Chemokines: signal lamps for trafficking of T and B cells for development and effector function

Kim, Chang H.; Broxmeyer, Hal E.

doi:10.1002/jlb.65.1.6

Cited by 327 publications

(263 citation statements)

References 103 publications

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“…Moreover, the use of PTX clearly demonstrated that the survivalenhancing effect was mediated through G␣i proteins. SDF-1/ CXCL12 as well as other chemokines are known to mediate their chemotactic effects for myeloid progenitors and other more mature cells through G ␣i proteins (5)(6)(7)(8)21). To establish additional controls for the enhanced survival of RSV-SDF-1/CXCL12 transgenic myeloid progenitors, we tested the survival of bone marrow and spleen cells from other transgenic mice we produced in which SDF-1/CXCL12 transgene expression was under the control of an LCK promoter (30), which limited expression of the SDF-1/ CXCL12 transgene to lymphoid cells (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Transgenic Expression of Stromal Cell-Derived Factor-1/CXC Chemokine Ligand 12 Enhances Myeloid Progenitor Cell Survival/Antiapoptosis In Vitro in Response to Growth Factor Withdrawal and Enhances Myelopoiesis In Vivo

Broxmeyer

Cooper

Kohli

et al. 2003

The Journal of Immunology

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153

143

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Hemopoiesis is regulated in part by survival/apoptosis of hemopoietic stem/progenitor cells. Exogenously added stromal cell-derived factor-1 ((SDF-1)/CXC chemokine ligand (CXCL)12) enhances survival/antiapoptosis of myeloid progenitor cells in vitro. To further evaluate SDF-1/CXCL12 effects on progenitor cell survival, transgenic mice endogenously expressing SDF-1/CXCL12 under a Rous sarcoma virus promoter were produced. Myeloid progenitors (CFU-granulocyte-macrophage, burst-forming unit-erythroid, CFU-granulocyte-erythrocyte-megakaryocyte-monocyte) from transgenic mice were studied for in vitro survival in the context of delayed addition of growth factors. SDF-1-expressing transgenic myeloid progenitors were enhanced in survival and antiapoptosis compared with their wild-type littermate counterparts. Survival-enhancing effects were due to release of low levels of SDF-1/CXCL12 and mediated through CXCR4 and Gαi proteins as determined by ELISA, an antagonist to CXCR4, Abs to CXCR4 and SDF-1, and pertussis toxin. Transgenic effects of low SDF-1/CXCR4 may be due to synergy of SDF-1/CXCL12 with other cytokines; low SDF-1/CXCL12 synergizes with low concentrations of other cytokines to enhance survival of normal mouse myeloid progenitors. Consistent with in vitro results, progenitors from SDF-1/CXCL12 transgenic mice displayed enhanced marrow and splenic myelopoiesis: greatly increased progenitor cell cycling and significant increases in progenitor cell numbers. These results substantiate survival effects of SDF-1/CXCL12, now extended to progenitors engineered to endogenously produce low levels of this cytokine, and demonstrate activity in vivo for SDF-1/CXCL12 in addition to cell trafficking.

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Section: Discussionmentioning

confidence: 99%

Transgenic Expression of Stromal Cell-Derived Factor-1/CXC Chemokine Ligand 12 Enhances Myeloid Progenitor Cell Survival/Antiapoptosis In Vitro in Response to Growth Factor Withdrawal and Enhances Myelopoiesis In Vivo

Broxmeyer

Cooper

Kohli

et al. 2003

The Journal of Immunology

Self Cite

153

143

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“…Chemokines and their chemokine receptors are key mediators of leukocyte recruitment to sites of inflammation. The different migratory properties of Th1 and Th2 cells relate to the expression of different chemokine receptors that are tightly regulated during their differentiation and activation processes [10,11]. Activated/memory Th1 cells have been shown to be associated with the expression of CCR5 (receptor for`Regulated upon Activation Normally T cell Expressed and Secreted' (RANTES), and`Macrophage Inflammatory Protein' (MIP-1a,-1b) and CXCR3 (receptor for`Interferon g Inducible Protein' (IP-10) and`Monokine Induced by IFNg' (MIG)) [12,13], while activated memory Th2 cells express the chemokine receptors CCR3 (receptor for Eotaxin) [14] and CCR4 (receptor for Thymus and Activation-Regulated Chemokine' (TARC)) [15].…”

Section: Introductionmentioning

confidence: 99%

Switch in Chemokine Receptor Phenotype on Memory T Cells without a Change in the Cytokine Phenotype

et al. 2001

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Induction of CCR5 expression on Th2 clones was associated with secretion of some IFN-g. Moreover, the Th2-associated chemokine receptor CCR3 could be expressed on both Th1-dominant cell lines, and clones of Th1 and Th0 type after culture conditions with IL-4. This expression of CCR3 was associated with a reduced IFN-g production, but no IL-4 production could be induced. The IL-4-treated Th1 clones had a reduced migratory capacity against chemokines produced by ST cells compared to nonmanipulated T-cell clones. In contrast, the same IL-12-treated Th1 clones showed an increased migratory potential. Induction of the Th2-associated marker CCR3 on memory Th1 cells demonstrates that a change in chemokine receptor phenotype related to the Th2 type can be induced on terminally differentiated Th1 cells, without a change in the cytokine profile.

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“…In addition, circulating B cells show selective migratory responses to the specific chemokines such as CCL-2, -19, -21, CXCL-1, -8, -12, and -13, which are the ligands for CCR-2, -7, CXCR-1, -2, -4, or -5. [13][14][15] In the nonpathological endometrium, MAdCAM-1, VCAM-1, CCL-2, -19, -21 and CXCL-8, and -13 are expressed throughout the menstrual cycle or temporally during the secretory phase, whereas selectin E, and CXCL12 are not detectable in any phase in the cycle. [16][17][18][19][20][21][22][23] The presence of these adhesion molecules and chemokines in the endometrium with chronic endometritis, however, remains undetermined.…”

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confidence: 99%

Aberrant expression of selectin E, CXCL1, and CXCL13 in chronic endometritis

2010

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Chronic endometritis is often identified in the patients with unexplained infertility, and is histopathologically characterized by infiltration of plasmacytes within the endometrial stroma. In parallel with stromal plasmacyte infiltration, the endometrial functional layer in chronic endometritis is invaded by B cells, which are a rare leukocyte subset residing within the basal layer in the nonpathological endometrium. In this study, we investigated the molecular expression underlying this unusual increase of B cells in chronic endometritis. Twenty-two out of 76 infertile patients were diagnosed with chronic endometritis from the stromal plasmacyte infiltration, and the endometrium contained numerous stromal B-cell aggregates and glandular single B cells. However, the other major leukocyte subsets, including T cells, natural killer cells, macrophages, and neutrophils were comparable in densities in chronic endometritis and nonpathological endometrium. The microvascular endothelium showed immunoreactivity to adhesion molecule selectin E and chemokine CXCL13 along with immunoreactivity to CXCL1 in the glandular epithelium in chronic endometritis, but not in the nonpathological endometrium. Lipopolysaccharide significantly induced surface selectin E expression and CXCL13 secretion in uterine microvascular endothelial cells, and CXCL1 secretion in endometrial epithelial cells in vitro. These findings indicated that the aberrant local microenvironment triggered possibly by bacterial infection has a role in selective extravasation of circulating B cells in chronic endometritis.

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Chemokines: signal lamps for trafficking of T and B cells for development and effector function

Cited by 327 publications

References 103 publications

Transgenic Expression of Stromal Cell-Derived Factor-1/CXC Chemokine Ligand 12 Enhances Myeloid Progenitor Cell Survival/Antiapoptosis In Vitro in Response to Growth Factor Withdrawal and Enhances Myelopoiesis In Vivo

Transgenic Expression of Stromal Cell-Derived Factor-1/CXC Chemokine Ligand 12 Enhances Myeloid Progenitor Cell Survival/Antiapoptosis In Vitro in Response to Growth Factor Withdrawal and Enhances Myelopoiesis In Vivo

Switch in Chemokine Receptor Phenotype on Memory T Cells without a Change in the Cytokine Phenotype

Aberrant expression of selectin E, CXCL1, and CXCL13 in chronic endometritis

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