CD86 (B7-2) on human B cells: A functional role in proliferation and selective differentiation in IgE and IgG4-producing cells

Jeannin, Pascale; Delneste, Yves; Ellis, Jonathan H.; Bonnefoy, Jean‐Yves

doi:10.1016/s0165-2478(97)85422-3

Cited by 45 publications

(60 citation statements)

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“…Anti-CD80 mAb (clone L307.4) and anti-CD86 mAb (clone IT2.2; both from BD PharMingen; used at 1 g/ml) have been shown to generate intracellular signals in B cells when cross-linked (28,29). In preliminary validation experiments we found that isolated DCs did not require any additional cross-linking of these Abs to show a biologic effect (because DCs themselves are potent cross-linkers of Abs, as demonstrated by their ability to cross-link anti-CD3 Abs and activate T cells).…”

Section: Blocking Absmentioning

confidence: 99%

Ligation of B7-1/B7-2 by Human CD4+ T Cells Triggers Indoleamine 2,3-Dioxygenase Activity in Dendritic Cells

Munn

Sharma

Mellor

2004

The Journal of Immunology

427

339

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Human monocyte-derived dendritic cells (DCs) are capable of expressing the tryptophan-degrading enzyme indoleamine 2,3-dioxygenase (IDO), which allows them to suppress Ag-driven proliferation of T cells in vitro. In DCs that express IDO, the activity of the enzyme is tightly regulated, with the protein being constitutively expressed, but functional activity requiring an additional set of triggering signals supplied during Ag presentation. We now show that triggering of functional IDO obligately requires ligation of B7-1/B7-2 molecules on the DCs by CTLA4/CD28 expressed on T cells. When this interaction was disrupted, IDO remained in the inactive state, and the DCs were unable to inhibit T cell proliferation. Inhibition could be fully restored by direct Ab-mediated cross-linking of B7-1/B7-2. Although both CD4+ and CD8+ T cells were susceptible to inhibition once IDO was induced, the ability to trigger functionally active IDO was strictly confined to the CD4+ subset. Thus, the ability of CD4+ T cells to induce IDO activity in DCs allowed the CD4+ population to dominantly inhibit proliferation of the CD8+ population via the bridge of a conditioned DC. We hypothesize that IDO activation via engagement of B7-1/B7-2 molecules on DCs, specifically, engagement by CTLA4 expressed on regulatory CD4+ T cells, may function as a physiologic regulator of T cell responses in vivo.

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Section: Blocking Absmentioning

confidence: 99%

Ligation of B7-1/B7-2 by Human CD4+ T Cells Triggers Indoleamine 2,3-Dioxygenase Activity in Dendritic Cells

Munn

Sharma

Mellor

2004

The Journal of Immunology

427

339

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“…B7-H1 has an intracellular domain consisting of one potential site for protein kinase phosphorylation and it shares 16% of its identity with B7-2. Thus, it is possible that B7-H1 can transmit signals just like B7-2 (22). Ligation of B7-H1 using mAb induces activation of naive T cells and apoptosis of activated T cells (11).…”

Section: Man Cd19mentioning

confidence: 99%

Cross-Linking of B7-H1 on EBV-Transformed B Cells Induces Apoptosis through Reactive Oxygen Species Production, JNK Signaling Activation, and fasL Expression

Kim

Park

Lee

et al. 2008

The Journal of Immunology

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“…Specifically, B7-2 demonstrates reverse signaling on B cells, resulting in differentiation and class switching (17). B7-H1 is expressed on activated human and mouse T cells (14,18).…”

Section: Introductionmentioning

confidence: 99%

Costimulating aberrant T cell responses by B7-H1 autoantibodies in rheumatoid arthritis

Dong¹,

Strome²,

Matteson³

et al. 2003

J. Clin. Invest.

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A pathogenic hallmark of rheumatoid arthritis (RA) is persistent activation of self-reactive CD4 + T cells. The cause of this aberrant activity remains elusive. We report here detection of autoantibodies against B7-H1, a recently described member of the B7 family, in 29% of patients with RA versus 4% of healthy donors. High-level expression of cell surface B7-H1 are found on activated human CD4 + , CD8 + , and CD45RO + T cells. Immobilized autoantibodies to B7-H1 are capable of costimulating the proliferation of CD4 + T cells in vitro, and the presence of these autoantibodies correlates with active disease status. Using immobilized B7-H1 mAb's and programmed death 1Ig, we demonstrate that engagement of B7-H1 on CD4 + T cells costimulates proliferation and secretion of IL-10, and subsequently leads to programmed cell death, accompanied with upregulated expression of TNF-related apoptosis-inducing ligand and activation of caspase-3. Taken together with our previous findings, these data indicate a bidirectional signaling role of B7-H1 in T cell costimulation and apoptosis and implicate B7-H1 autoantibodies as contributing to the progression of RA by inducing aberrant T cell responses.

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CD86 (B7-2) on human B cells: A functional role in proliferation and selective differentiation in IgE and IgG4-producing cells

Cited by 45 publications

References 0 publications

Ligation of B7-1/B7-2 by Human CD4+ T Cells Triggers Indoleamine 2,3-Dioxygenase Activity in Dendritic Cells

Ligation of B7-1/B7-2 by Human CD4+ T Cells Triggers Indoleamine 2,3-Dioxygenase Activity in Dendritic Cells

Cross-Linking of B7-H1 on EBV-Transformed B Cells Induces Apoptosis through Reactive Oxygen Species Production, JNK Signaling Activation, and fasL Expression

Costimulating aberrant T cell responses by B7-H1 autoantibodies in rheumatoid arthritis

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