Modulation of ongoing human immunoglobulin synthesis by natural killer cells

Kimata, Hajime; Shanahan, Fergus; Brogan, Michael; Targan, Stephan R.; Saxon, Andrew

doi:10.1016/0008-8749(87)90267-x

Cited by 38 publications

(25 citation statements)

References 30 publications

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“…NK cells are thought to play an important role in tissue damage as well as in modulation of B cell activity (23). Wouters et al (14) found a lower number of CD57 + cells in peripheral blood in DLE.…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical characterization of the cellular infiltrate in discoid lupus erythematosus

Xie

Jinnin

Zhang

et al. 2011

BST

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Section: Discussionmentioning

confidence: 99%

Immunohistochemical characterization of the cellular infiltrate in discoid lupus erythematosus

Xie

Jinnin

Zhang

et al. 2011

BST

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“…For example, it has been shown that NK cells are involved in the regulation of B lymphocyte functions (5)(6)(7)(8). Donor type-activated NK cells promote marrow engraftment and B cell development during allogeneic bone marrow transplantation in mice (9) and in humans (10).…”

Section: Cd2mentioning

confidence: 99%

Human B Cell Activation by Autologous NK Cells Is Regulated by CD40-CD40 Ligand Interaction: Role of Memory B Cells and CD5+ B Cells

Blanca

Bere

Young

et al. 2001

The Journal of Immunology

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NK cells are a subpopulation of lymphocytes characterized primarily by their cytolytic activity. They are recognized as an important component of the immune response against virus infection and tumors. In addition to their cytolytic activity, NK cells also participate either directly or indirectly in the regulation of the ongoing Ab response. More recently, it has been suggested that NK cells have an important role in the outcome of autoimmune diseases. Here, we demonstrate that human NK cells can induce autologous resting B cells to synthesize Ig, including switching to IgG and IgA, reminiscent of a secondary Ab response. B cell activation by the NK cell is contact-dependent and rapid, suggesting an autocrine B cell-regulated process. This NK cell function is T cell-independent, requires an active cytoplasmic membrane, and is blocked by anti-CD40 ligand (anti-CD154) or CD40-mIg fusion protein, indicating a critical role for CD40-CD40 ligand interaction. Depletion studies also demonstrate that CD5+ B cells (autoreactive B-1 cells) and a heterogeneous population of CD27+ memory B cells play a critical role in the Ig response induced by NK cells. The existence of this novel mechanism of B cell activation has important implications in innate immunity, B cell-mediated autoimmunity, and B cell neoplasia.

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“…NK cell activity is decreased in autoimmune diseases such as SLE (7), Sjogren's syndrome (8), and multiple sclerosis (9). The regulatory role of NK cells is unclear since these cells have also been shown to support Ig production (10)(11)(12). Mechanisms reported to be involved in NK cell regulatory effects have included perturbation of Fcy receptors (CD16) (6), or NK cell-derived cytokines such as TNF-ol and IFN-y (4,12).…”

mentioning

confidence: 99%

The role of transforming growth factor beta in the generation of suppression: an interaction between CD8+ T and NK cells.

Gray

Hirokawa

Horwitz

1994

The Journal of Experimental Medicine

136

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CD8+ T cells have suppressor effector functions, but the mechanisms involved in the generation of this activity are poorly understood. We report that natural killer (NK) cells have an important role in the acquisition of this function. CD8+ cells induce NK cells to produce transforming growth factor-beta (TGF-beta) which, in turn, stimulates CD8+ T cells to become suppressors of antibody production. Using a monocyte-dependent and -independent method to induce antibody production, we first observed that the addition of NK cells to CD8+ cells was required for optimal suppression. Next, we determined that the interaction of CD8+ T cells with NK cells resulted in a striking increase NK cell TGF-beta mRNA and its production. This cytokine appeared to be involved in the induction of T suppressor cell activity since: (a) anti-TGF-beta 1 completely abrogated the suppression of immunoglobulin G synthesis; (b) TGF-beta 1 could substitute for NK cells in inducing CD8+ T cells to develop suppressor activity; and (c) a short exposure of T cells to TGF-beta 1 in the absence of B cells was sufficient for the generation of suppressor activity by CD8+ T cells. Interferon gamma did not have this property. These studies provide strong evidence that in addition to its suppressive properties, TGF-beta is involved in the generation of CD8+ T suppressor effector cells. Because NK cell function is decreased in many autoimmune diseases, these cells may fail to interact properly with these individuals' CD8+ cells in generating suppressors of aggressive anti-self responses.

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Modulation of ongoing human immunoglobulin synthesis by natural killer cells

Cited by 38 publications

References 30 publications

Immunohistochemical characterization of the cellular infiltrate in discoid lupus erythematosus

Immunohistochemical characterization of the cellular infiltrate in discoid lupus erythematosus

Human B Cell Activation by Autologous NK Cells Is Regulated by CD40-CD40 Ligand Interaction: Role of Memory B Cells and CD5+ B Cells

The role of transforming growth factor beta in the generation of suppression: an interaction between CD8+ T and NK cells.

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