All Cytokines I can find mentioned in Immuno + Cell Receptors, Other molecules of importance

IL-4

• Th2 activation

• Stimulation of B cells to make IgE

• Alternate activation of macrophages, inducing an anti-inflammatroy effect

Il-5

• activates eosinophilic inflammation

• secreted by Th2 cells and innate lymphoid cells

Il-13

• intestinal motility

• muscous secretion

• secreted by Th2 cells

• Alternate activation of macrphages, inducing an anti-inflammtroy effect

IFN-γ

• Classical activation of macrophages

• In Many cell types Increases expression of classes I and II MHC

• Proliferating B cells → Induces class switch to IgG2a, blocks IL-4- induced class switch to IgE and IgG1

• Th2 cells → Inhibits proliferation

• Phagocytic cells → Mediates effects important in DTH, treatment for CGD

Il-17

• Produced by Th17 cells

• Increases inflammation. Attracts PMNs, induces IL-6, IL-1, TGFβ, TNFα, IL-8

TGFβ

• Promotes class switching to IgA in mucosal immunity

• Also has Anti-inflammatory properties

• Some tumors express this cytokine to evade immune response and inflammation

IL-7

• Growth factor for common lymphoid progenitor that eventually makes NKs, B cells, and T cells.

• SCID results fron failure in the y chain of this cytokine (among many others), as the y (gamma) chain is the signaling subunit

IL-15

• Major Cytokine in NK cell proliferation and maturation

TNFα

• Pro-inflammatory cytokine

• Produced by Macrphages, T cells, and mast cells

IL-6

IL-3

• Stimulates differentiation of hemocytoblast into Common Myeloid progenitor cells, which later make granulocytes

IL-11

• Induces thrombocyte production

NF-kB

• A transciption factor

• when activated induces the transcription of cytokines

NOD-like receptor (NLR)

• Cytoplasmic receptor

• Targets components of bacterial peptidoglycans

• plays a role in inflammasome activation

• plays a role in the secretion of IL-1beta via signaling of NF-kB

• causes acute inflammation

• macrophage activation

IL-1β

• Cytokine that causes acute inflammation

• Fever

• Promotes leukocyte migration

• Induces Th17 differentiation!

RIG-like receptors (RLR)

• Cytosolic receptor

• targets viral RNA

• causes interferon production

Toll-like Receptor 1,2,6

• Extracellular receptor

• targets bacterial lipopeptides

• Causes activation of NF-kB and cytokine transcription

Toll-like receptor 2

• Extracellular receptor

• targets bacterial peptidoglycan

• Causes activation of NF-kB and cytokine transcription

Toll-like Receptor 4

• Extracellular receptor

• targets Lipopolysaccharide (LPS)

• Causes activation of NF-kB and cytokine transcription

Toll-like Receptor 5

• Extracellular receptor

• targets flagellin

• Causes activation of NF-kB and cytokine transcription

IL-10

• Anti-inflammatory cytokine

Granzyme B

• Secreted by NKs

• Causes cell Lysis

Perforin

• Secreted by NKs

• punches holes in cell membranes

IL-12

• Induces Th1 differentiation

• in NKs and T cells induces IFN-y production and increased cytotoxic activity

IFN-α/β

• produced by virus infected cells in response to intracellular TLR signaling

• By binding to receptors on neighboring cells and causing subsequen cascades, they inhibit viral replication

• Also enhance the ability of NKs to kill infected cells

IL-6

• Promotes terminal differentiation into plasma cells

IL-15

• NK and T cell proliferation

IL-22

• Secreted by Th17 cells

• Stabilizes endothelial barrier, induces secretion of microbials

C3a and C5b

• Proteins in the complement cascade responsible for inflammation

C3b

• Protein in the complement cascade responsible for opsonization and phagocytosis

C6, C7, C8, C9

• Proteins in the complement cascade that make up the Membrane Attack Complex (MAC)

• Results in lysis of microbes

C1 INH

• Inhibits complement cascade

• loss in this molecule will result in Hereditary Angioedema

  • Note: with this condition you will see low C4 levels due to overconsumption

DAF

• Dissociates C3 converteases in the complement cascade

• Loss in this molecule will result in Paroxysmal Nocturnal Hemoglobinuria

  • specifically seen in RBCs → causes lysis

Factor I, Factor H

• Cleaves C3b (responsible for opsonisation) into inactive fragments

• Specifically dissociates the alternative pathway

• Loss in these molecules results in Atypical Hemolytic Uremic Syndrome

Effector Functions of IgM

• classical complement activation

• Naive B-cell antigen receptor

• Heavy chain u

Effector Functions of IgD

• Naive B-cell antigen receptor

• Heavy chain delta

Effector Functions of IgG

• Classical pathway complement activation

• Neutralization

• Opsonization

• ADCC (antigen dependent cellular cytotoxicity)

• Placental Transport

• Heavy chain y (gamma)

Effector Functions of IgA

• Neutralization in mucosal immunity

• Heavy chain alpha

Effector Functions of IgE

• ADCC

• Trigger mast cell granule release

• Heavy chain epsilon

FOXP3

• considered the master regulator of regulatory T cell development and function.

• It regulates the production of anti-inflammatory cytokines such as interleukin-10 (IL-10) and transforming growth factor-beta (TGF-β), which contribute to the suppressive activity of Tregs.

• This is a transciption factor

BCL-2

• Anti-apoptotic protein

Fas and FasL interaction

• Causes activation induced cell death in self reactive T cells

• NO B7 expression → Low IL-2 and IL-2R levels → expression of these Death receptors

• Interaction between two cells with these receptors leads to the death of both of them

Bad, PUMA

• pro-apoptotic proteins

• self reactive T Cell will mediate its own death (eg, it doesn’t need to interact with another one)

CTLA-4

• Tregs express this receptor

• engages with B7 molecules on APCs, preventing their interaction with CD28 on T cells

• T cell activation is inhibited

IL-2R

• Cell receptor on Tregs that consumes IL-2 produced by activatied T cells

• Its action causes inhibition of T cell proliferation

PD-1

• play a crucial role in regulating the immune system, particularly in modulating T cell responses.

• expressed primarily on the surface of activated T cells, B cells, natural killer (NK) cells

• Its expression is induced upon T cell activation and plays a key role in controlling the amplitude and duration of immune responses.

• When this molecule interacts with its ligand, it transmits inhibitory signals into the T cell. These signals dampen T cell activation and function, leading to T cell exhaustion, reduced proliferation, and diminished cytokine production.

PD-L1

• expressed on the surface of various cell types, including tumor cells, antigen-presenting cells (such as dendritic cells and macrophages), and certain non-immune cells. Its expression can be induced by inflammatory signals, cytokines, and other stimuli.

• functions as a negative regulator of immune responses by engaging PD-1 on activated T cells. This interaction transmits inhibitory signals to T cells, leading to T cell exhaustion, reduced proliferation, and diminished cytokine production.

• Its therapeutic blockade represents a major advancement in cancer treatment and has significantly improved outcomes for patients with certain types of cancer.

  • eg, cancer presents this to downregulate T cells

IL-8

• Chemotatactic for Neutrophils

• Induces adherence to endothelium and extravasation into tissues