Cloning of Human and Mouse EBI1, a Lymphoid-Specific G-Protein-Coupled Receptor Encoded on Human Chromosome 17q12-q21.2

Schweickart, Vicki L.; Raport, Carol J.; Godiska, Ronald; Byers, Mary G.; Eddy, Roger L.; Shows, Thomas B.; Gray, Patrick W.

doi:10.1006/geno.1994.1553

Cited by 90 publications

(74 citation statements)

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“…41 They are implicated in migration of leukocytes, inflammatory responses and regulation of tumor growth, as well as hematopoiesis. [42][43][44] SDF1a and its receptor CXCR4 play important roles in migration of HSC from the fetal liver to the fetal BM 45,46 as well as in postnatal life.…”

Section: Discussionmentioning

confidence: 99%

BCR/ABL-mediated downregulation of genes implicated in cell adhesion and motility leads to impaired migration toward CCR7 ligands CCL19 and CCL21 in primary BCR/ABL-positive cells

et al. 2005

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The mechanism underlying p210 BCR/ABL oncoprotein-mediated transformation in chronic myelogenous leukemia (CML) is not fully understood. We hypothesized that p210 BCR/ABL suppresses expression of genes which may explain at least some of the pathogenetic features of CML. A subtractive cDNA library was created between BCR/ABL-enhanced-green-fluorescentprotein (GFP)-transduced umbilical cord blood (UCB) CD34 þ cells and GFP-transduced UCB CD34 þ cells to identify genes whose expression is downregulated by p210 BCR/ABL . At least 100 genes were identified. We have confirmed for eight of these genes that expression was suppressed by quantitative realtime-RT-PCR (Q-RT-PCR) of additional p210 BCR/ABL -transduced CD34 þ UCB cells as well as primary early chronic phase (CP) bone marrow (BM) CML CD34 þ cells. Imatinib mesylate reversed downregulation of some genes, to approximately normal levels. Several of the genes are implicated in cell adhesion and motility, including L-selectin, intercellular adhesion molecule-1 (ICAM-1), and the chemokine receptor, CCR7, consistent with the known defect in adhesion and migration of CML cells. Compared with GFP UCB or normal (NL) BM CD34 þ cells, p210 UCB and CML CD34 þ cells migrated poorly towards the CCR7 ligands, CCL19 and CCL21, suggesting a possible role for CCR7 in the abnormal migratory behavior of CML CD34 þ cells.

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Section: Discussionmentioning

confidence: 99%

BCR/ABL-mediated downregulation of genes implicated in cell adhesion and motility leads to impaired migration toward CCR7 ligands CCL19 and CCL21 in primary BCR/ABL-positive cells

et al. 2005

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“…This could suggest the convergence or competition of LIGHT and CD40L signaling for Ig secretion for a limiting step that, thus, could not be modified by additional stimulation. In addition to stimulation by TNF/TNFR family members, interaction of ICOS [4], which is a member of the B7 family of costimulatory molecules, with its ligand [5] has also an important role in B cell physiology. ICOS is expressed on both CD4 + and CD8 + activated T lymphocytes [6].…”

Section: Light Stimulation Enhances Ig Secretionmentioning

confidence: 99%

LIGHT costimulates CD40 triggering and induces immunoglobulin secretion; a novel key partner in T cell‐dependent B cell terminal differentiation

et al. 2004

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The T cell-dependent differentiation and function of B lymphocytes are tightly regulated by TNF ligands (L) and receptors interactions, such as CD40/CD40L, CD27/CD70 and CD134/ CD314L. The LIGHT/HVEM system [homologous to lymphotoxin, inducible expression, competing for GpD of herpes virus, that binds to the herpes virus entry mediator (HVEM), and is expressed on activated T lymphocytes) focused our attention since HVEM has a large distribution that, in addition to T cells, DC or NK, includes tumor and normal B lymphocytes. HVEM was expressed on memory and naive B cells from peripheral blood or tonsils, but not on germinal center (GC) B cells. Costimulation by CD40L+LIGHT induced LIGHT expression at the B lymphocyte surface by a transcriptional mechanism since we detected de novo expression of LIGHT-specific mRNA. LIGHTexpression was further enhanced by triggering of surface IgM, a stimulus that mimics a normal step of B cell physiology, i.e. specific antigen encounter. Stimulation by LIGHT increased the B cell proliferation induced by CD40L, and induced IgG and IgM (but not IgA) secretion. We conclude that LIGHT costimulation, that mimics the B cell encounter with activated LIGHT-expressing T lymphocytes, enhances both B cell proliferation and Ig production, and thus has a central importance for humoral immunity development.

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“…CCR7 expression is expected on naive B cells because its ligands SLC and CK␤-11 readily attract freshly isolated human and murine B cells well [47,53,58,59]. CCR7 expression is up-regulated in activated B cells by Epstein-Barr virus (EBV) infection [77,90,91]. CCR2 is expressed on both resting and activated CD19 ϩ B cells [92].…”

Section: Chemokines For Activated or Memory Lymphocytesmentioning

confidence: 99%

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

Kim

Broxmeyer

1999

Journal of Leukocyte Biology

327

251

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Cloning of Human and Mouse EBI1, a Lymphoid-Specific G-Protein-Coupled Receptor Encoded on Human Chromosome 17q12-q21.2

Cited by 90 publications

References 0 publications

BCR/ABL-mediated downregulation of genes implicated in cell adhesion and motility leads to impaired migration toward CCR7 ligands CCL19 and CCL21 in primary BCR/ABL-positive cells

BCR/ABL-mediated downregulation of genes implicated in cell adhesion and motility leads to impaired migration toward CCR7 ligands CCL19 and CCL21 in primary BCR/ABL-positive cells

LIGHT costimulates CD40 triggering and induces immunoglobulin secretion; a novel key partner in T cell‐dependent B cell terminal differentiation

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

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