement activation+++---
Opsonization++-+--
ADCC+- --+
Mast cell degranulation----++
Crosses placenta+----
Crosses mucous membranes--++--
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EPITOPE CLASSLOCATIONCOMMENT
IsotypeConstant region - define each class of Ig heavy chains, identical in all of a species.
AllotypeConstant region - vary among individuals. IgG exhibits the most allotypic differences. (Allo = different.)
IdiotypeVariable regionThese epitopes differ among Abs because of different antigen-binding specificities. Monoclonal Abs have the same idiotype.
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Hypersensitivity Rxns

RxnONSET TIMEKEY FEATURESBENEFICIAL EFFECTSPATHOLOGIC EFFECTS
Type I Rxn<30 minIgE-dependent release of various mediatorsAntiparasitic responses&toxin neutralizationLocalized allergies (e.g., hay fever, asthma), Systemic anaphylaxis
Type II Rxn*<8 hrAb-&Ab (with complement)-mediated cytotoxicityOpsonization&direct lysis of extracellular bact&other susceptible microbesHemolytic anemias (e.g., transfusion rxns, Rh disease, Hapten [penicillin]), modified red blood cells, Organ-specific tissue damage in some autoimmune diseases (e.g.,Goodpasture syndrome), AutoAb activation of receptors (e.g., Graves disease, myasthenia gravis)
Type III Rxn*<8 hrDeposition of soluble antigen-Ab complexes, which activate complementAcute inflamm rxn at site of extracellular microbes&their clearanceArthus rxn (localized), Serum sickness&drug rxns (generalized) (e.g., hypersensitivity pneumonitis [farmer's lung], glomerulonephritis [Streptococcus pyogenessequelae]) , Systemic autoimmune diseases (e.g., systemic lupus erythematosus)
Type IV Rxn24-72 hr (acute); >1 wk (chronic)Delayed release of TH1 cytokines; activation of Mphages&cytotoxic lymphocytesProtection vs infection by fungi, intracellular bact,&virusesAcute: contact dermatitis, tuberculosis skin test, Chronic: granuloma formation, graft rejection
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Clinical Manifestations of Delayed-Type Hypersensitivity Rxns

TYPEANTIGENCLINICAL&HISTOLOGIC FEATURES
Contact dermatitis (1-3 days)): Epidermal (e.g., poison ivy, chemicals, cosmetics)Eczema with edema, Raised epidermis, many Mphages
Tuberculin rxn (1-3 days)Dermal (e.g., purified protein derivative, other mycobact&fungal antigens)Local induration&swelling ± fever, T cells, fewer Mphages
Graft rejection (Chronic (>1 wk))Persistent exposure to alloantigensThrombosis&necrosis of graft, T cells, many Mphages
Granuloma formation (Chronic (>1 wk))Persistent exposure to infectious or noninfectious agentsSkin induration, Nodule composed of epithelioid cells (activated Mphages), giant cells,&helper T cells; fibrosis ± caseous necrosis
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Effectors in Antimicrobial Responses

EFFECTOREXTRACELLULAR BactINTRACELLULAR BactVIRUSESFUNGIPARASITES
Nphils++--++
Mphages+++++-
Complement++----
Natural killer cells--+--
CD4 TH1 cells+++++++
CD8 cytotoxic lymphocytes-+++--
Secreted Ab+++++++ (IgE)*
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Autoimmune

Organ-Specific Diseases
DISEASEPROBABLE PATHOLOGIC MECHANISMSCLINICAL FEATURES
Autoimmune hemolytic anemiaType II rxn vs RBC (phagocytosis of RBCs)Anemia, + direct Coombs test
Goodpasture syndromeType II rxn vs capillary basement membranes in kidneys&lungsLung hemorrhages; nephritis with proteinuria, hematuria, renal failure
Graves diseaseStim of receptor for thyroid-stimulating hormone by autoAb (type II)Hyperthyroidism, diffuse goiter, ophthalmic symptoms (exophthalmos)
Hashimoto diseaseType II&IV rxns (damage to thyroid tissue); inhibition of iodine uptake by autoAb to thyroid peroxidase&thyroglobulinThyroiditis, goiter, hypothyroidism
Type 1 diabetes mellitus (insulin dependent)Type II&IV rxns vs pancreatic β cellsNo insulin production; insulitis
Myasthenia gravisBlocking of neural stim of muscle by autoAb vs ACh receptorMuscle weakness, fatigue
Pernicious anemiaInhibition of vit B12 uptake by autoAb to intrinsic factor (type II); type IV rxn vs gastric parietal cellsAbnormal erythropoiesis caused by deficiency of vit B12
Poststrep rheumatic feverType II&III rxns induced by cross-rxn of antistrep Abs with host tissuesHeart valve lesions, myocarditis, arthritis, chorea
Poststrep glomerulonephritisType III rxns induced by strep antigen, C3 complexesKidney damage&dysfunction
Thrombocytopenic purpuraType II rxn (lysis of platelets)Bleeding disorders due to platelet deficiency
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Systemic Diseases
DISEASEPROBABLE PATHOLOGIC MECHANISMSCLINICAL FEATURES
Multiple sclerosisType IV rxn vs central nervous system leading to demyelination&inflamm lesionsPeriodic episodes of weakness, incoordination, speech disturbances, paresthesia
Rheumatoid arthritisType III&Th17 responses rxn vs connective tissue&IgGChronic inflamm of joints marked by granulation tissue, subcutaneous nodules,&vasculitis
Systemic lupus erythematosusType III rxn involving autoAbs vs DNA, histones, RBCs, clotting factors,&other tissue antigensVasculitis, erythematous rash, arthritis, nephritis
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B Cell Deficiencies
DISEASEIMMUNOLOGIC DEFECTS*OTHER FEATURES
Bruton agammaglobulinemiaDefect in maturation of B cells: ↓ B cell count; ↓ Ig of all isotypesRecurrent pyogenic infections (e.g., Streptococcus pneumoniae); small lymph nodes with poorly developed germinal centers; X-linked recessive
Common variable hypogammaglobulinemiaDefect in differentiation of B cells to plasma cells: ↓ Ig of all isotypesRecurrent pyogenic infections (e.g., Streptococcus species, pneumoniae, giardiasis); often associated with blood or autoimmune disorders
Selective IgA deficiencyFailure of B cells expressing membrane IgA to differentiate into plasma cells: ↓ IgA&secretory IgA but normal levels of other isotypesRecurrent respiratory&gastrointestinal infections (giardiasis); most common congenital B cell defect
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T Cell Deficiencies
DISEASEDEFECTS*OTHER
Chronic mucocutaneous candidiasisAbsence of T cell response to Candida species despite normal T cell count&functionRecurrent candidal skin&mucous membrane infections; often associated with endocrine dysfunction
DiGeorge syndromeThymic aplasia due to defect in development of third&fourth pharyngeal arches: ↓ T cell count; ↓ or normal Ig levelsRecurrent viral, fungal,&protozoan infections due to absent thymus; tetany resulting from hypocalcemia due to absent parathyroid glands
Hyper-IgM syndrome↓ B cell activation&class switching due to T cell defect: ↑ IgM;↓ IgG&IgAPoor response to thymus-dependent antigens; recurrent infections, especially by Pneumocystis jiroveci; often associated with autoimmune blood disorders
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Combined B&T Cell Deficiencies
DISEASEDEFECTS*OTHER
Ataxia-telangiectasia↓ T cell count&function; ↓ IgA, IgE,&IgG2Cerebellar dysfunction (ataxia), dilation of small vessels (telangiectasia); recurrent bact infections of respiratory tract; autosomal recessive
Severe combined immunodeficiency (SCID)Various defects that interrupt early lymphocyte development: ↓ T&B cell counts; ↓ Ig of all isotypesRecurrent infections of all types; short life span; may be X-linked (X-SCID) or autosomal recessive (e.g., adenine deaminase deficiency)
Wiskott-Aldrich syndromePoor response to polysaccharide antigens&depressed T cell function: ↓ IgM; ↑ IgA&IgEEczema, thrombocytopenia,&recurrent infections with encapsulated pyogenic bact; X-linked recessive
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