MIP-1α Induces Binding of Nuclear Factors to the κB DNA Element in Human B Cells

Omoike, Obe I.; Teague, Ryan M.; Benedict, Stephen H.; Chan, Marcia A.

doi:10.1006/mcbr.2000.0247

Cited by 4 publications

(11 citation statements)

References 27 publications

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“…1C) and PI3K (14) and that MIP-1␣ activates a pathway leading to NF-B. (13) We also determined that formation of protein/ DNA complexes containing NF-B was almost completely inhibited in cells pretreated with 100 M parthenolide, (13) which prevents activation of NF-B by inhibiting IB kinase. (38) In an effort to link these observations, we investigated the role that NF-B activity might play in MIP-1␣-mediated B cell migration.…”

Section: Mip-1␣-mediated B Cell Migration Is Dependent On Nf-b Activitymentioning

confidence: 93%

“…Based on our previous data showing that MIP-1␣ regulates the activation of the transcription factors NF-B (13) and c-Jun (Fig. 2), we investigated the possible role MIP-1␣ may have in regulating B cell gene expression.…”

Section: Mip-1␣ Induces An Increase In Ib Gene Expression In Tonsil Bmentioning

confidence: 99%

“…(9,10) MIP-1␣ is a known chemoattractant for T cells (11) and is involved in T cell signal transduction by inducing the activation of signal transducers and activators of transcription (Stat) proteins. (12) In human tonsil B cells, we have demonstrated that MIP-1␣ induces activation of the transcription factor nuclear factor (NF)-B (13) as well as other signaling molecules, such as proline-rich tyrosine kinase (PYK-2) and phosphatidylinositol-3 kinase (PI3K). (14) MIP-1␣ also has been shown to induce B cell chemotaxis (11,14,15) and selectively enhance interleukin-4 (IL-4)-mediated IgE and IgG4 production in a dose-dependent manner.…”

Section: Introduction Mmentioning

confidence: 99%

“…(13) The NF-B family of transcription factors includes p65/RelA, RelB, p105/p50, p100/p52, and c-Rel, each of which exists in an inactive state, bound to the inhibitor IB in the cytoplasm of quiescent cells. (31,32) When the cell is stimulated, IB is phosphorylated and rapidly degraded, allowing the nuclear translocation of NF-B proteins.…”

Section: Introduction Mmentioning

confidence: 99%

“…(32) We demonstrated previously that MIP-1␣ activates NF-B transcription factors in tonsil B cells, and this appeared to correspond with IB degradation in peripheral blood lymphocyte (PBL) B cells. (13) Although transcription factor activation has been associated with MIP-1␣ treatment in T and B lymphocytes, (12,13) the effect MIP-1␣ has on regulation of B cell gene expression has not been investigated.…”

Section: Introduction Mmentioning

confidence: 99%

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MIP-1αInduces Differential MAP Kinase Activation and IκB Gene Expression in Human B Lymphocytes

Teague

Harlan

Benedict

et al. 2004

Journal of Interferon & Cytokine Research

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. The NF-B pathway is understood to be controlled in an autoregulatory fashion, so expression of IB is thought to provide a means by which B cells modulate this pathway after stimulation with MIP-1␣. Although the idea of NF-B autoregulation is not novel, this is the first report to suggest the regulation of B cell gene expression by MIP-1␣. In addition, we observed the activation of Jun N-terminal kinase (JNK) and p38 mitogenic-activated protein kinase (MAPK), but not extracellular signal-related kinase (ERK) in response to MIP-1␣. Although p38 and NF-B activity were both necessary for B cell migration, IB gene expression was not affected by p38 inhibition, suggesting that p38 is involved in a separate MIP-1␣-mediated signal transduction pathway. 403

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Section: Mip-1␣-mediated B Cell Migration Is Dependent On Nf-b Activitymentioning

confidence: 93%

Section: Mip-1␣ Induces An Increase In Ib Gene Expression In Tonsil Bmentioning

confidence: 99%

Section: Introduction Mmentioning

confidence: 99%

Section: Introduction Mmentioning

confidence: 99%

Section: Introduction Mmentioning

confidence: 99%

See 3 more Smart Citations

MIP-1αInduces Differential MAP Kinase Activation and IκB Gene Expression in Human B Lymphocytes

Teague

Harlan

Benedict

et al. 2004

Journal of Interferon & Cytokine Research

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Essential contribution of a chemokine, CCL3, and its receptor, CCR1, to hepatocellular carcinoma progression

Yang

Fujii

et al. 2005

Intl Journal of Cancer

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We previously observed that a chemokine, macrophage inflammatory protein-1 a/CCL3, and its receptor, CCR1, were aberrantly expressed in human hepatocellular carcinoma (HCC) tissues. Here, we show that CCL3 and CCR1 are also expressed in 2 different models of this cancer; N-nitrosodiethylamine (DEN)-induced HCC and HCC induced by hepatitis B virus surface (HBs) antigen-primed splenocyte transfer to myelo-ablated syngeneic HBs antigen transgenic mice. At 10 months after DEN treatment, foci number and sizes were remarkably reduced in CCR1-and CCL3-deficient mice, compared with those of wild-type (WT) mice, although tumor incidence were marginally, but significantly, higher in CCR1-and CCL3-deficient mice than in WT mice. Of note is that tumor angiogenesis was also markedly diminished in CCL3-and CCR1-deficient mice, with a concomitant reduction in the number of intratumoral Kupffer cells, a rich source of growth factors and matrix metalloproteinases (MMPs). Among growth factors and MMPs that we examined, only MMP9 and MMP13 gene expression was augmented progressively in liver of WT mice after DEN treatment. Moreover, MMP9, but not MMP13, gene expression was attenuated in CCR1-and CCL3-deficient mice, compared with that of WT mice. Furthermore, MMP9 was expressed mainly by mononuclear cells but not hepatoma cells, and MMP9-expressing cell numbers were decreased in CCR1-or CCL3-deficient mice, compared with WT mice. These observations suggest the contribution of the CCR1-CCL3 axis to HCC progression. ' 2005 Wiley-Liss, Inc.

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A critical role for CCL2 and CCL3 chemokines in the regulation of polymorphonuclear neutrophils recruitment during corneal infection in mice

et al. 2007

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While the role of CC chemokines in mononuclear cell trafficking and activation has been well studied, the functional role of CC chemokines in the regulation of polymorphonuclear neutrophil (PMN) recruitment in vivo has not been widely examined. Bacterial infection of the cornea (keratitis) is a relatively common, sometimes sight-threatening disease, which features acute inflammation with ulceration and PMN infiltration. Here, we demonstrate a critical role for the chemokines, CCL2 and CCL3, in the Pseudomonas aeruginosa-induced model of corneal infection in BALB/c mice. Treatment of mice with anti-CCL2 or anti-CCL3 antibodies resulted in a significant reduction in severity of corneal damage and PMN infiltration at 1 and 7 days after infection compared to control antibody-treated eyes, but did not significantly alter the rate of bacterial clearance from the cornea. Our findings provide strong evidence that CCL2 and CCL3 are critical regulators of PMN recruitment, and may lead to therapeutic strategies via targeting of the CC chemokines, CCL2 and CCL3, in the management of P. aeruginosa keratitis.

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MIP-1α Induces Binding of Nuclear Factors to the κB DNA Element in Human B Cells

Cited by 4 publications

References 27 publications

MIP-1αInduces Differential MAP Kinase Activation and IκB Gene Expression in Human B Lymphocytes

MIP-1αInduces Differential MAP Kinase Activation and IκB Gene Expression in Human B Lymphocytes

Essential contribution of a chemokine, CCL3, and its receptor, CCR1, to hepatocellular carcinoma progression

A critical role for CCL2 and CCL3 chemokines in the regulation of polymorphonuclear neutrophils recruitment during corneal infection in mice

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