Cytokines & Cells Online Pathfinder Encyclopaedia
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[natural killer T-cells] NKT-cells, called also NK-like T-cells [natural killer-like T-cells], constitute a small fraction of circulating lymphocytes. Their development is thymus-dependent (Berzins et al, 2004; Pear et al, 2004; Pellicci et al, 2002; Gapin et al, 2001) and the development of at least some subsets requires IL7 (Sandberg et al, 2004) or IL15 (Ranson et al, 2003). NKT-cells and NK-cells share expression of some cell surface antigens, including expression of NK1.1 (Godfrey et al, 2004). By definition, NKT-cells are specialized T-cells because they express the T-cell receptor. NKT-cells cells are, therefore, not identical with NK-cells (which are neither T-cells nor B-cells, and do not express the T-cell receptor).
NKT-cells were identified originally as CD4(-) CD8(-) T-cells that rapidly produce large amounts of IL4 upon cell activation (Zlotnbik et al, 1992; Yoshimoto et al, 1995), NKT-cells differ from conventional T-cells by using a limited and unique set of T-cell receptor variable chains. Most NKT-cells in mice express an invariant TCR alpha chain (Valpha14-Jalpha281) with a conserved CDR3 region together with various beta chains (typically Vbeta8.2, Vbeta2, or Vbeta7) (Fowlkes et al, 1987; Budd et al, 1987; Lantz and Bendelac, 1994). Human NKT-cells express Valpha24-Jalpha18 alpha chain together with a Vbeta11 beta chain (Bendelac, 1995; Lantz and Bendelac, 1994; Dellabona et al, 1994; Porcelli et al, 1993, 1996; Lee et al, 2002). The restricted use of T-cell receptor variants suggests that these cells also have a restricted range of targets (Porcelli et al, 1993).
Mice and human NKT-cells displaying these characteristic T-cell receptor variants depend on CD1d for antigen presentation. Such antigens are ignored by conventional T-cells. Recognition of CD1d by the T-cell receptor does not require CD4 or CD8 coreceptors, but other costimulatory molecules, including CD80 or CD86 with CD28, CD154 with CD40, and ICOS with B7H, which critically contribute to cell activation of CD1d restricted NKT-cells (Kaneda et al, 2005). Handling of antigenic signals by NKT-cells differs from peptide antigen presentation to conventional T-cells, which involves MHC molecules. Also, the antigens recognized are glycolipids rather than proteins (Beckman et al, 1994). This type of antigen recognition involving human CD1d or murine CD1 is highly conserved through mammalian evolution (Brossay et al, 1998; Kashiwase et al, 2003). CD1d is important for antigen presentation and also is important for the development of NKT-cells. Mice lacking CD1d are severely depleted in their NKT-cell pools (Chen et al, 1997; Mendiratta et al, 1997).
Cells expressing the invariant forms of the T-cell receptor and using CD1 for antigen presentation (which distinguishes NKT-cells from classical NK-cells) are frequently being referred to as classical NKT-cells, Va14i NKT-cells, invariant NKT-cells (abbr. iNKT-cells, invNKT-cells), or type 1 NKT-cells (Dale et al, 2004). The term CD1d restricted T-cells is used in a more inclusive sense and includes cells that use a diverse TCR repertoire (also referred to as diverse NKT-cells or noninvariant NKT-cells). Unlike invariant NKT-cells, these cells are not activated by the synthetic compound alpha-galactosylceramide (KRN7000) (Behar and Cardell, 2000). Non-classical NKT-cells are CD1d unrestricted and express gamma-delta T-cell receptors. NKT-cells are phenotypically and functionally diverse (Hammond et al, 1999; Emoto and Kaufmann, 2003) and there is no unique markier that would identify these cells (Hammond et al, 2001). At least two subsets of NKT-cells are distinguishable further. They are either CD4(+) or CD4(-) (Eberl et al, 1999). Some of these cells in humans (but not in mice) may also express CD8 (Prussin and Foster, 1997). They differ from CD4(+) iNKT-cells and CD4(-) CD8(-) iNKT-cells in that they do not produce IL4. However, they appear to produce higher levels of IL10 and IL13 (Takahashi et al, 2002). Lee et al (2002) have reported that CD4(+) NKT-cells and CD4(-) CD8(-) NKT-cell subsets expressing the Valpha24 T-cell receptor represent functionally distinct lineages with marked differences in their profile of cytokine secretion and pattern of expression of chemokine receptors, integrins, and NK receptors. CD4(+) NKT-cells exclusively produce IL4 and IL13 upon primary stimulation, whereas CD4(-) CD8(-) NKT-cells have a strict Th1 profile. Gumperz et al (2002) have reported that one subset of CD4(-) NKT-cells selectively produce the Th1 cytokines IFN-gamma and TNF-alpha, and expressed NKG2d, a marker associated with cytolysis of microbially infected and neoplastic cells. This subset upregulates expression of perforin after exposure to IL2 or IL12. The CD4(+) subset of NKT-cells produce both Th1 and Th2 cytokines, upregulate perforin in response to stimulation by phorbol 12-myristate 13-acetate and ionomycin but not IL2 or IL12, and can be induced to express CD95L. Antigenic stimulation induces cytokine production but not perforin expression in both subsets, whereas exposure to inflammatory factors enhances perforin expression but does not stimulate cytokine production. Hameg et al (2000) have reported the existence of an NKT-cell subset that expresses the canonical Valpha14-Jalpha281 T-cell receptor alpha-chain and Vbeta8 TCR-beta segments, as well as CD1d. They lack expression of the NK-cell marker NK1.1 marker. This subset of NKT-cells can engage their own surface CD1d in an autocrine and/or paracrine manner. In response to alpha-galactosylceramide, these cells produce high amounts of IL4 and moderate amounts of IFN-gamma.
A widely used and most potent agonist for cell activation of NKT-cells is alpha-galactosylceramide (abbr. alpha-GalCer) (Hayakawa et al, 2004). This compound is a synthetic glycolipid based on the structures of related lipids purified from marine sponges, which were identified originally by their ability to induce tumor regression in experimental animal models (Morita et al, 1995). The compound is active on human and murine NKT-cells (Brossay et al, 1998). Facile identification of such specialized NKT-cells exploits the ability of tetrameric complexes of CD1d loaded with alpha-galactosylceramide to bind to the invariant T-cell receptor (Benlagha et al, 2000; Gumpertz et al, 2002). Responses of NKT-cells to alpha-galactosylceramide and derivatives differ quantitatively and qualitatively (Parekh et al, 2004). A variety of other glycolipid structures have been shown also to stimulate NKT-cells. Zhou et al (2004) have reported that the lysosomal glycosphingolipid isoglobotrihexosylceramide (iGb3) is an endogenous ligand for NKT-cells. iGb3 is recognized both by mouse and human NKT-cells. Severe NKT-cell deficiency is observed in mice in which the generation of lysosomal iGb3 is impaired due to the lack of beta-hexosaminidase b.
NKT-cells have been implicated in a variety of biological processes, including direct influences on B-cell proliferation and antibody production (Galli et al, 2003), cell-mediated suppression of tissue destruction, autoimmunity, antitumor responses, host defense, allergy and inflammation (Seino and Taniguchi, 2005, Dale et al, 2004; Godfrey et al, 2004). Nonobese diabetic mice (NOD mice), which serve as a model of autoimmune diabetes, have been shown to be deficient in thymic NKT-cells (Godfrey et al, 1997) and also have reduced numbers of peripheral NKT-cells (Baxter et al, 1997). Diabetes can be prevented in these mice by the introduction of NKT-cells (Hammond et al, 1998; Lehuen et al, 1998). The onset of systemic lupus erythematosus in lupus-prone mouse strains also correlates with a depletion of NKT-cells (Mieza et al, 1996). CD1d restricted NKT-cells have been implicated in granuloma formation during infections with Mycobacterium tuberculosis (Apostolou et al, 1999), immune responses against Listeria monocytogenes via a mechanism mediated by MCP-1 (Flesch et al, 1997), inhibition of infection with Plasmodium yoelii malaria sporozoites (Pied et al, 2000), antitumor responses (Smyth et al, 2000; Nicol et al, 2000), cytotoxic potential for epithelial cells in colitis (Fuss et al, 2004), and development of transplantation tolerance (Ikehara et al, 2000). IL10 secreted by NKT-cells has been shown to be essential for the differentiation of antigen-specific regulatory T-cells in systemic tolerance (Sonoda et al, 2001). IL13 derived from these cells can prevent effective tumor eradication mediated by cytotoxic T-cells (Moodycliffe et al, 2001).
NKT-cells, after ligation of the T-cell receptor, release a variety of cytokines. Depending upon the circumstances, the details of which have not been elucidated completely, NKT-cells can make typical Th1 cytokines (such as IFN-gamma, TNF-alpha), Th2 cytokines (such as IL4, IL10, and IL13), and TGF-beta simultaneously. These cells, therefore, show a Th0 pattern of cytokine secretion. Several conditions exist in which this secretion profile can be skewed either towards a predominance of IFN-gamma (Wilson et al, 1998; Arase et al, 1996) or towards IL4 (Bendelac et al, 1995; Gombert et al, 1996). Thus, NKT-cells, by virtue of the cytokines they secrete, can condition immune responses for subsequent adaptation and have the capacity to shift the balance between Th1 cells and Th2 cells. This would also depend on relative and absolute numbers of NKT-cells. In some systems, these cells may have immunosuppressive activities, whereas in other systems, they may promote enhanced cell-mediated immunity (Smyth and Godfrey; 2000; Wilson and Delovitch, 2003). Matsumoto et al (2004) have reported that cell activation of NKT-cells from mice lacking expression of CD11a LFA-1-/- mice show increased production of IL4, IL5, and IL13, which demonstrates that CD11a is required to polarize cytokine production.
Currently, it is impossible to predict whether cell activation of NKT-cells will suppress or promote immune reactions. This may, at least in part, be due also to the presence of different subpopulations of NKT-cells with different activities. Various scenarios the promotion or suppression of immune responses have been discussed (Dale et al, 2004; Kronenberg, 2004). Functionally different subsets of NKT-cells may be more or less efficient in promoting/suppressing immune responses. Preferential secretion of pro-inflammatory cytokines or anti-inflammatory cytokines may depend critically upon the types of signals received from the microenvironment. This may depend on the balance of signals received through one or more receptors, or, for example, different types of T-cell receptor simulation. The production of a typical identical set of cytokines produced by NTK-cells after cell activation may depend on the time of, or after, cell activation. It has been described, for example, that resting NKT-cells store or pre-form mRNAs for some cytokines even before cell activation through exogenous antigens (Matsuda et al, 2003; Stetson et al, 2003) and that IL4 production by NKT-cells ceases considerably earlier than IFN-gamma production (Crowe et al, 2003). IFN-gamma production by NKT-cells requires longer T-cell receptor stimulation than is required for IL4 production (Oki et al, 2004). Again, different responder cells types may sense the balance of these factors rather than individual factors.
Murine Valpha14Jalpha18(+) cells account for 30-50 % of hepatic T-cells. Human Valpha24Vbeta11(+) NKT-cells are found in small numbers in healthy liver (0.5 % of CD3(+) cells) and blood (0.02 %) and include CD4(+), CD8(+), and CD4(-) CD8(-) cells. Many cells express the NK-cell markers CD56, CD161, and/or CD69. Stimulated human hepatic Valpha24(+) T-cells are potent producers of IFN-gamma and TNF-alpha, but not IL2 or IL4 (Kenna et al, 2003).
Studies in vitro and in vivo have demonstrated that NKT-cells have the capacity to express many different bioactive mediators, which may be engaged in autocrine, paracrine or endocrine interactions that can affect many other cell types. Subsets of NKT-cells may differ in their expression patterns, and these may be influenced also by the state of cell activation and the stimuli leading to it, and may differ, depending of whether the cells were adult or neonatal cells (Kadowaki et al, 2001). Species differences in the capacity of NKT-cells to produce various mediators have been observed also.
NKT-cells have been shown to possess the capacity to express the proteins listed below. Please note the following general observation: expression may be influenced by tissue localization, may occur only in discrete subpopulations of cells, may vary between established cell lines, primary cells, embryonic cells, mature cells, fully differentiated cells, activated cells, non-activated cells or growth conditions (confluent vs. sparse cultures), may be influenced by various disease states (including cancer environment), and may differ between species.
Note also: expression profile information lists entities only for which there is an entry in COPE or one of its subdictionaries.
The meaning of • and •• is as follows: • factor/protein is expressed; •• receptor (or, in some instances, binding sites) for this factor/protein is expressed. For further explanations concerning format, "hidden" information, and/or ambiguities see my remarks in the entry cell types.
• CCL1 (CC chemokine ligand 1, chemokine (C-C motif) ligand 1, SCYA1, I-309, TCA-3, T-cell activation-3, P500, SIS-epsilon) (Kennedy et al, 2000)
•• CCL2 (CC chemokine ligand 2, chemokine (C-C motif) ligand 2, GDCF, Glioma-derived monocyte chemotactic factor-2, GDCF-2, HC11, JE, LDCF, MCAF, MCP, monocyte chemoattractant protein, MCP-1, monocyte chemoattractant protein-1, SMC-CF, smooth muscle cell chemotactic factor, TDCF, tumor-derived chemotactic factors, TSG-8, tumor necrosis factor-stimulated gene sequence-8, SCYA2) receptors (Kawakami et al, 2001)
• CCL3 (CC chemokine ligand 3, chemokine (C-C motif) ligand 3, MIP-1-alpha, macrophage inflammatory protein-1-alpha, 464.1, GOS-19-1, L2G25B, LD78, LD78-alpha, SCI, stem cell inhibition factor, stem cell inhibitor, TY5, SCYA3, SCYA3L1) (Kennedy et al, 2000)
• CCL4 (CC chemokine ligand 4, chemokine (C-C motif) ligand 4, SCYA4, ACT-2, Immune activation gene-2, 744.1, G26, H400, HC21, Cytokine 21, human, LAG-1, lymphocyte activation gene-1, MIP-1-beta, macrophage inflammatory protein-1-beta, SIS-gamma) (Kennedy et al, 2000)
• CCL5 (CC chemokine ligand 5, chemokine (C-C motif) ligand 5, RANTES, EoCP-1, Eosinophil chemotactic polypeptide-1, SIS-delta, TCP228, T-cell-specific protein p228, SCYA5) (Faunce and Stein-Streilein, 2002)
• CCR1 (CC-Chemokine receptor 1, RANTES receptor, MIP-1-alpha receptor, LD78 receptor, CC-CKR1, HM145, YT4, CD191, CMKBR1, chemokine-beta receptor 1) (Thomas et al, 2003; Kim et al, 2002)
• CCR2 (CC-Chemokine receptor 2, CC-CKR2A, CCR2A, CC-CKR2B, CCR2B, MCP-1 receptor A, MCP-1 receptor B, CMKBR2, chemokine-beta receptor 2, CD192) (Thomas et al, 2003; Kim et al, 2002)
• CCR4 (CC-Chemokine receptor 4, CC-CKR4, CKR4, CMKBR4, chemokine-beta receptor 4, K5-5, CD194) (Thomas et al, 2003)
• CCR5 (CC-Chemokine receptor 5, CC-CKR5, CMKBR5, ChemR13, CD195) (Wang et al, 2004; Thomas et al, 2003; Fleuridor et al, 2003; Kim et al, 2002; Motsinger et al, 2002)
• CCR6 (CC-Chemokine receptor 6, GPRCY4, STRL22, DRY6, CKR-L3, CMKBR6, chemokine-beta receptor 6, GPR29, CD196) (Thomas et al, 2003; Kim et al, 2002; Liu et al, 2005)
• CCR7 (CC-Chemokine receptor 7, EBI-1, EBV induced gene-1, blr-2, CMKBR7, Burkitt lymphoma receptor-2, CD197) (Johnston et al, 2003)
• CD11a (ITGAL, integrin-alpha-L, LFA-1, Ly15, Ly21, LFA-1, lymphocyte function-associated antigen-1, LFA-1-alpha, lymphocyte function-associated antigen-1-alpha, neutrophil adherence receptor alpha-M subunit, OND(a), OND) (Franitzka et al, 2004; Gansuvd et al, 2003)
• CD28 (T90/44, Tp44) (Kaneda et al, 2005; Hayakawa et al, 2001)
• CD38 (ADP-ribosyl cyclase, ADP-ribosyl cyclase-1, cyclic ADP-ribose hydrolase, ecto-NAD+ glycohydrolase, Ecto-nicotinamide adenine dinucleotide glycohydrolase, EC3.2.2.5, Leu17, T10) (Fleuridor et al, 2003)
• CD40 ligand (CD40L, CD40LG, TRAP, TNF-related activation protein, CD154, 5c8, gp39, Ly62, T-BAM, IMD3, TNFSF5, TNF ligand superfamily member 5) (Galli et al, 2003)
• CD45R0 (UCHL-1, B220, HuLy-m4, LCA, leukocyte common antigen, Ly5, OX1, OX22, OX30, PTPRC, protein tyrosine phosphatase receptor type C, EC3.1.3.4, T200) (Fleuridor et al, 2003; Gansuvd et al, 2003)
• CD49b (Br alloantigen, DX5, ECMR-2, extracellular matrix receptor-2, GPIa, HPA-5, human platelet antigen-5, ITGA2, integrin-alpha-2, platelet glycoprotein Ia/IIa, VLA-2, very late activation antigen 2, VLAA2, VLA2 receptor alpha 2 subunit, Zav alloantigen) Stenstrom et al, 2004; Yang et al, 2003; Chakir et al, 2001)
• CD49d (ITGA4, integrin-alpha-4, VLA-4, very late activation antigen 4, VLAA4, VLA4 receptor alpha 4 subunit) (Franitzka et al, 2004)
• CD44 (CD44H, AnWj blood group antigen, ECMR-3, extracellular matrix receptor-3, HCAM, homing-associated cell adhesion molecule, Hermes-1, Hermes antigen, HUTCH-1, Indian blood group antigen, In blood group antigen, Ly24, MC56, MDU2, MDU3, MIC4, MUC 2-63, OX49, PGP1, PGP1.1, phagocytic glycoprotein-1) (McKallip et al, 2005)
• CD56 (5.1.H11, BASCA, brain-associated small cell lung cancer antigen, Leu19, MSK39, NCAM, neural cell adhesion molecule, NCAM1, neural cell adhesion molecule-1, NKH-1, PSA-NCAM, polysialylated NCAM, E-NCAM, embryonic NCAM, embryonic neural cell adhesion molecule) (Gansuvd et al, 2003; Kenna et al, 2003; Van de Wetering et al, 2009)
• CD66 (CD66a, BGP, biliary glycoprotein, BGP-1, biliary glycoprotein 1, CEACAM-1, CEA-related cell adhesion molecule 1, CCAM, cell-cell adhesion molecule, CEACAMPS, NCA-160, nonspecific crossreacting antigen 160) (Markel et al, 2002)
• CD69 (AIM, activation inducer molecule, BL-AC/P26, CLEC2C, C-type lectin domain family 2 member C, EA1, early antigen 1, early T-cell activation antigen p60, gp34/28, Leu23, MLR3, VEA) Stenstrom et al, 2004; Kenna et al, 2003)
• CD93 (AA4, C1q receptor, C1qR1, C1qRp, collectin receptor, GR11, Ly68, MXRA4) (Dean et al, 2000, 2001; Lovik et al, 2000)
• CD94 (KP43, KLRD1, killer cell lectin-like receptor subfamily D member 1) (Wilhelm et al, 2003; Coquet et al, 2007)
• CD161b (NKR-P1B) (Carlyle et al, 2004)
• CD161c (NK1.1, NKR-P1C, natural killer cell receptor P1C, NK-cell receptor P1C, NKR-P1.9, Ly55) (Kenna et al, 2003; Fleuridor et al, 2003; Asea and Stein-Streilein, 1998)
• CD161d (NKR-P1D, Ly55d, KLRB1D) (Carlyle et al, 2004)
• CD229 (hly9, HumLy9, Lgp100, Ly9, SLAMF3, signaling lymphocyte activation molecule family member 3, T100 (Sintes et al, 2007)
•• CX3CL1 (fractalkine, FKN, FK, CX3C membrane-anchored chemokine, C3Xkine, neurotactin, NTT, NTN, ABCD-3, SCYD1) receptors (CX3CR1) (Thomas et al, 2003)
•• CXCL1 (CXC chemokine ligand 1, chemokine (C-X-C motif) ligand 1, SCYB1, CINC-1, Cytokine induced neutrophil chemoattractant-1, fsp, fibroblast secretory protein, GRO1, GRO-alpha, KC, MGSA, melanoma growth stimulatory activity, MGSA-alpha, melanoma growth stimulatory activity-alpha, NAP-3, neutrophil-activating protein-3, N51) receptors (Faunce et al, 2001)
•• CXCL16 (CXC chemokine ligand 16, chemokine (C-X-C motif) ligand 16, SR-PSOX, scavenger receptor that binds phosphatidylserine and oxidized lipoprotein, SCYB16) receptors (Shimaoka et al, 2000)
• CXCR3 (CXCR3A, CXC-Chemokine receptor 3, IP-10 receptor, Mig receptor, CKR-L2, GPR9, CD183) (Johnston et al, 2003; Wang et al, 2004; Thomas et al, 2003; Beider et al, 2003; Kim et al, 2002; Liu et al, 2005)
• CXCR4 (CXC-Chemokine receptor 4, LESTR, leukocyte-derived 7-transmembrane domain receptor, HUMSTR, NPYRL, neuropeptide Y receptor-like, NPY3R, neuropeptide Y receptor Y3, HM89, Fusin, LCR-1, FB22, LAP3, Lipopolysaccharide-associated protein 3, SDF-1 receptor, CD184) (Johnston et al, 2003 Franitzka et al, 2004; Thomas et al, 2003; Beider et al, 2003; Fleuridor et al, 2003)
• CXCR5 (MDR15, monocyte-derived receptor 15, blr-1, Burkitt lymphoma receptor-1, CD185) (Johnston et al, 2003)
• CXCR6 (CXC-Chemokine receptor 6, TYMSTR, T-lymphocyte-expressed seven-transmembrane domain receptor, Bonzo, STRL33, CD186) (Johnston et al, 2003; Wang et al, 2004; Shimaoka et al, 2004; Thomas et al, 2003; Kim et al, 2002; Motsinger et al, 2002; Huang et al, 2006)
•• G-CSF (Granulocyte colony stimulating factor, CSF-3, colony stimulating factor-3, CSF-beta, colony stimulating factor-beta, G-CSA, granulocytic neutrophil colony stimulating activity, Pluripoietin-beta) receptors (CD114, CSF3R) (Crough et al, 2004)
• glycosylation inhibiting factor receptors (Sugie et al, 1999)
• GM-CSF (Granulocyte-macrophage colony stimulating factor, BPA, burst promoting activity, CSF-2, colony stimulating factor-2, GM-CSA, Granulocyte-macrophage colony stimulating activity, MGI-1GM, macrophage-granulocyte inducer, Pluripoietin-alpha) (Leite-de-Moraes et al, 2002)
• granulysin (T-cell activation gene 519, T-lymphocyte activation gene 519, TLA519, 519, NKG5, Perforin-enhancing protein, PEPr) (Gansert et al, 2003)
• Granzyme A (GZMA, granzyme 1, Hanukah factor, H factor, HFSP, Hanukah factor serine protease, CTLA-3, cytotoxic T-lymphocyte-associated serine esterase-3, SE-1, serine esterase-1, TSP-1, MTPS-1, T-cell-derived serine proteinase-1, HuTSP, Human T-cell specific proteinase) (Bade et al, 2005)
• Granzyme B (GZMB, Granzyme 2, serine protease B, SE-2, serine esterase-2, CSP-B, cytotoxic serine protease B, CCP1, cytotoxic cell protease-1, Asp-ase, CGL1, cathepsin G-like-1, CTLA-1, cytotoxic T-lymphocyte-associated serine esterase-1, fragmentin-2, RNKP1, rat natural killer protease-1) (van der Vliet et al, 2001; Ohkawa et al, 2001)
• Granzyme K (GZMK, granzyme 3, tryptase-2, fragmentin-3) (Bade et al, 2005)
• Granzyme M (GZMM, Met-ase, Lymphocyte Met-ase 1, Natural killer cell Met-ase) (Bade et al, 2005)
• ICOS (inducible T-cell co-stimulator, H4, AILIM, Activation-inducible lymphocyte immunomediatory molecule, Crp1, CD28-related protein-1, CD278) (Kaneda et al, 2005; Buonfiglio et al, 2000)
• IFN-gamma (IFNG, interferon-gamma, Gamma-Interferon, gIFN) (Chen and Paul, 1997; Chamoto et al, 2004; Kitamura et al, 1999; Oki et al, 2004; Gansuvd et al, 2003; Kennedy et al, 2000; Hayakawa et al, 1992; Matsuda et al, 2003; Gumpertz et al, 2002; Simon et al, 2009)
• IL2 (Interleukin-2, BF, blastogenic factor, EDF, eosinophil differentiation factor, KHF, killer cell helper factor, LMF, lymphocyte mitogenic factor, LPF, lymphocyte proliferation factor, MAF-C I, macrophage-activating factor for cytotoxicity I, PFC-EA, plaque forming cell enhancing factor, SCIF, secondary cytotoxic T-cell inducing factor, TCGF, T-cell growth factor, TCPA, T colony-promoting activity, TDF, thymocyte differentiation factor, T-LPF, T-lymphocyte promotor factor, TMF, thymocyte mitogenic factor, T-cell maturation factor, T-cell mitogenic factor, TRF-3, T-cell replacing factor-3, TSF, thymocyte stimulating factor) (Kim et al, 2002; Hayakawa et al, 1992; Metelitsa et al, 2001)
•• IL2 (Interleukin-2, BF, blastogenic factor, EDF, eosinophil differentiation factor, KHF, killer cell helper factor, LMF, lymphocyte mitogenic factor, LPF, lymphocyte proliferation factor, MAF-C I, macrophage-activating factor for cytotoxicity I, PFC-EA, plaque forming cell enhancing factor, SCIF, secondary cytotoxic T-cell inducing factor, TCGF, T-cell growth factor, TCPA, T colony-promoting activity, TDF, thymocyte differentiation factor, T-LPF, T-lymphocyte promotor factor, TMF, thymocyte mitogenic factor, T-cell maturation factor, T-cell mitogenic factor, TRF-3, T-cell replacing factor-3, TSF, thymocyte stimulating factor) receptors (CD25, TAC antigen, Ly43, OX39) (CD122, CD132) (Lin et al, 2004; Beider et al, 2003; Gumpertz et al, 2002; Coquet et al, 2007)
• IL3 (Interleukin-3, 20-alpha-hydroxysteroid dehydrogenase inducing factor, BPA, burst promoting activity, CFU-S, colony-forming unit spleen, CSF-2-alpha, colony stimulating factor-2-alpha, CSF-2-beta, colony stimulating factor-2-beta, ECSF, erythroid colony stimulating factor, Eo-CSF, eosinophil colony stimulating factor, HCGF, Hematopoietic cell growth factor, HP2, Hematopoietin-2, HPGF, hematopoietic cell growth factor, MCGF, mast cell growth factor, MCSA, multi-colony stimulating activity, MEG-CSF, megakaryocyte colony stimulating factor, MGF, mast cell growth factor, Mixed colony stimulating factor, Multi-CSF, Multi-colony stimulating factor, multi-HGF, multilineage hemopoietic growth factor, Multipoietin, NC cell growth factor, natural cytotoxic cell growth factor, Neutrophil-granulocyte colony stimulating factor, PSF, progenitor stimulating factor, PSH, panspecific hemopoietin, SAF, stem cell activating factor, Thy1 inducing factor) (Leite-de-Moraes et al, 2002)
• IL4 (Interleukin-4, BCDF-epsilon, B-cell differentiation factor-epsilon, BCDF-gamma, B-cell differentiation factor-gamma, BCGF-gamma, B-cell growth factor-gamma, BCGF-1, B-cell growth factor-1, Binetrakin, BSF-1, B-cell stimulating factor-1, BSF-p1, B-cell stimulating factor p1, EL4-BCGF, EL4 B-cell growth factor, HCGF, Hodgkin's cell growth factor, IgE-EF, IgE enhancing factor, IgG1-enhancing factor, IgG1-induction factor, LMW-BCGF, low molecular weight B-cell growth factor, MaGEF, Mast cell growth enhancing factor, MCGF-2, mast cell growth factor-2, MFF, macrophage fusion factor, Pitrakinra, TCGF-2, T-cell growth factor-2) (Zlotnbik et al, 1992; Yoshimoto et al, 1995; Chen and Paul, 1997; Chamoto et al, 2004; Oki et al, 2004; Kim et al, 2002; Kennedy et al, 2000; Hayakawa et al, 1992; Takahashi et al, 2002; Matsuda et al, 2003; de Lalla et al, 2004; Simon et al, 2009)
• IL5 (Interleukin-5, B151-TRF, B151 T-cell replacing factor, BCDF, B-cell differentiation factors, BCDF-alpha, B-cell differentiation factor-alpha, BCDF-mu, B-cell differentiation factor-mu, BCGF-2, B-cell growth factor-2, DL-BCGF, Dennert line B-cell growth factor, BGDF, B-cell growth and differentiation factor, CFU-Eo GSF, colony-forming unit eosinophil growth stimulating factor, EDF, eosinophil differentiation factor, Eo-CSF, Eosinophil colony stimulating factor, Eo-DF, eosinophil differentiation factor, ESP, eosinophil stimulation promoter, IgA-EF, IgA enhancing factor, KHF, killer helper factor, TRF-1, T-cell replacing factor-1) (Hayakawa et al, 1992; Louis et al, 2002)
• IL6 (interleukin-6, 26 kDa protein, BSF-2, B-cell stimulating factor-2, CDF, CAT development factor, choline acetyltransferase development factor, Cytolytic differentiation factor for T-lymphocytes, FDGI, fibroblast-derived growth inhibitor, HGF, hybridoma growth factor, HPGF, hybridoma/plasmacytoma growth factor, HSF, hepatocyte stimulating factor, HSF-1, hepatocyte stimulating factor-1, ILHP1, Interleukin-hemopoietin-1, MGI-2A, Macrophage-granulocyte inducer-2A, Myeloma GF, myeloma growth factor, NKAF, natural killer cell activating factor, TAF, T-cell activating factor, Thymocyte growth factor, TSF, thymocyte stimulating factor) (Gansuvd et al, 2003)
•• IL7 (Interleukin-7, B-cell precursor growth-promoting activity, Lpo-1, lymphopoietin-1, LP-1, PBGF, Pre-B-cell growth factor, serum factor from patients with ulcerative colitis, Thymocyte growth factor) receptors (CD127) (Lin et al, 2004; van der Vliet et al, 2001)
•• IL8 (interleukin-8, SCYB8, 3-10C, 9E3, ANAP, anionic neutrophil-activating peptide, Chemotaxin, CEF-4, CT/IL8, CXCL8, CXC chemokine ligand 8, chemokine (C-X-C motif) ligand 8, EDNAP, endothelial-derived neutrophil-activating peptide, EMF-1, embryo fibroblast protein 1, Emoctakin, ENAP, Endothelial cell neutrophil-activating peptide, FDNAP, Fibroblast-derived neutrophil-activating peptide, FINAP, fibroblast-derived neutrophil-activating protein, GCF, granulocyte chemotactic factor, GCP, granulocyte chemotactic peptide, LAI, leukocyte adhesion inhibitor, LCF, lymphocyte chemotactic factors, LDNAP, leukocyte-derived neutrophil-activating peptide, LIF, leukocyte inhibitory factor, LUCT, lung carcinoma-derived chemotaxin, LYNAP, lymphocyte-derived neutrophil-activating peptide, MDNAP, monocyte-derived neutrophil-activating peptide, MDNCF, monocyte-derived neutrophil chemotactic factor, MOC, monocyte-derived chemotaxin, MONAP, monocyte-derived neutrophil-activating peptide, NAF, neutrophil-activating factor, NAP-1, neutrophil-activating protein-1, NCF, neutrophil chemotactic factor, NCP, neutrophil chemotactic protein, PLF, psoriatic leukotactic factor, TCF, T-cell chemotactic factor, TSG-1, Tumor necrosis factor-stimulated gene sequence-1) receptors (CXCR1 and/or CXCR2) (Thomas et al, 2003)
• IL10 (interleukin-10, B-TCGF, B-cell derived T-cell growth factor, CSIF, cytokine synthesis inhibitory factor, TGIF, T-cell growth inhibitory factor) (Gansuvd et al, 2003; D’Orazio and Niederkorn, 1998; Takahashi et al, 2002; Sonoda et al, 2001)
•• IL12 (IL12A, IL12-alpha IL12B, IL12-beta, IL12-p35, IL12-p40, IL12-p70, Interleukin-12, Interleukin-12A, Interleukin-12B, CLMF, cytotoxic lymphocyte maturation factor, NKSF, natural killer cell stimulatory factor, NKSF1, natural killer cell stimulatory factor-1, NKSF2, natural killer cell stimulatory factor-2, TcMF, CTL maturation factor, TSF, T-cell stimulating factor) receptors (Lin et al, 2004; Habu et al, 2004; Kitamura et al, 1999; Brigl et al, 2003; Gumpertz et al, 2002; Chakir et al, 2001)
• IL13 (Interleukin-13, NC30, P600) (Kawano et al, 1997; Spada et al, 1998; Gansuvd et al, 2003; Takahashi et al, 2002; de Lalla et al, 2004)
•• IL15 (Interleukin-15, IL-T, Interleukin T) receptors (Lin et al, 2004; Ranson et al, 2003; Chakir et al, 2001; van der Vliet et al, 2001; Coquet et al, 2007)
•• IL18 (interleukin-18, IGIF, IFN-gamma inducing factor, IL1-gamma, IL1F4, IL1 family member 4, Iboctadekin) receptors (Dao et al, 1998; Chakir et al, 2001; Leite-De-Moraes et al, 2001; Van de Wetering et al, 2009)
• IL21 (interleukin-21) (Coquet et al, 2007)
•• IL21 (interleukin-21) receptors (Coquet et al, 2007)
•• IL23 (interleukin-23, IL12B, IL12-p40, IL23-p40, p19, IL23-p19, IL23A, SGRF, IL6 G-CSF related factor) receptors (Van de Wetering et al, 2009)
• JAM2 (Junctional adhesion molecule 2, VEJAM, vascular endothelial junctional adhesion molecule, JAM-B, Junctional adhesion molecule B) receptors (JAM3) (Liang et al, 2002)
• Ly49 (Skold et al, 2003; Shimizu et al, 2001; Maeda et al, 2001)
• Mer (Behrens et al, 2003)
• osteopontin (OPN, OP, Osp, 2ar, 44 kDa bone phosphoprotein, 66 kDa bone phosphoprotein, bone sialoprotein, bone sialoprotein-1, BSP, BSP1, BSPI, Calcium oxalate crystal growth inhibitor protein, Eta-1, early T-lymphocyte activation protein 1, Nephropontin, Spp-1, Secreted Phosphoprotein-1, transformation-related phosphoprotein, tumor-secreted phosphoprotein, urinary stone protein, Uropontin) (Diao et al, 2004)
• perforin-1 (pore-forming protein-1, perforin, pore-forming protein, PFP, PFN, PRF1, PFN1) (Ohkawa et al, 2001)
• Survivin (SVV, Apoptosis inhibitor 4, API4, TIAP, Thiol inhibitor of apoptosis, BIRC5, baculoviral IAP repeat-containing protein-5) (Korten et al, 2005)
• TNF-alpha (tumor necrosis factor-alpha, TNFSF2, TNF ligand superfamily member 2, Cachectin, CF, cytotoxic factor, CTX, cytotoxin, DIF, differentiation inducing factor, EP, endogenous pyrogens, Hemorrhagic factor, Macrophage-derived cytotoxic factor, J774-derived cytotoxic factor, MCF, macrophage cytotoxic factor, MCT, macrophage cytotoxin, MD-FGF, monocyte-derived fibroblast growth factor, PCF, peritoneal cytotoxic factor, RCF, Released cytotoxic factor) (Kenna et al, 2003; Gumpertz et al, 2002)
• TGF-beta (transforming growth factor-beta, TGFB, B-TGF, Aqueous humor lymphocyte inhibitory activity, DIF, differentiation-inhibiting factor, EGI, epithelial cell-specific growth inhibitor; epithelial growth inhibitor, EIF, Epstein-Barr virus inducing factor, Epithelial cell growth inhibiting factor, G-TsF, glioma-derived T-cell suppressor factor, MDGF, milk-derived growth factor, MGF, milk growth factor, Polyergin, Simian BSC-1 cell growth inhibitor, SP factor, TCGF, transformed cell growth factor, TGI, tissue-derived growth inhibitor, TIF-1, tumor inducing factor-1) (Gansuvd et al, 2003; D’Orazio and Niederkorn, 1998)
• TLR-2 (Toll-like receptor-2, TIL-4, Toll-interleukin-1 receptor-like-4, Ly105, lymphocyte antigen 105, CD282) (Hiromatsu et al, 2003; Shimizu et al, 2002)
• XCL1 (chemokine C motif ligand-1, CL1, lymphotactin, Ltn, Lptn, SCM-1-alpha, Single C motif-1-alpha, ATAC, activation induced T-cell derived and chemokine related, SCYC1) (Kennedy et al, 2000)
For related information see also: Cell types, Cell lines in Cytokine Research, Cell culture.
For other entries pertaining to hematopoiesis see also the Hematology Dictionary section of this encyclopedia.
LAST MODIFIED: March 2009
See REFERENCES for entry NKT-cells
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