First Aid Immunology

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site of B-cell localization and proliferation

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Follicle of lymph node

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differentiate primary and secondary follicles

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primary - dense and dormant
secondary - pale central germinal centers and are active

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house T cells and enlarges in an extreme cellular immune response

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paracortex

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where are T cells found in the spleen

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periarterial lymphatic sheath in the white pulp of the spleen

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why are asplenic patients susceptible to encapsulated organisms

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decreased IgM leads to decreased C3b opsonization
Salmonella, S. pneumo, H. influenzae, N. meningitidis

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Howell-Jolly bodies

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postsplenectomy
either physically or with sickle cell anemia that destroys spleen

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does RBC express MHC I

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No

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this immune antigen is paired with B2-microglobulin which aids it for transport to cell surface

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MHC I

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this immune antigen is loaded following release of invariant chain in an acidified endosome

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MHC II

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A3

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hemochromatosis

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B27

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psoriasis
Ankylosing spondylitis
inflammatory bowel disease
Reiter's syndrome

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B8

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Grave's disease

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DR2

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MS
hay fever
SLE
Goodpasture's

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DR3

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DM type 1

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DR4

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RA
DM type 1

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DR5

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pernicious anemia
Hashimoto's thyroiditis

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DR7

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steroid-responsive nephrotic syndrome

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only lymphocyte member of innate immune system
activity enhanced by IL-12, IFN-B, and IFN-a

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NK cell

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site of positive selection in thymus

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cortex
cell is CD4/CD8 T cell

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site of negative selection in thymus

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medulla
T cell is differentiated into CD4 or CD8

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Interleukins associated with inducing formation of Th1 or Th2 cell from Helper T cell

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IL-12 --> Th1
IL-4 --> Th2

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antigen presenting cells

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macrophages
Dendritic cells
B cells

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two signals needed for APC to activate CD4 cell

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APC (MHC II and B7)
CD4 (TCR and CD28)

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two signals needed for activation of cytotoxic T cell

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MHC I (virus-infected cell) recognized by TCR
IL-2 from Th1

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two signals needed for activation of B cell class switching

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IL-4,5,6 from Th2 cell
CD40 receptor on B cell binds CD40L on Th2 cell

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regulates cell-mediated response by activating macrophages and CD8 T cells (IL-2)

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Th1 cell

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regulates humoral response by activating B cell to make antibodies (IL-4 and 5)

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Th2 cell

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what inhibits Th1 cells

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IL-10 secreted by Th2 cell

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what inhibits Th2 cells

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IFN-y secreted by Th1 cell

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amino terminal of an antibody

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antigen-binding end

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carboxy terminal of an antibody

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constant portion

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complement binding part of an antibody

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IgG and IgM antibodies can activate complement via CH2 portion of their heavy chain

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which two antibodies are expressed on the surface of mature B lymphocytes

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IgM and IgD

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differentiate IgA antibody when in circulation vs. when secreted

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monomer in circulation
dimer when secreted

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antibody associated as being the primary, immediate response to an antigen

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IgM

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antibody associated with hypersentivity and mediating immunity to worms by activating eosinophils

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IgE

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antigen that stimulates release of IgM antibodies only and does not result in immunologic memory

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thymus-independent antigen:
LPS from cell envelope
polysaccharide capsule

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what do DAF and C1 esterase inhibitor prevent

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complement activation on self-cells

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leads to hereditary angioedema

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C1 esterase deficiency

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associated with severe, recurrent pyogenic sinus and respiratory tract infections and increased susceptibility to type III hypersensitivity reaction

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C3 deficiency

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associated with Neisseria bacteremia

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C5-8 deficiency

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associated with paraxysmal nocturnal hemoglobinuria

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DAF deficiency

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defends against gram(-) bacteria

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MAC

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what activates the alternative complement system

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endotoxin
peptidoglycan

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what two pathways cleave C2 and C4

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Lectin - mannan binding
Classic - antigen-antibody complexes

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major chemotactic factor for neutrophils

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IL-8

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interluekin associated with fever

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IL-1

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mediates septic shock

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TNF-a

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induce the production of ribonuclease that inhibit viral protein synthesis by degrading viral mRNA

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Interferons

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stimulates growth of helper and cytotoxic T cells

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IL-2

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T cell markers

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TCR
CD3
CD28
CD4
CD8

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B cell markers

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IgM and IgD
CD19
CD20
CD21
CD40
MHC II
B7

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NK cell markers

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CD16 (binds Fc of IgG)
CD56

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CD14

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macrophage

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how do endotoxins directly stimulate macrophages

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bind to CD14

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results in the uncoordinated release of IFN-y from Th1 cells and subsequent release of IL-1,6 and TNF-a from macrophages

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superantigens (S. pyogenes and S. aureus)

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immunity associated with rapid onset, but short life span of antibodies

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passive immunity

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differentiate the hypersensitivities

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ACID:
Anaphylactic (type I)
Cytotoxic (antibody mediated) (type II)
immune complex (type III)
Delayed T-cell mediated (type IV)

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anti-dsDNA
anti-Smith

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SLE

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antihistone

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drug-induced lupus

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anti-IgG

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rheumatoid arthritis

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anticentromere

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scleroderma (CREST)

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anti-Scl-70 (anti-DNA topoisomerase I)

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scleroderma (diffuse)

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antimitochondrial

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primary biliary cirrhosis

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antigliadin
antiendomysial

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celiac disease

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anti-basement membrane

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goodpasture's syndrome

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anti-desmoglein

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pemphigus vulgaris

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anti-Jo-1

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polymyositis
dermatomyositis

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anti-SS-A/B

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Sjogren's syndrome

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Anti-U1 RNP (ribonucleoprotein)

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mixed connective tissue disease

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c-ANCA

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Wegener's granulomatosis

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anti-glutamate decarboxylase

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type 1 DM

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X-linked recessive defect in BTK, a tyrosin kinase gene that blocks B-cell differentiation

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Bruton's agammaglobinemia

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defective CD40L on helper T cells - inability to class switch

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hyper-IgM syndrome

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when does children with Bruton's get infections

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after 6 months - when maternal IgG decreases

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associated with sinus and lung infection and anaphylaxis on exposure to blood products

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IgA deficiency
blood products that contain IgA produce anaphylaxis

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associated with a defect in B-cell maturation, normal number of B cells but decreased plasma cells and immunoglobin

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common variable immunodeficiency

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22q11 deletion associated with tetany and congenital heart and great vessel defects

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Thymic aplasia (DiGeorge syndrome)

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Decreased Th1 response and IFN-y

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IL-12 receptor deficiency

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Hyper-IgE syndrome (Job's syndrome)

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FATED:
coarse Facies
staph Abscesses
retained primary Teeth
increased IgE
Dermatologic problems (eczema)

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two types of SCID

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x-linked defect in IL-2 receptor -decreased T cell activation
adenosine deaminase deficiency - increased adenine which is toxic to B and T cells

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ataxia, spider angiomas, and IgA deficiency
Cause

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Ataxia-telangietasia
Defect in DNA repear

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x-linked recessive defect with progressive deletion of B and T cells associated with:
thrombocytopenic purpura
Infections
Eczema
decreased IgM

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Wiskott-Aldrich syndrome

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defect in LFA-1 integrin (CD18) on phagocytes

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Leukocyte Adhesion deficiency (type-1)

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autosomal recessive defect in microtubular function with decreased phagocytosis

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Chediak-Higashi syndrome

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lack of NADPH oxidase resulting in decreased superoxide and absent respiratory burst in neutrophils

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Chronic granulomatous disease

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increased susceptibility to catalase-positive organisms with a negative nitroblue tetrazolium dye reduction test

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chronic granulomatous disease

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hyperacute rejection

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type II hypersensitivity due to presence of preformed antidonor antibodies that occludes graft vessels causing ischemia and necrosis

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graft-versus-host disease

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immunocompetent T cell from the graft attack the immnocompromised host resulting in severe organ dysfunction (usually bone marrow and liver transplant)

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T-cell and antibody-mediated vascular damage in transplant rejection

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chronic rejection (months to years later)