Neutrophil oxidative burst activates ATM to regulate cytokine production and apoptosis

Author:

Harbort C. J.1,Soeiro-Pereira Paulo Vitor2,von Bernuth Horst34,Kaindl Angela M.567,Costa-Carvalho Beatriz Tavares8,Condino-Neto Antonio9,Reichenbach Janine10111213,Roesler Joachim14,Zychlinsky Arturo1,Amulic Borko1

Affiliation:

1. Department of Cellular Microbiology, Max Planck Institute for Infection Biology, Berlin, Germany;

2. Department of Pathology, Federal University of Maranhão, Maranhão, Brazil;

3. Department of Pediatric Pneumology and Immunology, Outpatient Clinic for Primary Immunodeficiencies, Charité Medical School, Berlin, Germany;

4. Labor Berlin, Section for Immunology, Charité–Vivantes GmbH, Berlin, Germany;

5. Institute of Cell Biology and Neurobiology,

6. Department of Pediatric Neurology, and

7. Sozialpädiatrisches Zentrum (SPZ), Charité–Universitätsmedizin Berlin, Berlin, Germany;

8. Department of Pediatrics, Federal University of São Paulo Medical School, São Paulo, Brazil;

9. Department of Immunology, Institute of Biomedical Sciences–University of São Paulo, São Paulo, Brazil;

10. Division of Immunology, University Children’s Hospital, and Children’s Research Centre,

11. Swiss Center for Regenerative Medicine,

12. Center for Applied Biotechnology and Molecular Medicine, and

13. Zurich Centre for Integrative Human Physiology (ZIHP), University of Zürich, Zürich, Switzerland; and

14. Department of Pediatrics, University Hospital TU Dresden, Dresden, Germany

Abstract

Key Points Activation of ATM kinase modulates neutrophil functions and is dependent on the oxidative burst. Neutrophils from ataxia telangiectasia patients overproduce inflammatory cytokines and have a prolonged lifespan.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Reference52 articles.

1. The genetic defect in ataxia-telangiectasia.;Lavin;Annu Rev Immunol,1997

2. Selective defects in T cell function in ataxia-telangiectasia.;Levis;Clin Exp Immunol,1979

3. Selective deficiency of CD4+/CD45RA+ lymphocytes in patients with ataxia-telangiectasia.;Paganelli;J Clin Immunol,1992

4. Deficiencies in CD4+ and CD8+ T cell subsets in ataxia telangiectasia.;Schubert;Clin Exp Immunol,2002

5. Spontaneous and oxidative stress-induced programmed cell death in lymphocytes from patients with ataxia telangiectasia (AT).;Schubert;Clin Exp Immunol,2000

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