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Lange:

IL-1: made by APCs (incl. B-cells) and induce helper t-cells to proliferate/activate.

IL-2: made by helper T-cells to activate the response (activate Helper Cells-CD4 andcytotoxic CD8 cells)

IL4: made by CD4 cells to induce B-cells -> B-cell Growth factor

IL-5: made by CD4 cells to induce B-cells -> B-cell differentiation (isotype switching)

Gamma interferon: activates macrophages for delayed hypersensitivity response;

increases microbicidal activity of macrophages; upregulates the immune response

by increasing # of MHC class II proteins on APCs; inhibits production of Th2 cells

IL-12: made by macrophages to increase TH1 cell production (increases

hypersensitivity response)

IL-10 produced by TH2 cells, inhibits IL-12 production and drives it away from cell-

med response, to focus on Humoral Response!

IL-8: made by macrophages to attract neutrophils and T cells to site of infection.

Costimulatory signal: B7 (on APC) & CD28 (on T-cell) -> need to bound for full

activation to occur; activates helper T-cell to produce IL-2; CTLA-4 made by thehelper T-cell inhibits B7.

ICAM-1 (on APCs) & TFA-1 (on T-cells)

For B-cells: in addition to all the cell adhesion molecs, CD40 (on APCs) & CD40L (onhelper T cells) for class-switching (ex. IgM-> IgG)

IL-6: inhibits Treg cells -> so T-cells can now fight against a pathogenic microbe.

Innate Response-

1. to neutralize toxins/viruses2. opsonize bacteria

innate immunity -> pattern recognition receptors -> self vs non-self

-ag => turns on PRR => macrophage makes specific cytokine to ag based on what

PRR is stimulated => cytotoxic/humoral response elicited.

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LPS: on all gram neg bacteria, TLR4 = PRR, stimulates cytokines IL1,6,8, TNF, B7 (to

activate Helper t-cells)

Gram + & yeasts => TLR2

MBL-> binds mannose from bacterial cells, stimulates

1. complement to kill ag,2. phagocytosis

IL -1, 6, TNF = pro-inflamm cytokines

TH1 cells: activate cytotoxic cell function (IL-2) and delayed hypersensitivityresponse (Gamma IFN)Cell-Mediated Immunity activated

TH2 cells: activate B-cell function (IL-4, IL-5)Humoral Immunity activated

IL-12 induces nave T-helper cell to become TH1 cells and secrete IL-2 and IFN

Gamma

IL-4 induces nave helper T-cell to become Th2 cells and secrete IL-4 & IL-5

T-cells can be induced when they are stimulated by mitogens (concanavalin A &

phytohemagglutinin) LPS is mitogen only for B-cells

Delayed hypersensitivity => imp for intracellular pathogens

Cytotoxicity ->perforins and granzymes- perforate cell and release of cell contents,

capsases -> apoptosis, Fas-FasLigand -> fas bound to infected cell and when

cytotoxic t-cell recognizes fsa protein, fas ligand made in CD-8 cell. When fas-fasLigand interact, apoptosis occurs in cell. (used by CD-8 and NK cells)

T-cell independent: no helper t-cells involved = no class switching, so more IgM Abs& no memory cells made.

T-reg cells: imp in inhibiting autoimmune diseases. Have CD25 in them.

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Memory B-cells -> have IgG receptors (some have IgM); in 2ndary response: the

memory T-cells secrete interleukins to induce memory B cells to make Abs.

Macrophages ->

1. phagocytosis2. antigen presentation3. cytokine production

have Fc receptors and C3B receptors for opsonization of microbes; make IL-1, TNF,IL-8; they are attracted to site of infection by c5a -> part of complement cascade.

Dendritic cells = the primary inducers of Ab response.

Follicle dendritic cells: have no MGC class proteins, but have Fc receptors that bind

Ag-Ab complexes