M1 Block 2 Immunology

Front 1

initial response cytokines

Back 1

TNF-α, IL-1α, IL-1β, and IL-6

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initial response chemokines

Back 2

CXCL8 and IL-8

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CD14

Back 3

LPS receptor (innate) on monocyte and macrophages that comes together with TLR4 and MD2 to generate intracellular signaling cascade

Front 4

NLRPs

Back 4

"nucleotide-binding domain, leucine-rich repeat containingproteins"

evolutionarily conserved family of cytoplasmic receptor proteins that bind microbialcompounds and stress-associated self molecules and activate protective responses such asapoptosis

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alternative pathway

Back 5

complement proteases are directly activated by factorspresent on the surface of a microbe and the resulting cascade causes the cleavage of C3

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lectin pathway

Back 6

This pathway is initiated by the binding of a protein in plasma calledmannose-binding lectin (MBL) to high mannose proteoglycans that are characteristically presenton the surfaces of yeast and certain bacteria. Binding of MBL to a microbial surface initiates theproteolytic cleavage cascade.

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classical pathway

Back 7

When either C-reactive protein (CRP) or certain antibody types bindto the surface of a microbe, a complement component called C1q is recruited to the surface of themicrobe. C1q is structurally homologous to MBL and activates the proteolytic cleavage cascade.

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factors H and I

Back 8

Plasma proteins that work together to cleave C3bmolecules that are bound to cell surfaces into a form that is no longer active. Factor H has abinding site for sialic acid which is abundantly expressed on mammalian cells

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DAF

Back 9

decay-accelerating factor that destabilizes and cleaves C3b molecules that bind to the cell surface

Front 10

MCP

Back 10

membrane co-factor protein that destabilizes and cleaves C3b molecules that bind to the cell surface

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MyD88

Back 11

Adaptor protein that associates with the intracellular portion of bound TLRs to activate kinase cascade that results in the translocationto the nucleus of a protein called "nuclear factor κB" (NFκB), which is a major transcriptionfactor that turns on a number of genes associated with inflammatory responses, includingcytokines and other proteins.

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TRIF/TRAM

Back 12

Adaptor proteins that are an alternative to MyD88. Leads to the nuclear translocation of a different transcription factorcalled interferon response factor 3 (IRF3). IRF3 activates the transcription of type I interferons (e.g. IFNα and IFNβ), which arecytokines that activate innate intracellular defense mechanisms of most cell types. These defensemechanisms are particularly effective in protecting against viral infections.

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Ig signaling subunit

Back 13

Igα and Igβ or CD79

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CD3 complex

Back 14

TCRs are always expressed at the cell surface in a complex with a group of four other transmembrane proteins that together is called the CD3 complex.

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Class I MHC molecule

Back 15

Composed of a transmembrane chain that associates with asoluble protein called β2-microglobulin (β2m). Class I molecules are expressed on all nucleatedcells. Bind peptides that come from within the cell.

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Class II MHC molecule

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Composed of two transmembrane chains (α and β). Class IImolecules are expressed only on cells of the immune system that undergo specialized interactions with T cells, for example, dendritic cells, monocytes, macrophages, and B cells. Bind peptides that come from extracellular sources.

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T cell co-stimulation

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CD80 and CD86 on (B7) on the surface of the antigen presenting cell (that also bears the cognate MHC/peptide complex recognized by the TCR) stimulate CD28

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B cell co-stimulation

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The process of T cell help begins when a B cell's BCR binds an antigen that also contains an epitope (e.g. a peptide) that can be recognized by a T cell's TCR. The antigen is internalized by the BCR, chopped up, and its peptides loaded into the B cell's MHC molecules. When a helper T cell comes along that has a TCR that recognizes an antigenic peptide, it up-regulates a molecule on its cell surface called CD40L. This delivers a signal to a co-stimulatory molecule on the B cell called CD40.

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IL-6

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major inflammatory cytokine released by phagocytic cells and TH2 cells, facilitates B cell division

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IL-10

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produced by TH2 cells, facilitates B cell division and differentiation into plasma cells

Front 21

IL-4

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produced by TH2 cells and promotes TH2 polarization, causes B cells to differentiate into memory B cells, associated with promoting IgE class switching

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IFN-γ

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produced by TH1 cells and promotes TH1 polarization, activates macrophages to destroy engulfed bacteria, inhibits IgE class switching and promotes certain IgG subtypes, enhances acquisition of cytolytic effector functions by CTLs

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Regulatory T cells

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Serve to inhibit immune responses and are often specific for self antigens. Inhibit the activation of other immune cells and prevent autoimmunity.

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IgM

Back 24

triggers classical complement pathway

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IgA

Back 25

transported across epithelial surfaces, and therefore is important for immunity atmucosal surfaces of the body, involved in neutralization

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IgG

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1. triggers classical complement pathway

2. binds to Fc receptors on cytolytic cells and triggers cytolysis of antibody coated cells through a process called antibody-dependent cell-mediated cytotoxicity (ADCC),

3. important for immunity in utero and for neonates

4. Involved in neutralization (some in opsonization)

5. Diffuses into extravascular sites

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IgE

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associated with allergic responses, and is particularly effective at triggeringdegranulation by Mast cells (thus producing histamine and other vasoactive compounds), IL-4 promotes IgE class switching

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IL-12

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high amounts promote TH1 polarization (low amounts promote TH2 polarization), enhances acquisition of cytolytic effector functions by CTLs

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IL-2

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stimulates T cells to proliferate, made by T cells and CD8 cells require more IL-2 to proliferate

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Fc fragment

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Constant fragment of an Ig heavy chain that contains conserved sites thatare critical for the effector functions of antibodies, and also has sites for associating with othermolecules that transmit activation signals triggered by antigen recognition into the B cell.

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Fc receptor

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Receptor on certain immune cell types (e.g. NK cells, mastcells) that activates specific responses (e.g. cytolysis, histamine release).

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Type I hypersensitivity

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Immediatehypersensitivity (allergy) – IgE antibodies bind to mast cells, causing releaseof histamine (occurs within 15 min of blood-stream exposure to antigen)

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Type II hypersensitivity

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Antibody-mediatedhypersensitivity – IgM or IgG bind to hapten-labeled cell surfaces and fixcomplement (minutes to hours after exposure)

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Type III hypersensitivity

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Immune-complexhypersensitivity – antigen-antibody immune complexes are deposited in smallblood vessels or alveoli of the lungs and activate phagocytes (at least 12hours after exposure)

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Type IV hypersensitivity

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Delayedhypersensitivity - mediated by T cells that respond to peptide epitopesacquired by cells in peripheral tissues (1-3 days after exposure)

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IL-1

Back 36

secreted by macrophages, stimulates proliferation of B-lymphocytes, chemotactic for neutrophils

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CD19

Back 37

B cell co-receptor

Front 38

IL-5

Back 38

released by TH2 cells, promotes production of eosinophils in the bone marrow and release into circulation

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IL-8

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recruits neutrophils, released by activated phagocytic cells

Front 40

TNF-α

Back 40

major inflammatory cytokine released by activated macrophages, monocytes, and T cells