Regulation of cytokine production by soluble CD23: costimulation of interferon gamma secretion and triggering of tumor necrosis factor alpha release.

Armant, Myriam; Ishihara, Hideki; Rubio, Manuel; Delespesse, Guy; Sarfati, M

doi:10.1084/jem.180.3.1005

Cited by 60 publications

(28 citation statements)

References 36 publications

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“…This effect was inhibited by Abs to CD69, LFA-1, and ICAM-1 (38). Other studies have shown that cytokine production is induced in monocytes by soluble CD23 (39,40). In monocytes, the counterligands for CD23 are CD11b/CD18 and CD11c/CD18 rather than CD21 (41).…”

Section: Discussionmentioning

confidence: 80%

Differential Induction of IL-1β and TNF by CD40 Ligand or Cellular Contact with Stimulated T Cells Depends on the Maturation Stage of Human Monocytes

Burger¹,

Molnarfi²,

Gruaz³

et al. 2004

The Journal of Immunology

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Cellular contact with stimulated T cells potently induces cytokine production in monocytes, a mechanism that is likely to be relevant to chronic inflammation. Although the identity of surface molecules involved in this process remains elusive, CD40 and its ligand, CD40L, are thought to be implicated, considering that they are expressed at the inflammatory site. To ascertain the involvement of CD40L, we compared the activation of three different types of human monocytic cells, i.e., freshly isolated monocytes, monocytes primed with IFN-γ (IFN-γ-macrophages), and THP-1 cells. These cells were activated by either membranes isolated from stimulated T cells (HUT-78 or T lymphocytes) to mimic cellular contact, soluble extracts from isolated membranes, or CD40L trimer (CD40LT). The production of TNF and IL-1β was induced by membranes of stimulated T cells in the three types of target cells, whereas CD40LT induced TNF production in IFN-γ-macrophages only. Similar results were obtained with soluble extracts of T cell membranes, demonstrating that the difference between membranes and CD40LT was not due to the particulate form of membranes. CD40LT induced neither transcript nor protein of cytokines in monocytes, whereas in IFN-γ-macrophages, IL-1β and TNF mRNA were observed, but only TNF was measured in cell supernatants. Finally, anti-CD40L Abs failed to inhibit TNF and IL-1β production induced in IFN-γ-macrophages by solubilized membranes, whereas TNF production induced by CD40LT was inhibited. These results demonstrate that CD40L is not required in monocyte activation by direct cellular contact with stimulated T cells, although soluble CD40LT induces the production of TNF in IFN-γ-macrophages.

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Section: Discussionmentioning

confidence: 80%

Differential Induction of IL-1β and TNF by CD40 Ligand or Cellular Contact with Stimulated T Cells Depends on the Maturation Stage of Human Monocytes

Burger¹,

Molnarfi²,

Gruaz³

et al. 2004

The Journal of Immunology

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“…51,52,64,69 Furthermore, we and others 34,38,39,41,[70][71][72] found that engagement of ␤ 2 integrins by different methods, including binding to specific mAbs, adherence to surface coated with fibrinogen, incubation with sCD23, and direct contact with T cells, plays an important role in the production of IL-1␤ and TNF-␣ on monocytes. However, using sTNFR or IL-1Ra (data not shown), we showed that, in our system, expression of MIP-1␣, MIP-1␤, and IL-8 induced by engagement of CD11b or CD11c was not mediated by prior secretion of TNF-␣ or IL-1␤.…”

Section: Discussionmentioning

confidence: 99%

Ligation of CD11b and CD11c β2 integrins by antibodies or soluble CD23 induces macrophage inflammatory protein 1α (MIP-1α) and MIP-1β production in primary human monocytes through a pathway dependent on nuclear factor–κB

Rezzonico

Imbert

Chicheportiche

et al. 2001

Blood

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Chemokines and adhesion molecules such as integrins play a major part in the trafficking, extravasation, and recruitment of leukocytes to inflammatory sites. This study investigated the effects of ␤ 2 integrin engagement on chemokine production by freshly isolated human monocytes. We found that ligation of CD11b or IntroductionRecruitment of circulating leukocytes to an inflammatory site in response to stimuli such as infectious agents (viruses, bacteria, and protozoans) or noninfectious processes (trauma, autoimmune disorders, and ischemia-reperfusion injury) is a crucial step in the development of both acute and chronic inflammatory responses. In all these conditions, extravasation of circulating leukocytes requires communication with vascular endothelial cells that in turn depends on an interrelated network of events involving the finely regulated action of inflammatory cytokines (ie, interleukin [IL] 1 and tumor necrosis factor [TNF]-␣), adhesion molecules (notably integrins), and chemoattractant cytokines called chemokines.Chemokines are highly conserved, small, secreted or membranebound cytokines with molecular masses of 6 to 14 kd and a characteristic 4-cysteine motif in their amino acid sequence. [1][2][3] Two main subfamilies are defined according to the position of the first 2 cysteine residues. In the CXC (or ␣-chemokine) subfamily, these residues are separated by one amino acid, whereas in the CC (or ␤-chemokine) subfamily, they are adjacent. The ␤-chemokines, which include monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein (MIP) 1␣, MIP-1␤, and regulated on activation, normal T-cell expressed and secreted (RANTES) molecules, are potent chemotactic agents for monocytes. 4,5 The migratory behavior of monocytes in response to a concentration gradient of these soluble chemotactic factors also depends on adhesion molecules, particularly the leukocyte-specific ␤ 2 integrins.Integrins are part of a family of heterodimeric transmembrane glycoproteins that recognize a variety of ligands or counterreceptors, including extracellular matrix and cell-surface and plasma proteins, and that consequently control numerous physiologic functions, such as adhesion, locomotion, chemotaxis, and phagocytosis. 6 Expression of ␤ 2 integrins is restricted to leukocytes, with distribution varying among leukocyte subtypes. The ␤ 2 integrins share a common ␤ chain (CD18) and have at least 4 distinct ␣ chains noncovalently associated with CD18: lymphocyte functional antigen 1 (␣ L ␤ 2 , CD11a/CD18), macrophage antigen 1 (Mac-1; ␣ M ␤ 2 , CR3, CD11b/CD18), p150,95 (␣ X ␤ 2 , CR4, CD11c/ CD18), and a newly characterized member, ␣ D ␤ 2 (CD11d/ CD18). 7-9 Interestingly, some chemokines (MCP-1, MIP-1␣, MIP-1␤, and RANTES) increase surface expression of CD11b/CD18 and CD11c/CD18 on human monocytes. [10][11][12] The best characterized ligands of CD11a/CD18 are intracellular adhesion molecule (ICAM) 1 (CD54), ICAM-2 (CD102), and ICAM-3 (CD50), all of which are members of the immunoglobulin superfamily. [13][14...

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“…The imbalance in cytokine production we have described reflects the pattern ofcytokine expression in chronic human synovitis and CAEV-associated arthritis (6, 13). Th2 cytokines can contribute to pathogenesis by driving synovial production of antibodies and formation ofimmune complexes, or by inducing expression of metalloproteases (23) and inflammatory mediators, such as soluble CD23 (24) . Alternatively, Th2 cytokines may contribute to pathogenesis by suppressing Th1-mediated clearance of (auto)antigens or inappropriately activated cells (25) .…”

Section: Discussionmentioning

confidence: 99%

Regulation of the balance of cytokine production and the signal transducer and activator of transcription (STAT) transcription factor activity by cytokines and inflammatory synovial fluids.

Fu-shen

Sengupta

Zhong

et al. 1995

The Journal of Experimental Medicine

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SummaryThe balance between type 1 and 2 T helper cell cytokine production plays an important role in several animal models ofautoimmunity, and skewed patterns of cytokine expression have been described in human inflammatory diseases . Many cytokines activate signal transducer and activation of transcription (STAT) transcription factors, which, in turn, activate transcription ofinflammatory effector genes. We used mononuclear cell priming cultures and inflammatory synovial fluids (SFs) derived from arthritis patients to examine the regulation of cytokine production and STAT activity by an inflammatory synovial microenvironment. Exposure to SFs during priming resulted in an 81% inhibition of interferon (IFN) -'y, but not interleukin (IL) 4, production by effector cells generated in priming cultures . SF suppression was mediated by IL-4 and IL-10 and inhibition ofIL-12 expression, and it was reversed in a dominant fashion by exogenous IL-12 . SFs blocked the sustained activity of transcription factor Statl, but not Stat3, during the priming period, and Statl activity was differentially regulated by cytokines in parallel with their positive or negative regulation of IFN-y production . Active Stat3, but not Statl, was detected in cells from inflamed joints . These results suggest a role for altered balance of Statl and Stat3 transcriptional activity in the regulation of T cell differentiation and in the pathogenesis ofinflammatory synovitis .

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Regulation of cytokine production by soluble CD23: costimulation of interferon gamma secretion and triggering of tumor necrosis factor alpha release.

Cited by 60 publications

References 36 publications

Differential Induction of IL-1β and TNF by CD40 Ligand or Cellular Contact with Stimulated T Cells Depends on the Maturation Stage of Human Monocytes

Differential Induction of IL-1β and TNF by CD40 Ligand or Cellular Contact with Stimulated T Cells Depends on the Maturation Stage of Human Monocytes

Ligation of CD11b and CD11c β2 integrins by antibodies or soluble CD23 induces macrophage inflammatory protein 1α (MIP-1α) and MIP-1β production in primary human monocytes through a pathway dependent on nuclear factor–κB

Regulation of the balance of cytokine production and the signal transducer and activator of transcription (STAT) transcription factor activity by cytokines and inflammatory synovial fluids.

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