The circulating lymphocyte profiles in patients with discoid lupus erythematosus and systemic lupus erythematosus suggest a pathogenetic relationship

Wouters, Carine; Diegenant, C; Ceuppens, Jan L.; Degreef, Hugo; Stevens, Erik

doi:10.1111/j.0007-0963.2004.05883.x

Cited by 54 publications

(45 citation statements)

References 22 publications

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“…In short, our study substantiated Akasu and Wolfgang's findings that numerous B lymphocytes may be found in DLE lesions. In a circulating lymphocyte study (14), the percentage of CD19 + B cells was increased in DLE patients compared with healthy controls, which was compatible with earlier studies that demonstrated increased percentages of cytoplasmic immunoglobulin-containing and immunoglobulinsecreting cells in the DLE peripheral blood. The role of B lymphocytes in DLE is unknown, but local secretion of specific antibodies is possible, which may act through mechanisms such as opsonization and activation of the complement system.…”

Section: Discussionsupporting

confidence: 89%

“…The decreased number of circulating CD8 + T cells found in their study might result from a shift of these cells to the skin that may be involved in T-cell mediated cytotoxic damage of basal keratinocytes. This may be compatible with the immunohistological finding of CD8 + T cells close to damaged keratinocytes in lesional epidermis (14).…”

Section: Discussionsupporting

confidence: 88%

“…The CD4/CD8 ratio, which ranged approximately from 0.7 to 1.7 (mean 1.0), was a slight decrease compared to that in normal skin (1.1), but there was no statistical significance between them. Wouters et al (14) studied the circulating lymphocyte profiles in patients with DLE and found that the levels of CD4 + T cells were similar in DLE patients and healthy controls, but that CD8 + T cells were decreased both in absolute numbers and percentages, which resulted in a mild increase of the CD4/CD8 ratio. The decreased number of circulating CD8 + T cells found in their study might result from a shift of these cells to the skin that may be involved in T-cell mediated cytotoxic damage of basal keratinocytes.…”

Section: Discussionmentioning

confidence: 99%

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Immunohistochemical characterization of the cellular infiltrate in discoid lupus erythematosus

Xie

Jinnin

Zhang

et al. 2011

BST

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Section: Discussionsupporting

confidence: 89%

Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

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Immunohistochemical characterization of the cellular infiltrate in discoid lupus erythematosus

Xie

Jinnin

Zhang

et al. 2011

BST

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“…The clinical relevance of these data was assessed in a study of lupus patients (Table S2). As reported (25), in the line with IFN-α effects on CD4 cells, active (n = 49) compared with inactive lupus patients (n = 103) or HD exhibited lymphopenia (P = 0.002 and P < 0.001, respectively), a lower blood CD4 T-cell percentage, and among them, a reduced number of CD25 bright nTregs (Fig. 4A).…”

Section: Impact On Ntreg Physiology Of Innate Immune Components Expresupporting

confidence: 76%

IFN-α and CD46 stimulation are associated with active lupus and skew natural T regulatory cell differentiation to type 1 regulatory T (Tr1) cells

Buanec

Gougeon

Mathian

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Immune suppressive activities exerted by regulatory T-cell subsets have several specific functions, including self-tolerance and regulation of adaptive immune reactions, and their dysfunction can lead to autoimmune diseases and contribute to AIDS and cancer. Two functionally distinct regulatory T-cell subsets are currently identified in peripheral tissues: thymus-developed natural T regulatory cells (nTregs) controlling self-tolerance and antiinflammatory IL-10-secreting type 1 regulatory T cells (Tr1) derived from Ag-stimulated T cells, which regulate inflammation-dependent adaptive immunity and minimize immunopathology. We establish herein that cell contact-mediated nTreg regulatory function is inhibited by inflammation, especially in the presence of the complement C3b receptor (CD46). Instead, as with other T-cell subsets, the latter inflammatory conditions of stimulation skew nTreg differentiation to Tr1 cells secreting IL-10, an effect potentiated by IFN-α. The clinical relevance of these findings was verified in a study of 152 lupus patients, in which we showed that lupus nTreg dysfunction is not due to intrinsic defects but is rather induced by C3b stimulation of CD46 and IFN-α and that these immune components of inflammation are directly associated with active lupus. These results provide a rationale for using anti-IFN-α Ab immunotherapy in lupus patients. autoimmunity | lupus pathogenesis | regulatory T cell functional diversity | inflammation-driven regulatory T cell regulation | anti-IFNα immune therapy

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“…Lymphopenia is commonly observed in SLE manifested by decreased numbers of T cells, including CD4 + and CD8 + cells (Wouters et al 2004), as well as B cells (Odendahl et al 2000). Homeostasis within peripheral B cells from SLE patients is disturbed and can be characterized by an increased frequency of CD27 + cells (Odendahl et al 2000;Jacobi et al 2003).…”

Section: Introductionmentioning

confidence: 99%

CD40-activated B cells from patients with systemic lupus erythematosus can be modulated by therapeutic immunoglobulins in vitro

Néron

Boire

Dussault

et al. 2009

Arch. Immunol. Ther. Exp.

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Introduction: Aberrant signaling within and between B and T cells, considered to be central in systemic lupus erythematosus (SLE), could depend on enhanced CD40-CD154 activation. As a result, autoreactive B cells, normally anergic, differentiate and secrete antibodies attacking several normal tissues. Thus restorating B cell homeostasis might help control this disease. In this study, two facets of SLE B cells were investigated, namely their in vitro response to CD40-CD154 and the effect of treatment with human immunoglobulins for intravenous use (IVIg). Materials and Methods: Blood samples from SLE patients and healthy volunteers were obtained and used to isolate B cells, which were activated through CD40 in the presence or absence of IVIg. The phenotype, proliferation, and differentiation of the SLE B cells were determined and compared with those of control B cells using flow cytometry and standard ELISA. Results: In this model, CD40-activated SLE B cells, as control B cells, proliferated and differentiated and were characterized by the emergence of CD19 lo CD38 ++ CD138 + CD27 ++ cells. IVIg treatment of the CD40-activated SLE B cells resulted in higher differentiation, characterized by increased secretion rates of IgG and IgM, as reported previously for control B cells. Conclusions: Taken as a whole, such accelerated differentiation of CD40-activated B cells suggests that IVIg may participate in re-equilibration of the antibody repertoire by replacing pathological antibodies by de novo harmless antibodies.

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The circulating lymphocyte profiles in patients with discoid lupus erythematosus and systemic lupus erythematosus suggest a pathogenetic relationship

Cited by 54 publications

References 22 publications

Immunohistochemical characterization of the cellular infiltrate in discoid lupus erythematosus

Immunohistochemical characterization of the cellular infiltrate in discoid lupus erythematosus

IFN-α and CD46 stimulation are associated with active lupus and skew natural T regulatory cell differentiation to type 1 regulatory T (Tr1) cells

CD40-activated B cells from patients with systemic lupus erythematosus can be modulated by therapeutic immunoglobulins in vitro

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