Expansion of cytokine-producing CD4-CD8- T cells associated with abnormal Fas expression and hypereosinophilia.

Simon, Hans‐Uwe; Yousefi, Shída; Dommann-Scherrer, Corina; Zimmermann, Dieter R.; Bauer, Stefan; Barandun, Jonas; Blaser, Kurt

doi:10.1084/jem.183.3.1071

Cited by 143 publications

(98 citation statements)

References 56 publications

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“…In two cases the effect of immunosuppressive therapy could be studied and in both, expression of soluble CD95 and clonal T cell expansions were markedly reduced. In view of previously published data, 16,22 one might speculate that the clonal T cell expansions might represent autoaggressive T cell populations and that high levels of soluble CD95 may protect them from apoptotic removal. Overexpression of soluble CD95 might then equally favor survival and proliferation of eosinophils and self-reactive T cells.…”

Section: Soluble Cd95: a Survival Factor For Autoaggressive T Cells?mentioning

confidence: 99%

“…[13][14][15] But somatic variations in CD95 expression have also recently been shown in two adult individuals, one with idiopathic eosinophilia and the second with HIV infection. 16 Recently, we described a deranged expression pattern of CD95 isoforms in a single Accepted for publication April 11, 1999. M. M. and U. W. contributed equally to this work.…”

Section: Churg-strauss Syndrome (Css) Was For the First Time Describementioning

confidence: 99%

“…Consecutive immunosuppressive treatments led to clinical improvement within 1 month. Patient WI was recently described 16 and is a 48-yearold woman with a 22-year history of asthma. She presented in 1992 for the first time with severe alveolar hemorrhage.…”

Section: Patientsmentioning

confidence: 99%

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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: Soluble Cd95: a Survival Factor For Autoaggressive T Cells?mentioning

confidence: 99%

Section: Churg-strauss Syndrome (Css) Was For the First Time Describementioning

confidence: 99%

See 1 more Smart Citation

Involvement of Soluble CD95 in Churg-Strauss Syndrome

Müschen

Warskulat

Perniok

et al. 1999

The American Journal of Pathology

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“…1). As for CD3 + CD4 ) CD8 ) cells, deficient Fasmediated apoptosis may account for uncontrolled clonal proliferation (39).…”

Section: The Lymphocytic Variantmentioning

confidence: 99%

Recent advances in pathogenesis and management of hypereosinophilic syndromes

Roufosse

Cogan

Goldman

2004

Allergy

129

150

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Idiopathic hypereosinophilic syndrome is a largely heterogeneous disorder defined until now as persistent marked hypereosinophilia of unknown origin generally complicated by end‐organ damage. Recent studies clearly indicate that many patients fulfilling the diagnostic criteria of this syndrome can now be classified as presenting one of two major disease variants: the myeloproliferative or the lymphocytic variant. Research in cellular and molecular biology has provided firm evidence for the existence of discrete hematological disorders underlying these variants, questioning the pertinence of continued reference to ‘idiopathic’ hypereosinophilic syndrome in such patients. Furthermore, identification of these variants has a number of prognostic and therapeutic implications that must be taken into consideration for adequate management of these patients.

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“…There is an augmented proof that T cells play very crucial task in eosinophilia [15] and subgroup of idiopathic eosinophilia [16,17]. …”

Section: Allergic Inflammation Due To Delayed Eosinophils Apoptosismentioning

confidence: 99%

Apoptosis: A Therapeutic Strategy in Eosinophilia

Qasim¹

2013

PAB

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Eosinophils have crucial role in allergic inflammation and asthma. Prolong survival and pathological accumulation at the site of inflammation exclusively related to destructive activity of these pathogenic granulocytes by releasing tissue toxic and inflammatory granule proteins. Any deficiency in eosinophil apoptosis may put in to condition of eosinophilia. Thus, removal of eosinophils by inducing apoptosis has been proposed as potential anti inflammatory strategy in eosinophilia. Apoptosis proves to be beneficial for development of future airway drugs. For therapeutic instances, many reviews illustrate the importance of glucocorticoids as potent anti-inflammatory agent and known to induce apoptosis in eosinophils. Apart from glucocorticoids, theophylline and histamine are well studied apoptosis inducing agents in eosinophil related inflammation. This review elaborates the anti-inflammatory characters of apoptosis in asthma and allergic inflammation.

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Expansion of cytokine-producing CD4-CD8- T cells associated with abnormal Fas expression and hypereosinophilia.

Cited by 143 publications

References 56 publications

Involvement of Soluble CD95 in Churg-Strauss Syndrome

Involvement of Soluble CD95 in Churg-Strauss Syndrome

Recent advances in pathogenesis and management of hypereosinophilic syndromes

Apoptosis: A Therapeutic Strategy in Eosinophilia

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