Microbiology Choi's Lectures

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Koch's Postulates

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1.) microbe must be present in every case of the disease
2.) Microbe must be isolated from host and grown in pure culture.
3.) Disease must be reproduced when pure culture is introduced into a non-diseased susceptible host.
4.) Microbe must be recoverable from an experimentally infected host.

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2° Immune Response characteristics

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1.) Shorter Lag
2.) Higher levels of Ig
3.) Longer persistence of Igs
4.) Affinity maturation
5.) Class switching.

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Epitope/determinant

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specific region of an antigenic molecule that interacts with the Ab.

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Adjuvant

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a substance (such as alum) that non-specifically enhances the immune response to an Ag.

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Cross Reaction

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ability of a specific Ab to bind to an Ag that is similar but not identical to its original Ag.

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Polyclonal Antiserum

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a multi-determinant Ag will activate multiple clones of B cells, causing a heterogenous soup of Abs for its many epitopes.

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Multiple Myeloma

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a plasma cell tumour in the bone marrow, creating a monoclonal spike because all the B-cells are identical and making the same Ig (usu. IgG or IgA). More light chains are made than heavy chains, and excess light chains are excreted in urine. Resistant to most chemotherapies.

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Hybridoma

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a cell fusion between a normal B-cell making Ags and a myeloma cell (not making Ags), producing a monoclonal, immortal strain making Ags.

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Hypervariable Region (CDR; complementarity determining region)

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the Ag binding site on the Fab portion of an Ig.

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Idiotype

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The unique Ag-combining characteristic of an Ig molecule.

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J-chain (Joining Chain)

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A piece that connects the individual IgM together to form the pentameric IgM. Also connects dimeric IgA. It's made by the plasma cell.

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Secretory Component (secretory piece)

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a piece attached to dimeric IgA before it is released into the lumen of mucosa-lined organs as secretory IgA.

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IgM

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Pentameric IgMs bound to J-chain. IgM is made during the 1° response, then undergoes class switching (IgG usu., IgA in mucosa). It activates complement.

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IgA

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Associated with mucosal immunity. It is dimeric, connected by J-chain, and tacked on with a secretory component by the epithelial cell before release into lumen. Most abundant Ig in the body. Two subclasses, IgA1, IgA2.

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IgG

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Most abundant Ig in the serum (10mg/mL); crosses placenta and provides maternal immunity. Released in 2° response. Activates complement, like IgM. Involved in opsonisation; binds to Fc receptors on phagocytes.

4 subtypes: IgG1, 2, 3, and 4.

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IgE

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Very rare; associated with allergic responses. Binds to Fc RR on mast cells and basophils.

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IgD

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Very rare; function unclear, found as cell surface RR on B-cells.

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agglutination (immune complex formation)

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Ab, cells, and/or large particles agglutinate. Larger immune complexes are better cleared by phagocytes.

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affinity

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strength of binding (dissociation constant) between an epitope and one Fab CDR on an Ig.

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avidity

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overall binding energy between the entire Ig and a multivalent Ag. IgM has the highest avidity.

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hapten

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A low MW-compound that becomes immunogenic after attachment to a carrier. Abs generated against this complex will attack free hapten. However, free hapten alone will never generate a 2°response. The carrier usually provides a peptide portion for the T-cell to recognise. The actual Abs are generated against the non-protein hapten.

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ELISA (Enzyme-Linked ImmunoSorbent Assay)

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Used for testing serum Ab against HIV, indicating contact with virus. Colour rxn occurs if human Ab are bound to HIV-Ag, which are in turn anchoured to well by specific Ag.

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isohaemogluttinins

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Abs against RBC Ags, causing transfusion rxns. Type A person makes αB isohaemogluttinin. All are IgM, and are thus too big to cross the placenta to cause haemolytic disease.

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Direct Callie Coombs test

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Used to detect anti-Rh Ab ; cord blood used. Rabbit anti-IgG is added; agglutination means RBCs are coated with maternal IgGs against Rh.

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Indirect Callie Coombs test

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Rh-Ab test. Mother's serum is combined with Rh-RBCs. If anti-Rh Abs are present, they will coat the RBCs, and cause agglutination when rabbit anti-IgG is added.

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C3b

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Most important component of the complement pathway; binds to C3b RR (CR1) on many cell types, and synergises with Fc RRs.

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C5a

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chemotactic factor for neutrophils. Along with C3a, are anaphylatoxins that cause vasodilation.

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Hereditary Angioneurotic Oedema (HANE)

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Deficiency: C1INH (C1 inhibitor).
Sxs: severe abdomnial colic due to swelling, vomitting; airway obstruction from swelling.
Tx: androgens; purified C1NH

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Paroxysmal Nocturnal Haemoglobinuria

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Deficiency: Decay Accelerating Factor (DAF); C3 can't dissociate from convertase. Tons of C5 cleaved.

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Terminal Deoxynucleotide Transferase (TdT)

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Adds random nucleotides to the space btw D and J chains on the heavy chain in Ab, introducing "N-sequence diversity". However if it doesn't add a multiple of 3 nucleotides, the reading frame is shifted, and the Ab is busted. Also works on TCRs.

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somatic hypermutation

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mutation rate (especially of the hypervariable regions) are 1Mx greater than normal. Occurs after B-cell encounter with Ag, and contributes to affinity maturation.

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allelic exclusion

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Since each B-cell only makes one type of Ag and humans are diploid, one allele is inactivated.

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alternative RNA splicing

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In mature B-cells, μ and δ-chains are simultaneously expressed (both IgM and IgD). RNA splicing can remove the C-μ and make δ-mRNA

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Heavy-chain Class switching

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secondary DNA-rearrangement that's more permanent than alternative RNA splicing; unused C-regions are lost.

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intracellular μ chain

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hallmark of a pre-B cell (stem cell→pro-B cell→pre-B cell). Pre-B don't express surface IgM; a pre-B R has the μ chain attached to a "surrogate light chain".

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thymus-dependent antigen

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Most Ags; requires T-cell to help B-cell make Abs. These are Ags with a protein component that requires processing and presentation to the T-cell.

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thymus-independent (TI) antigens

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Non-protein (polysaccharide, etc.) Ags that do no rquire T-cells for B-cell Ab production. They tend to be simple and polymeric, and cross links Ig-RR to activate. However, they don't stimulate 2° response (no memory), affinity maturation, or class switching.

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mitogen

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a type of TI-Ag that are polyclonal stimulators (don't elicit Ag-specific response). Example: LPS

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cytokines

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activated T-cells secrete these to bind to and activate B-cells. Cytokines are not Ag-specific, and will activate any B-cell in proximity.

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cell-cell contact activation

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In addition to secreting cytokines, a T-cell can activate the B-cell directly by binding its CD40L to the B-cell's CD40.

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Interleukin-2 (IL-2)

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A T-cell GF; acts as autocrine activator of CD4+, but paracrine on CD8+ CTLs. IL-2 must bind with the high-affinity R type.

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Interferon-γ (IFN-γ)

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Potent activator of macs; also ↑s MHC expression in APCs; associated with inflammatory response. Promotes TH1 responses, and inhibits TH2.

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Interleukin-4 (IL-4)

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induces B-cell activation and growth, class switching to IgE in Type I hypersensitivity (instead of IgG) along with IL-13, and allergic responses.

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Interleukin-12

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Promotes TH1 cell responses (cell-mediated) via NK cell activation, in concert with IFN-γ.

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Interleukin-10

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Made by TH2 cells, and inhibits TH1 type responses.

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Tumour Necrosis Factor-α (TNF-α)

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an endogenous pyrogen that mediates local inflammatory responses; activates vascular endothelial cells to ↑ permeability; induces cachexia, shock. LPS is a strong inducer of TNF-α

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Interleukin-1 (IL-1)

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Mediates inflammatory responses; lots of overlap with TNF-α.

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Chemokines

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low MW-cytokines made by activated mononuclear phagocytes; mediate acute inflammation; chemotaxic for leukocytes. Serves as co-receptor for HIV.

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NK cells (large granular lymphocytes)

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NOT a lymphocyte; independent of thymus for maturation. A component of innate immunity; no Ag-specific mechanisms. Will kill cells without MHC-I.

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High Endothelial Venules (HEV)

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The passageway from blood into lymph through which naive T-cells enter a lymph node during homing.

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Homing Receptor (L-selectin)

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Expressed by naive T-cells that allow attachment to addressins on endothelial cells, allowing organ-specific homing.

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Hyperacute Graft Rejection

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Occurs right in O.R.; due to preformed Abs against HLA (usually MHC-I) or isohaemogluttinins.

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Acute Graft Rejection

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Due to incompatibilities of HLA; takes days to weeks.

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Chronic Rejection

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Due to minor HC Ag.

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Graft vs. Host Disease

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Occurs in bone marrow transplantation; the recipient's immune system has been destroyed, so the graft actually begins rejecting the host!

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Positive Selection

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A +/+ T-cell with TCRs specific for self-MHC (creating MHC restriction) are positively selected and allowed to mature into +/- T-cells. Selection is largely independent of peptide-binding affinities in MHC.

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Negative Selection

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deletion of T-cell clones with high affinity for self-antigen and self-MHC in the thymus. Thus you are selecting for T-cells with intermediate affinity for self-Ags.

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Clonal anergy

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a state of non-responsiveness in a T-cell after becing exposed to Ag without co-stimulation. A precautionary mechanism against autoimmunity.

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molecular mimicry

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Situation in which an Ab is made against an Ag that's very similar to a self-Ag, casuing cross-rxn and autoimmunity.

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Type I Hypersensitivity

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IgE-mediated, involving TH2 cells and IL-4 against a foreign Ag.
Immediate Rxn: Histamine degranulation
Late-phase Rxn: PAF, prostaglandins, leukotrienes.

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Wheal-and-Flare

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A Type I hypersensitivity response; a suspected Ag is injected into the skin, and an immediate rxn is seen, caused by histamine release.

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Type II Hypersensitivity

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Autoimmune disorders involving Abs with self-specificity. IgG/IgM involved.

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Drug-induced Haemolytic Anaemia

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Type II disease: A drug binds to Abs, and acts as a carrier when it binds to an RBC, making the RBC its hapten.

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Grave's Disease

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Type II disease: Abs specific for TSH R is made; this Ab is actually an agonist, and causes excess TH secretion (hyperthyroidism).

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Myasthenia Gravis

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Type II disease: Abs against nicotinic-NMJ ACh RRs made. Disease caused by IgG; can cross placenta and affect foetus. Sxs more severe in younger pts; thymectomy helps in them.

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Goodpasture Syndrome

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Type II disease: Abs against Type IV collagen in BM; major effects on kidneys and lungs. "Ribbon-like" presentation?

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Autoimmune Thrombocytopenic Purpura

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Type II disease: Abs against platelet mem. proteins.

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Pemphigus Vulgaris

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Type II disease: Ab against intercellular jxns in skin.

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Rheumatic Fever

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Type II disease: Ab against Strep infections cross-react with cardiac mm (moleculary mimicry)

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Type III Hypersensitivity

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Immune Complexes formed in excess during zone of Ag excess, and are not cleared. Build up along BVs, joints, leading to complement activation and inflammatory response. Sxs can resolve as you make more Abs, causing immune complexes to become bigger and easier to clear.

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Arthus Reaction

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A type III rxn; inject an Ag subcutaneously into someone with a high titer of Ab against the Ab. A red indurated bump appears in 4-8 hours.

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Farmer's Lung

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Type III disease: repeated exposure to mould spores in hay leads to immune complex formation.

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Serum Sickness

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Type III rxn: when large amts of heterologous antiserum are injected as antitoxin, Abs are made against the antiserum, and the next time you try to give the antiserum, pt. will go into shock (memory).

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Systemic Lupus Erythematosus (SLE)

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Type III disease: ↑'d in black women. 10x more common in women.
Sxs: Glomerulonephritis (made progress to ESRD), arthritis, butterfly rash. Abs against dsDNA, histones, etc. are made, forming complexes.
Tx: antimalarials, anti-inflammatories.

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Type IV (Delayed-Type) Hypersensitivity

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Mediated by specific T-cells; Abs are NOT involved. Takes 24-72 hrs to evolve. TH1 mediated (activate macs with IFN-γ).
Ex.: poison ivy rash, beryllium, caeliac sprue.

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Contact Sensitivity

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Type IV rxn; skin rashes due to small foreign molecules (acting as hapten) binding to host proteins and altering them. No fever or general malaise with the rash.

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Tuberculin Skin Rxn

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Type IV rxn: small amt of tuberculin injected subcutaneously. Previous exposure leads to response. Mediated by TH1 and macs (Characteristic of Type IV)

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Granuloma

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Type IV disease: mycobacterial infections

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Acute Systemic Anaphylaxis

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Classic Type I disease: often caused by antibiotics that act as haptens (host proteins are carriers). Allergen captured by B-cells, presented to TH2, which then make IL-4 and IL-13 to induce class switch to IgE. IgE binds to FcεRI type Fc R on mast cells, causing degranulation.
Sxs: vomitting, swelling of face/throat, bronchoconstriction, urticaria, heart arrhythmia, myocardial ischemia, ↓BP.

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rheumatoid factor

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An Ab against Fc portion of IgG; may play a role in exacerbating rheumatoid arthritis after inflammation has begun.

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Bruton's X-linked agammaglobulinaemia

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B-cell deficiency
↓B-cells, all Igs ↓'d.
Defect: Bruton's tyrosine kinase (btk), a signal-transduction kinase. (-) B-cell maturation.
Tx: I.V. IgG, marrow transplant.

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Hyper IgM Immunodeficiency

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B-cell deficiency
Defect: lack of CD40L on T-cells means it can't activate B-cells. Abs can't be made. ↑[IgM] due to (-) class switching.

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Selective IgA Deficiency

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B-cell deficiency.
Often asymptomatic due to redundancy, but can ↑ resp. problems.

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DiGeorge Syndrome

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T-Cell deficiency.
Defect: block in T-cell maturation due to lack of thymus dev't. Severe congenital heart disease, ↑'d susceptibility to all pathogens.

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adenosine deaminase SCID

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lack of this enzyme lead to accumulation of toxic metabolites and thus ↓ B/T-cells.

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γ-c chain deficiency SCID

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γ-c chain is a component of different cytokine RR, including IL-2R. Thus, no T-cell activation.

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Bare Lymphocyte Syndrome

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One form due to lack of MHC II in all cells. Thus no humoral immunity, no presentation of exogenous Ag.

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Wiskott-Aldrich Syndrome

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Immunodeficiency
Defect: X-linked defect in WASP gene, involved in organising actin cytoskeleton for T/B-cell collaboration. CTL responses, IgM ↓'d.
Sxs: eczema, thrombocytopenia, reccurrent pyogenic infections.

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Bloom's Syndrome

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Immunodeficiency
Defect: DNA helicase

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Ataxia-Telangiectasia

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Immunodeficiency
Defect: selective IgA and T-cell deficiency.

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Burkitt's Lymphoma

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Lymphocyte tumour
Mature B-cell lineage; c-myc translocation, associated with EBV.

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Waldenstrom's Macroglobulinaemia

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Lympohcyte tumour
Single clone of B-cells making monoclonal IgM, causing hyperviscosity. Lack of bone lesions distinguishes from mutliple myeloma.