Fas ligand is not only expressed in immune privileged human organs but is also coexpressed with Fas in various epithelial tissues.

Xerri, Luc; Devilard, Élisabeth; Hassoun, Jacques; Mawas, Claude; Birg, Françoise

doi:10.1136/mp.50.2.87

Cited by 120 publications

(89 citation statements)

References 30 publications

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“…Because normal gastric epithelia are known to express CD95 but not CD95L, 23 extensive CD95L expression in the area of affected gastric mucosa could account for the ulcerative tissue damage observed in this case. The contribution of IEL to CD95L expression in ulcerative gastric mucosa was estimated by quantitative RT-PCR using CD3␦ chain-specific primers.…”

Section: Figure 4 T-cell Repertoire Diversity and Clonal Expansions mentioning

confidence: 99%

Involvement of Soluble CD95 in Churg-Strauss Syndrome

Müschen

Warskulat

Perniok

et al. 1999

The American Journal of Pathology

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Deficiency of CD95 (Apo-1/Fas)-mediated apoptosis has recently been found in some autoimmune lymphoproliferative disorders due to inherited mutations of the CD95 gene. In this study , impairment of CD95 ligand-mediated killing of lymphocytes and eosinophils in Churg-Strauss Syndrome (CSS) , which was a result of variation of CD95 receptor isoform expression , is demonstrated. Compared to those from healthy individuals , peripheral blood lymphocytes from eight CSS patients exhibit a switch from the membrane-bound CD95 receptor expression to its soluble splice variant , which protects from CD95L-mediated apoptosis. In five out of seven CSS patients recurrent oligoclonal T cell expansions were found, all using a V␤-gene from the V␤21 family associated with similar CDR3 motifs , indicating the predominance of T cell clones of a similar specificity in the CSS patients. In two of them , the effect of immunosuppressive therapy was studied. In both cases aberrant overexpression of the soluble CD95 receptor isoform and deviations from normal TCR V␤-gene usage normalized in parallel with the clinical improvement. Furthermore , soluble CD95 was identified as a survival factor for eosinophils rescuing eosinophils from apoptosis in the absence of growth factors in vitro. Churg-Strauss Syndrome (CSS) was for the first time described by Lotte Strauss and Jacob Churg in 1951 in The American Journal of Pathology, 1 defining a new entity with systemic vasculitis, blood and tissue eosinophilia, and a long-term history of asthma. Systemic vasculitis in this rare syndrome mainly affects the lower respiratory tract, kidneys, skin, and nervous system. 2 The gastrointestinal tract is involved in about 35% of the CSS cases. 2 Infiltrating eosinophils are frequently found in granulomatous lesions 3 and the fraction of eosinophils in the peripheral blood correlates with the course of the disease, 3,4 suggestive of a role of eosinophils in the pathogenesis of CSS. 5 On the other hand, T cells were frequently implicated in autoreactivity and inflammatory lesions. 6 However, a potential role of T lymphocytes in CSS and the molecular mechanisms underlying this disease have not yet been studied.One tool to analyze T cell populations in clinical samples at the molecular level is the Immunoscope technique. 5 This approach is based on the hypothesis that the expression of unique, rearranged T cell receptor (TCR) genes reflects the specificity of a given T cell. 7 Each TCR-␤ chain consists of a variable (V), diversity (D), joining (J), and a constant region, the first three determining the antigen specificity in their VDJ-junction, including complementarity-determining region III (CDR3). During T cell differentiation, unique variable region genes are created by recombination of V, D and J segments for the TCR-␤ locus. More than 70 V␤ gene segments have been characterized and are classified into 24 gene families 8 ( Figure 1A).In T cells the CD95/CD95 ligand system is a major pathway of apoptotic cell death and thus essential for prevention of lymp...

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Section: Figure 4 T-cell Repertoire Diversity and Clonal Expansions mentioning

confidence: 99%

Involvement of Soluble CD95 in Churg-Strauss Syndrome

Müschen

Warskulat

Perniok

et al. 1999

The American Journal of Pathology

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“…These tissues are called immune privileged tissues (Watanabe-Fukunaga et al, 1992;Leithauser et al, 1993;Hiramatsu et al, 1994;Galle et al, 1995;Xerri et al, 1997;Guller and LaChapelle, 1999;Bernstorff et al, 2002;Niederkorn, 2002). Immune privilege occurs because these tissues express CD95 ligand normally on their surface and normal monitoring immune cells carry the death receptors resulting in a clearing of the immune cells via apoptosis (Krammer, 1998).…”

Section: Death Receptor Proteinsmentioning

confidence: 99%

Synthetic retinoids as inducers of apoptosis in ovarian carcinoma cell lines

Holmes¹,

Soprano²,

Soprano³

2004

Journal Cellular Physiology

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Apoptosis is also known as programmed cell death. Apoptosis plays an essential role in maintaining normal tissue and cell physiology in multicellular organisms. Clearance of aberrant or pre-cancerous cells occurs through the induction of apoptosis. It has been reported that many tumors and tumor cell lines have dysfunctional apoptosis signaling, causing these tumors to escape immune monitoring and internal cellular control mechanisms. One potential cause of this dysfunctional apoptosis is the tumor suppressor p53, an important regulator of growth arrest and apoptosis that is mutated in over 50% of all cancers. Retinoids have great potential in the areas of cancer therapy and chemoprevention. While some tumor cells are sensitive to the growth inhibitory effects of natural retinoids such as all-trans-retinoic acid (ATRA), many ovarian tumor cells are not. 6-[3-(1-Admantyl)]-4-hydroxyphenyl]-2-naphthalene carboxylic acid (CD437) and fenretinide N-[4-hydroxyphenyl] retinamide (4-HPR) are conformationally restricted synthetic retinoids that induce growth arrest and apoptosis in both ATRA-sensitive and ATRA-resistant ovarian tumor cell lines. Recently, we have identified the molecular pathways of apoptosis induced by treatment of ovarian carcinoma cells with mutated p53 by CD437 and 4-HPR.

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“…It belongs to the TNF family and its main function is the induction of apoptosis in susceptible and Fas receptor expressing cells (Takahashi, et al 1994). There are two types of FasL: the pro-apoptotic membrane bound form, which is primarily expressed in activated T lymphocytes and immuneprivileged organs (Xerri, et al 1997) -and the soluble one (sFasL), which originates from the membrane-bound FasL by matrix metalloproteinase-mediated cleavage. The physiological role of sFasL is controversial since it has been reported to induce non-apoptotic signals, possibly including NF-kβ-mediated stimulation of cell proliferation, survival or inflammation within an elevated cytokine milieu (Suda, et al 1997, Mogi, et al 2001, Serrao, et al 2001).…”

Section: Introductionmentioning

confidence: 99%