CD69 molecule in human neutrophils: Its expression and role in signal-transducing mechanisms

Gavioli, Riccardo; Risso, Angela; Smilovich, Daniela; Baldissarro, Isabella; Capra, M.C.; Bargellesi, A.; Cosulich, Maria Elisabetta

doi:10.1016/0008-8749(92)90279-x

Cited by 55 publications

(44 citation statements)

References 27 publications

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“…These signaling events, together with the rapid expression of CD69, have led to the proposal that it may be involved in the ongoing activation of T cells through an as-yet unidentified ligand. CD69 is expressed on a variety of hematopoietic cells including monocytes [ 121, activated neutrophils [13], eosinophils [15] and platelets [ll] in addition to lymphocytes [16-191. In several of these cell types, the expression of CD69 is constitutive [11,121. In contrast, for lymphocyte and natural killer (NK) cells, CD69 is not expressed on resting populations, but is rapidly induced following activation [8,10,201.…”

Section: Introductionmentioning

confidence: 99%

Raf‐1 provides a dominant but not exclusive signal for the induction of CD69 expression on T cells

Taylor‐Fishwick

Siegel

1995

Eur J Immunol

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Stimulation of the T cell antigen receptor (TCR) induces a number of intracellular signaling pathways which lead to the transcription of a variety of new genes. Of the newly synthesized proteins, the earliest to be detected on the cell surface is the type II integral membrane protein CD69. Cross-linking of this activation antigen induces signaling events related to T cell activation. The proto-oncogene product Ras has been reported to up-regulate CD69. However, which of the potential effectors of Ras induces the expression of CD69 has remained unclear. Using transient transfection, we have shown a constitutively active form of the serine/threonine kinase Raf-1 to be sufficient to induce CD69 expression in human Jurkat T cells. Raf-1 was further shown to be necessary for PMA-induced CD69 expression, since transfection of a dominant inhibitory form of Raf-1 blocked the up-regulation of CD69 by PMA. In addition, studies with the calcium ionophore ionomycin identified a previously uncharacterized pathway regulating the expression of CD69 in T cells. Elevation of intracellular calcium induced the expression of CD69 in both Jurkat cells and peripheral blood T cells. This effect was sensitive to the immunosuppressive drug cyclosporin A, indicating that calcium-induced CD69 expression is mediated by the protein phosphatase calcineurin. Taken together, these results define Raf-1 as the major signaling mediator of CD69 expression in T cells and suggest that multiple mechanisms exist to regulate the level of CD69 expression following TCR stimulation.

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Section: Introductionmentioning

confidence: 99%

Raf‐1 provides a dominant but not exclusive signal for the induction of CD69 expression on T cells

Taylor‐Fishwick

Siegel

1995

Eur J Immunol

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“…We have previously shown that neutrophils contain a preformed intracellular pool of CD69 [14] that can be mobilised to the cell surface upon exposure to relevant stimuli [32]. We detected a time-dependent upregulation of CD69 on all viable neutrophils, and no CD69-expression on dead cells, indicating a role for CD69 primarily in the activation process.…”

Section: Discussionmentioning

confidence: 59%

“…The ligand of CD69 is still to be identified, but a membrane-bound molecule is more likely than a soluble factor, since cross-linking of CD69 is required for optimal stimulation [12,13]. Surface expression of CD69 has been observed on a variety of cells, for example activated T and B-cells [11,14,15], NK cells, [16], monocytes [17], neutrophils [18], platelets [19] and eosinophils, but the role of CD69 is, however, still obscure.…”

Section: Introductionmentioning

confidence: 99%

Lower apoptosis rate and higher CD69 expression in neutrophils from atopic individuals

et al. 2002

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“…Additionally, CD69 appears to be involved in signal transduction leading to T cell activation (36). The constitutive expression of CD69, on thymocytes (37), mucosal T lymphocytes (14), neutrophils, platelets, Langerhans cells, eosinophils, and myeloid precursors (4,18,29,39) suggests that CD69 also plays a significant biological role in hematopoietic cells (38). The purpose of this study was to determine whether gamma irradiation, which is known to activate Raf-1 (23), as well as protein tyrosine kinases (40,41), induces CD69 expression on both T and B lymphocytes.…”

mentioning

confidence: 98%

Gamma radiation induces CD69 expression on lymphocytes

et al. 1997

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Gamma radiation activates protooncogenes that are involved in early signal transduction, e.g., Raf‐1. Most studies of effects of gamma radiation on lymphocytes deal with regulation of gene expression. However, early surface receptor expression in response to radiation has not been reported. We studied the effect of radiation on lymphocyte CD69 expression and BrdU uptake in the absence or presence of phytohemagglutinin (PHA). Radiation induces CD69 expression on T and B cells in a dose‐ and time‐dependent manner. Four hours after a dose of 906 cGy, approximately 90% of B and 12% of T cells express CD69. CD69 expression diminishes after 6 h and requires de novo protein synthesis and protein phosphorylation. Radiation alone does not stimulate cell proliferation, as measured by BrdU incorporation, at any radiation dose tested. Furthermore, radiation enhances PHA induced CD69 expression at 2 h, but inhibits BrdU incorporation at day 3 in a dose‐dependent fashion. CD69 functions as a marker for response to radiation, but unlike antigen or mitogen, radiation‐induced CD69 expression does not lead to proliferation. Cytometry 30:304–312, 1997. © 1997 Wiley‐Liss, Inc.

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CD69 molecule in human neutrophils: Its expression and role in signal-transducing mechanisms

Cited by 55 publications

References 27 publications

Raf‐1 provides a dominant but not exclusive signal for the induction of CD69 expression on T cells

Raf‐1 provides a dominant but not exclusive signal for the induction of CD69 expression on T cells

Lower apoptosis rate and higher CD69 expression in neutrophils from atopic individuals

Gamma radiation induces CD69 expression on lymphocytes

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