MiG

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Related to CXCL9: CXCL10, CXCL11

MiG

 (mĭg)
n.
Any of a series of Russian fighter aircraft using piston and later jet engines, such as the MiG 15, an interceptor used during the Korean War, and the MiG 21, exported around the world during the 1970s.

[After Artem Ivanovich Mi(koyan) (1905-1970) and Mikhail Iosifovich G(urevich) (1892-1976), Russian aircraft designers.]

MiG

(mɪɡ)
n
(Military) any of various types of Russian and former Soviet fighter aircraft
[from Mi(koyan) and G(urevich), names of designers]

MiG

or Mig or MIG

(mɪg)

n.
any of several Russian-built fighter aircraft.
[after A. Mi(koyan) and M. G(urevich), Soviet aircraft designers]
References in periodicals archive ?
Relationship between Circulating Levels of IFNg, IL10, CXCL9 and CCL2 in Pulmonary and Extrapulmonary Tuberculosis is Dependent on Disease Severity.
(11-13) Immune system activation is a hallmark of HTLV-1 infection, resulting in spontaneous lymphoproliferation, increased expression of activation markers (HLA-DR, CD25), and exacerbated production of proinflammatory cytokines (IFN-[gamma], TNF) and chemokines (IL-8, CXCL9 and CXCL10).
Levels of the alpha-chemokines CXCL9 and CXCL10, which are expressed in muscle affected by idiopathic inflammatory myopathies such as dermatomyositis, declined strongly over the course of 12 weeks of treatment to an extent that was just shy of statistical significance.
Multicenter validation of urinary CXCL9 as a risk-stratifying biomarker for kidney transplant injury.
However, the majority of the DEGs that were associated with immune response, proliferation, and cytokine networks were downregulated, including Src-like-adaptor-1 (SLA-1), SLA-3, SLA-5, SLA-7, interleukin 10 receptor, beta (IL10RB), chemokine (C-X-C motif) ligand 9 (CXCL9), ubiquitin D (UBD), paired immunoglobulin-like type 2 receptor beta (PILRB), histone H2B type 1, sphingomyelin phosphodiesterase 3 (SMPD3), solute carrier family 7 member 2 (SLC7A2), thyrotropin-releasing hormone degrading enzyme (TRHDE), and serum amyloid A.
Levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), chemokine ligand 9 (CXCL9), IL-10, IL-11, B lymphocyte chemoattractant, and IL-17A have been shown to be elevated in HS skin (17, 18).
HSCs are capable of expressing different chemokine receptors; such as CXC chemokine receptor (CXCR) 3; C-C chemokine receptor (CCR) 5; CCR7; and ligands, including chemokine ligand (CCL) 2, CCL3, CCL5, CXC chemokine ligand (CXCL) 1, CXCL8, CXCL9, and CXCL10.
Genes that were most highly upregulated in DKO mice were CCl5 (by 5.19-fold), Cd40lg (by 2.54-fold), and Cxcl9 (by 5.89-fold).
Additionally, the expression of the following four macrophage polarization markers transglutaminase 2 (Tgm2), arginase 1 (Arg1), chemokine (C-X-C motif) ligand 9 (Cxcl9), and nitric oxide synthase 2 (Nos2) was also assessed (example gating schema in Supplementary Figure 8).
Among these upregulated proteins, cytokines (TNF-[alpha]) and chemokines (I-309, ICAM-1, MCP-1, M-CSF, CCL3, CXCL12, CXCL2, CXCL9, and CXCL10) were significantly downregulated by MST1 suppression compared with the expression in the negative control animals (Figure 7(d)).
Among them, we found the principal components of major regulatory clusters, involving inflammatory responses (IFNy, IL6, several members of the interleukin 1 pathway, including ILIA, IL1B, IL1RN, and the TNF pathway members TNF, TNFAIP6, TNFSF15, TNFRSF9), angiogenesis (CXCL10, PTGS2), immune regulation (CD80, CD274, CSF3, IL23R), leukocyte chemotaxis (CCL2, CCL3, CCL4, CCL20, CCL23, CCL3L3, CXCL1, CXCL2, CXCL5, CXCL9), transcriptional regulation (EGR1, GATA6, HEY1), proliferation (CDKN2B, FGFR1), adhesion (ITGB8), extracellular matrix remodeling (ADAMTS4), cell-cell communication (GJB2), cell signaling (EDNRB, IRS1, RIN2), ion transmembrane transport (KCNJ2, CLIC4), and response to oxidative stress (SOD2).
The PPI network consists of 27 upregulated proteins including LCK, CD3G, CD3E, CD3D, IFNG, VAV1, TNF, B2M, CXCR3, CCR5, CCL5, CXCL9, CXCL10, CXCR4, GNG2, IL1B, IL12B, IL2RB, IL2RA, IL2RG, STAT1, CD8A, CD86, PTPRC, PIK2CG, CD44, and HLADPA1 and 1 downregulated protein EGF.