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74 Cards in this Set
- Front
- Back
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Lymph node
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Follicle: B cells
primary: dense and dormant secondary: pale and active germinal centers Medulla: Cords: plasma cells Sinuses: macrophages Paracortex: T cells Between follicles sand medulla high endothelial venules; T and B cells enter from blood -enlarges during cellular immune response (viral) |
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Upper limb and lateral breast
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axillary nodes
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stomach
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celiac nodes
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duodenum, jejunum
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superior mesenteric nodes
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sigmoid colon
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colic to inferior mesenteric nodes
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rectum above pectinate line
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internal iliac nodes
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anal canal below pectinate line
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superficial inguinal nodes
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testes
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superficial and deep plexuses --> para-aortic nodes (retroperitoneal)
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scrotum
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superficial inguinal
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thigh
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superficial inguinal
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lateral side of dorsum of foot
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popliteal nodes
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right lymphatic duct
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drains right arm and right half of head
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thoracic duct
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drains everything else
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Spleen
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B cells in follicles
T cells in Paracortex, PALS (periarticular lymphatic sheath) **macrophages in marginal zone removes encapsulated bacteria |
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Thymus
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T cell differentiation and maturation (but first comes from bone marrow)
-from epithelium of 3rd branchial pouches -lymphocytes frome mesenchyme cortex: immature T cells medulla: mature T cells, epithelial reticular cells, Hassall's corpuscles At corticomedullary junction: Positive selection: MHC restriction Negative selection: nonreactive to self |
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Innate immunity
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Receptors that recognize pathogens are germline encoded
-response is fast and nonspecific, no memory PMNs, macs, dendritic cells, NK cells, complement |
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Adaptive immunity
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receptors that recognize pathogens undergo V(D)J recombination during lymphocyte development
-response is slow on first exposure, but memory response is faster and more robust -T cells, B cells, circulating a.b. |
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MHC I
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MHC I: binds TCR and CD8
encoded by HLA-A, B, C -expressed on all nucleated cells, not RBCs -antigen loaded in RER **viral immunity *pairs with beta2-microglobulin (aids in transport to cell surface) |
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MHC II
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Binds TCR and CD4
Encoded by HLA-DR, DP, DQ expressed only on APCs -antigen is loaded following release of invariant chain in an acidified endosome |
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NKs
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perforin and granzymes to induce apoptosis of virally infected and tumor cells
**only lymphocyte of innate immune system enhanced activity by IL-12, IFN-beta, IFN-alpha targets lack of MHC-I **CD16, 56 |
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B cells
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make antibodies
allergy: type I, IgE Cytotoxic: type II, IgG Immune complex: type III, IgG Hyperacute organ rejection |
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T cells
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CD4: help B cells make a.b. and produce IFN-gamma, which activates macs
CD8: kill virus-infected cells directly type IV hypersensitivity Acute and chronic rejection |
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CD4 cell activation
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1. TCR - MHCII on APC
2. CD28 - B7 on APC |
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CD8 cell activation
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1. TCR - MHC I on virus-infected cell
2. IL-2R - IL-2 on Th1 cell |
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B cell activation
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1. IL-4,5,6 from Th2 cell
2. CD40 - CD40L from Th2 |
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Cytotoxic T cells
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kill virus-infected, neoplastic, and donor graft cells by inducing apoptosis
-release cytotoxic granules containing: perforin: delivers granules granzyme: serine proteas, activates apoptosis granulysin: antimicrobial, induces apoptosis |
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Antibody
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Fab:
amino terminal antigen-binding fragment -determines idiotype: unique antigen-binding pocket Fc: constant carboxy terminal complement binding at Ch2 (for IgG and IgM) Carbohydrate side chains Determines isotype (type of antibody) |
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Antibody diversity
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Diversity generated by:
1. random "recombination" of VJ (light) or V(D)J (heavy) genes 2. random combination of heavy and light chains 3. somatic hypermutation following antigen stimulation 4. addition of nucleotides to DNA during "recombination" by terminal deoxynucleotidyl transferase |
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Thymus-independent antigens
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antigens lacking a peptide component; can't be presented by MHC to T cells (i.e. LPS from gram neg and polysach capsule)
-stimulate release of IgM a.b. only and do not result in memory |
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C1 esterase inhibitor deficiency
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hereditary angioedema (increased bradykinin)
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C3 deficiency
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severe, recurrent pyogenic sinus and resp infxns (strep pneumo, h flu)
-increases susceptibility to type III rxns (esp GN) |
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C5-c9 def
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Neisseria bacteremia
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DAF def
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GPI-anchored enzyme
-complement mediated lysis of RBCs and PNH |
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DAF & C1 esterase inhibitor
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DAF: CD55, CD59
both help prevent complement activation on self-cells |
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C3a, C5a
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anaphylaxis:
C3a: stim mast cells and basophils --> histamine --> vasc permeability --> swelling, hypotension C5a: pmn chemotaxis |
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Classic pathway
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activated by IgG and IgM
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Membrane attack complex
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defends against gram-negative bacteria
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Alternative pathway
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activated by microbial surface molecules (esp endotoxin)
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Antigen variation
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salmonella: 2 flagellar variants
borrelia (relapsing fever) Neisseria gon: pilus protein influenza: major shift, minor drift *DNA rearrangement and RNA segment reassortment trypanosomes: programmed rearrangement |
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Passive immunization
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To Be Healed Rapidly:
Tetanus Botulinum HBV Rabies +RSV to premies in winter |
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Type I hypersensitivity
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Anaphylactic and atopic:
free antigen cross-linked IgE on presensitized mast cells and basophils --> release histamine, etc. *due preformed antibody from prior exposure test: scratch test (wheal and flare), radioimmunosorbent assay |
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Type II hypersensitivity
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ANTIBODY TO SELF
Cytotoxic Antibody mediated: IgM, IgG bind to fixed antigen on "enemy" cell --> complement or phagocytosis 1. opsonize cells or activate complement 2. a.b. recruit pmns and macs 3. bind to normal cellular receptors and interfere with functioning test: direct and indirect Coombs |
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Type III hypersensitivity
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ANTIBODY TO ANTIGEN
Immune complexes: IgG-antigen; activates complement (decrease C3) -attracts pmns --> enzymes Serum sickness: 5-10days a.b. to foreign proteins are produced, deposit in membranes where they fix complement -usually drugs (sulfa) -fever, urticaria, arthralgias, proteinuria, LAD Arthus rxn: 5-12h local subacute rxn; intradermal injection induces a.b. --> edema, necrosis, complement test: immunofluorescent staining |
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Type IV hypersensitivity
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delayed (t-cell mediated)
-sensitized T cells encounter antigen, then release lymphokines --> mac activation, no antibody involved 4 T's: T cells Transplant rejection TB skin tests Touching (contact dermatitis) test: patch test (PPD) |
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Type IV examples
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MS
type I DM Guillain-Barre Hashimoto's GVHD PPD Contact dermatitis (sensitization phase (afferent), then elicitation phase (efferent)) |
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Type III examples
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SLE
RA PAN PSGN Serum sickness Arthus reaction Hypersensitivity pneumonitis (farmer's lung = IgG + actinomyces antigens) |
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Bruton's agammablobulinemia
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X-linked
BTK defect, tyrosine kinase --> blocks B-cell differentiation/maturation -recurrent bacterial infection after 6 months Labs: normal pro-B, decreased rest of B and Igs |
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Hyper-IgM syndrome
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Defective CD40L on helper T cells, can't class switch
**severe pyogenic infxns early in life Labs: high IgM, low IgG, IgA, IgE |
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Selective Ig deficiency
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IgA most common
defect in isotype switching **sinus and lung infxns (encapsulated), milk allergies, diarrhea **Anaphylaxis on exposure to blod products with IgA (have anti-IgA IgG) |
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CVID
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defect in B-cell maturation
*can be acquired in 20s-30s -increase risk autoimmune, lymphoma, sinopulm infxns -nl # B cells, decreased plasma and IGs |
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DiGeorge
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Thymic aplasia
-failure to develop 3rd and 4th pharyngeal pouches *no T cells -tetany (hypoCa) -recurrent viral/fungal infxns -congenital heart and great vessel defects Labs: hypoCa, low PTH, low T cells -absent thymic shadow on CXR |
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IL-12 receptor deficiency
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decrease Th1 response (don't stimulate Th1 to release IFNgamma to activate macs
**disseminated mycobacterial infxns Labs: decrease IFN-gamma |
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Hyper-IgE syndrome (Job's)
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It's my FATE to get this JOB
Th cells fail to produce IFN-gamma --> pmns can't respond to chemotactic stimuli -no suppression to Th2 --> high IgE FATE: Facies: coarse Abscess: cold, staph Teeth: retained primary E: IgE, eczema |
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Chronic mucocutaneous candidiasis
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T-cell dysfunction
*candida infxns of skin and mucous membranes |
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SCID
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Types:
X-linked: defective IL-2 receptor ADA def Failure to make MHCII antigens **B and T cell def -recurrent viral, bacterial, fungal, and protozoal infxns Tx: bone marrow transplant Labs: low IL-2R high adenine (toxic to B and T cells); low dNTPs, low DNA synthesis) -low IgGs |
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Ataxia-Telangiectasia
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-defect in DNA repair enzymes
Triad: Ataxia (cerebellar atrophy) Angiomas (spider) IgA def increase risk CA *recurrent sinopulm infxns; late oculocutaneous telangiectasias |
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Bruton's agammablobulinemia
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X-linked
BTK defect, tyrosine kinase --> blocks B-cell differentiation/maturation -recurrent bacterial infection after 6 months Labs: normal pro-B, decreased rest of B and Igs |
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Hyper-IgM syndrome
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Defective CD40L on helper T cells, can't class switch
**severe pyogenic infxns early in life Labs: high IgM, low IgG, IgA, IgE |
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Selective Ig deficiency
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IgA most common
defect in isotype switching **sinus and lung infxns (encapsulated), milk allergies, diarrhea **Anaphylaxis on exposure to blod products with IgA (have anti-IgA IgG) |
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CVID
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defect in B-cell maturation
*can be acquired in 20s-30s -increase risk autoimmune, lymphoma, sinopulm infxns -nl # B cells, decreased plasma and IGs |
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DiGeorge
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Thymic aplasia
-failure to develop 3rd and 4th pharyngeal pouches *no T cells -tetany (hypoCa) -recurrent viral/fungal infxns -congenital heart and great vessel defects Labs: hypoCa, low PTH, low T cells -absent thymic shadow on CXR |
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IL-12 receptor deficiency
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decrease Th1 response (don't stimulate Th1 to release IFNgamma to activate macs
**disseminated mycobacterial infxns Labs: decrease IFN-gamma |
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Hyper-IgE syndrome (Job's)
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It's my FATE to get this JOB
Th cells fail to produce IFN-gamma --> pmns can't respond to chemotactic stimuli -no suppression to Th2 --> high IgE FATE: Facies: coarse Abscess: cold, staph Teeth: retained primary E: IgE, eczema |
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Chronic mucocutaneous candidiasis
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T-cell dysfunction
*candida infxns of skin and mucous membranes |
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SCID
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Types:
X-linked: defective IL-2 receptor ADA def Failure to make MHCII antigens **B and T cell def -recurrent viral, bacterial, fungal, and protozoal infxns Tx: bone marrow transplant Labs: low IL-2R high adenine (toxic to B and T cells); low dNTPs, low DNA synthesis) -low IgGs |
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Ataxia-Telangiectasia
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-defect in DNA repair enzymes
Triad: Ataxia (cerebellar atrophy) Angiomas (spider) IgA def increase risk CA *recurrent sinopulm infxns; late oculocutaneous telangiectasias |
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Wiskott-Aldrich syndrome
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X-linked
progressive deletion of B and T cells TIE: Thrombocytopenic purpura Infections Eczema *high IgE, IgA; low IgM |
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Leukocyte adhesion deficiency (type 1)
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defect in LFA-1 integrin (CD18) on phagocytes
-recurrent bacterial infxns, absent pus formation, delayed separation of umbilicus Labs: neutrophilia |
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Chediak-Higashi syndrome
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Autosomal recessive
Defect in microtubular function with decreased phagocytosis CH-AIN of Ps: albinism partial infxns: pyogenic staph & strep neuropathy: peripheral |
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Chronic granulomatous disease
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lack of NADPH oxidase
-decrease ROIs and absent resp burst in pmns Increase susceptibility to catalase-positive organisms: S. aureus, E coli, Aspergillus, Serratia Labs: negative Nitroblue tetrazolium dye reduction test |
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Hyperacute rejection
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Type II (ab)
-preformed antidonor ab in recipient MINUTES **occludes graft vessels --> ischemia, fibrinoid necrosis PMN infiltration acute hemolytic transfusion rxn: anti-ABO a.b. binds donor antigens --> complement --> C3a & C5a; C5-C9 |
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Acute rejection
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Cell mediated due to cytotoxic T cells reacting against foreign MHCs
WEEKS after *reversible with immunosuppressants (cyclosporine, OKT3) *vasculitis of graft vessels with dense interstitial lymphocytic infiltrate (CD4 and CD8) |
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Chronic rejection
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T-cell AND AB mediated vascular damage
obliterative vascular fibrosis MONTHS-YRS *irreversible ClassI-MHC nonself perceived by CTLs as class I-MHCself presenting nonself antigen *fibrosis of tissue and vessels |
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GVHD
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Graft T cell sensitization against host MHC antigens
grafted immunocompetent T cells proliferate in the irradiated immunocompromised host and reject host proteins --> severe organ dysfunction *maculopapular rash, jaundice, HSM, diarrhea *usually in bone marrow and liver transplant (rich in lymphocytes) *can be potentially beneficial in bone marrow transplant |
