Michel Arock

Pitié-Salpêtrière Hospital

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Document Type

Co-Authors

Peter Valent

Medical University of Vienna

129

Wolfgang R. Sperr

Medical University of Vienna

Olivier Hermine

Hôpital Necker-Enfants Malades

Karin Hartmann

University of Basel

Cem Akin

University of Michigan–Ann Arbor

Andreas Reiter

Heidelberg University

Karl Sotlar

Paracelsus Medical University

Jason Gotlib

Stanford University

Massimo Triggiani

University of Salerno

Dean D. Metcalfe

National Institute of Allergy and Infectious Diseases

Cooperative Institutions

Inserm

492

Sorbonne Université

308

Université Paris Cité

302

Assistance Publique – Hôpitaux de Paris

297

Centre National de la Recherche Scientifique

263

Pitié-Salpêtrière Hospital

166

Universidad de Salamanca

154

Misgav Ladach

148

Medical University of Vienna

133

Sorbonne Paris Cité

131

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Clinical and Laboratory Parameters of Mast Cell Activation as Basis for the Formulation of Diagnostic Criteria

International Archives of Allergy and Immunology (2011)

Peter Valent Hans‐Peter Horny Massimo Triggiani Michel Arock

Mast cell (MC) activation occurs in a number of different pathologic conditions. Acute activation is commonly seen in patients with allergic reactions, with consecutive massive release of vasoactive and proinflammatory mediator substances from MCs, leading to the clinical signs and symptoms of anaphylaxis. In these patients, serum tryptase concentrations usually increase subtantially above baseline levels. Chronic MC activation is more difficult to diagnose, especially when symptoms are mild or atypical, and no underlying disease is found. In these patients, serum tryptase levels usually are normal. In a smaller group of patients, tryptase levels are constantly elevated and may point to an occult form of mastocytosis. These patients have to be examined for MC monoclonality, other criteria of a primary MC disease, non-MC hematopoietic neoplasms, and reactive disorders producing chronic MC activation or MC accumulation. In most patients in whom MC activation is found, histamine-induced symptoms can be documented and usually respond to treatment with histamine receptor antagonists or MC stabilizers. If this is not the case, alternative explanations for symptoms and differential diagnoses have to be considered.

Tryptase

Proinflammatory cytokine

10.1159/000323763

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Citations (51)

The serum tryptase test: an emerging robust biomarker in clinical hematology

Expert Review of Hematology (2014)

Peter Valent Wolfgang R. Sperr Karl Sotlar Andreas Reiter Cem Akin

During the past few years, a number of molecular markers have been developed in clinical hematology, most of them related to specific gene defects. However, there is also an unmet need to develop novel serologic parameters to improve diagnostics and prognostication in daily practice. Among these, the serum tryptase appears to be a most reliable biomarker of myeloid neoplasms. Elevated tryptase levels are found in subgroups of patients with mastocytosis, myelodysplastic syndrome, myeloproliferative neoplasm, acute myeloid leukemia, chronic myeloid leukemia and chronic eosinophilic leukemia. In these patients, the tryptase level is of diagnostic and/or prognostic significance. In mastocytosis, an elevated tryptase level is a minor criterion of systemic disease and in BCR-ABL1+ chronic myeloid leukemia, elevated tryptase at diagnosis correlates with treatment responses and overall survival. In patients with elevated tryptase, the enzyme also serves as follow-up parameter and can be employed to measure treatment-responses. In the current article, we review and update the perspectives of tryptase and provide recommendations for use of this conventional biomarker in daily practice.

Tryptase

Hematology

Myeloproliferative neoplasm

10.1586/17474086.2014.955008

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Citations (72)

Beyond HaT: Is there room for hereditary beta-tryptasemia?

Revue française d'allergologie (2023)

Y. Chantran S. Choi P. Hirsch L. Bouillet F. Castelain

Tryptase

10.1016/j.reval.2023.103389

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Citations (0)

[Demonstration of a protector effect of interleukin-1 against hematologic toxicity of azidothymidine (AZT)].

PubMed (1992)

Michel Arock A. Dedenon C. Damais Geneviève Averlant Guillosson Jj

3'-azido-3'-deoxythymidine (Azidothymidine or AZT) has attained wide critical utility in the treatment of acquired immunodeficiency syndrome (AIDS). Unfortunately, treatment with AZT is associated with the development of severe hematopoietic toxicity. The AZT sensitivity of marrow progenitors was different with an IC 50 of 10(-8) M and 10(-6) M for respectively BFU-E and CFU-GM/GEMM. Data reported here show that recombinant human interleukin-1 alpha (IL-1 alpha), a pleiotropic cytokine, was demonstrated to be efficient to protect normal human as well as murine hematopoietic progenitors (CFU-GM, CFU-GEMM and BFU-E) from the toxic effect of AZT. The maximal effect was observed with 30 U/ml (Human cells) or 100 U/ml (murine cells) IL-1 alpha for BFU-E and CFU-GM/GEMM, with a marked effect at 1 U/ml. The results demonstrate that marrow progenitors respond differently to AZT and point out the potential efficacy of IL-1 alpha to enhance the proliferation of hematopoietic stem cells treated with growth factors (IL-3, erythropoietin) and to minimize the hematopoietic toxicity associated with AZT treatment.

Interleukin 3

Source

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Citations (1)

Proposed diagnostic criteria and classification of basophilic leukemias and related disorders

Leukemia (2017)

Peter Valent Karl Sotlar K. Blatt Karin Hartmann Andreas Reiter

Basophilia

Basophilic

10.1038/leu.2017.15

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Citations (48)

Ligation of CD23 activates soluble guanylate cyclase in human monocytes via an L-arginine–dependent mechanism

Journal of Leukocyte Biology (1995)

Nathalie Paul‐Eugène Jean‐Pierre Kolb Marika Sarfati Michel Arock F Ouaaz

Abstract Transduction through FcR2/CD23 was analyzed in normal human monocytes using immunoglobulin E (IgE)-anti-IgE immune complexes (IgE ICs) and monoclonal antibodies (mAbs) to CD23. Anti-CD23 mAb and IgE IC triggered a time-dependent increase in cGMP and cAMP in interleukin-4–preincubated (CD23+) but not in unstimulated (CD23-) monocytes. Maximal cGMP and cAMP accumulations were observed 10 and 20 min, respectively, after the onset of CD23 ligation. The increase in cGMP was inhibited with Nω-monomethyl-l-arginine (L-NMMA), which also partially affected cAMP accumulation. Addition of an anti-CD23 mAb Fab fragment inhibited the IgE IC– and the anti-CD23 mAb–induced cGMP and cAMP accumulation, confirming the engagement of CD23. In addition, IgE IC and anti-CD23 mAb induced, at least in some donors, a production of nitrite that was inhibited in the presence of L-NMMA. Taken together, these findings suggest a possible involvement of the nitric oxide synthase pathway in IgE IC–mediated activation of CD23+ monocytes. J. Leukoc. Biol. 57: 160–167; 1995.

CD23

10.1002/jlb.57.1.160

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Citations (44)

Retinoids exert anti-inflammatory effects on human keratinocytes through inhibition of NO and TNF-α secretion

Journal of Investigative Dermatology (1994)

Pierre‐André Bécherel M. Djavad Mossalayi Liliane Le Goff Patrice Debré C. Françès

10.5555/uri:pii:0022202x94923345

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Citations (8)

Rôle des mastocytes dans le remodelage vasculaire de la maladie de Takayasu

La Revue de Médecine Interne (2020)

Alexandre Le Joncour A.C. Desbois P. Regner Anna Maciejewski‐Duval C. Comarmond

10.1016/j.revmed.2020.10.102

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Citations (0)

Distinctive Serum miRNA Profile in Mouse Models of Striated Muscular Pathologies

PLoS ONE (2013)

Nicolas Vignier Fatima Amor Paul Fogel Angélique Duvallet Jérôme Poupiot

Biomarkers are critically important for disease diagnosis and monitoring. In particular, close monitoring of disease evolution is eminently required for the evaluation of therapeutic treatments. Classical monitoring methods in muscular dystrophies are largely based on histological and molecular analyses of muscle biopsies. Such biopsies are invasive and therefore difficult to obtain. The serum protein creatine kinase is a useful biomarker, which is however not specific for a given pathology and correlates poorly with the severity or course of the muscular pathology. The aim of the present study was the systematic evaluation of serum microRNAs (miRNAs) as biomarkers in striated muscle pathologies. Mouse models for five striated muscle pathologies were investigated: Duchenne muscular dystrophy (DMD), limb-girdle muscular dystrophy type 2D (LGMD2D), limb-girdle muscular dystrophy type 2C (LGMD2C), Emery-Dreifuss muscular dystrophy (EDMD) and hypertrophic cardiomyopathy (HCM). Two-step RT-qPCR methodology was elaborated, using two different RT-qPCR miRNA quantification technologies. We identified miRNA modulation in the serum of all the five mouse models. The most highly dysregulated serum miRNAs were found to be commonly upregulated in DMD, LGMD2D and LGMD2C mouse models, which all exhibit massive destruction of striated muscle tissues. Some of these miRNAs were down rather than upregulated in the EDMD mice, a model without massive myofiber destruction. The dysregulated miRNAs identified in the HCM model were different, with the exception of one dysregulated miRNA common to all pathologies. Importantly, a specific and distinctive circulating miRNA profile was identified for each studied pathological mouse model. The differential expression of a few dysregulated miRNAs in the DMD mice was further evaluated in DMD patients, providing new candidates of circulating miRNA biomarkers for DMD.

Limb-girdle muscular dystrophy

Creatine kinase

10.1371/journal.pone.0055281

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Citations (99)

Le polynucléaire basophile : du contrôle de l’immunité à celui des leucémies

Annales Pharmaceutiques Françaises (2021)

Michel Arock

Malignant Transformation

Malignant cells

10.1016/j.pharma.2021.05.005

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Citations (2)