• 1993 MD, Semmelweis University School of Medicine, Budapest, Hungary
• 1999 PhD, Semmelweis University School of PhD Studies, Budapest, Hungary

• 1999-2002 Postdoctoral Fellow, University of California, San Francisco, USA
• 2002-present Assistant Professor, Dept. of Physiology, Semmelweis University School of Medicine, Budapest, Hungary

• 1997 EMBO Short Term Fellowship
• 1999 Veritas et Virtus Award, Semmelweis University School of PhD Studies
• 2002 Best Presentation Award, European Society for Clinical Investigation
• 2002 Bolyai Research Fellowship, Hungarian Academy of Sciences
• 2003 Young Investigator Award, Sigma-Aldrich Hungary
• 2004 Gedeon Richter Award, Richter Pharmaceuticals Ltd., Hungary
• 2004 International Senior Research Fellowship, The Wellcome Trust, UK
• 2004 EMBO-HHMI Scientist Award, EMBO Young Investigator Program

Phagocytic cells include a wide array of hematopoietic cell types like neutrophils, macrophages, dendritic cells and osteoclasts; these cells are involved in diverse physiological functions from innate and adaptive immunity to bone resorption. Despite their major biomedical importance, the mechanism of their function is poorly understood, in part because they need to undergo a complex differentiation program that is hard to attain under ex vivo culture conditions. This difficulty can now be overcome by gene knockout technology, allowing the analysis of primary cells carrying targeted deletions of genes of interest. This technology has dramatically enhanced the understanding of how phagocytic cells perform their physiological functions.

During the last several years, we have made considerable contribution to the application of gene targeting to the analysis of neutrophil functions. We have gathered important information about the intracellular signaling mechanisms used by neutrophil surface receptors like integrins, G-protein-coupled receptors and Fc-receptors. Our focus has more recently shifted to the analysis of osteoclast development and osteoclast-mediated bone resorption. Our results suggest that a signaling mechanism similar to that used by lymphocyte antigen receptors is required for osteoclast development and function both in vitro and in vivo.

• Jakus Z, Berton G, Ligeti E, Lowell CA and Mócsai A:
  Responses of neutrophils to anti-integrin antibodies depends on costimulation through low affinity Fc Rs: full activation requires both integrin and nonintegrin signals.
  J Immunol 2004, 173: 2068-2077.
• Mócsai A, Humphrey MB, Van Ziffle JA, Hu Y, Burghardt A, Spusta SC, Majumdar S, Lanier LL, Lowell CA and Nakamura MC:
  The immunomodulatory adapter proteins DAP12 and Fc receptor -chain (FcR ) regulate development of functional osteoclasts through the Syk tyrosine kinase.
  Proc Natl Acad Sci USA 2004, 101: 6158-6163.
• Newbrough SA, Mócsai A, Clemens RA, Wu JN, Silverman MA, Singer AL, Lowell CA and Koretzky GA:
  SLP-76 regulates Fc receptor and integrin signaling in neutrophils.
  Immunity 2003, 19: 761-769.
• Abtahian F, Guerriero A, Sebzda E, Lu MM, Zhou R, Mócsai A, Myers EE, Huang B, Jackson DG, Ferrari VA, Tybulewicz V, Lowell CA, Lepore JJ, Koretzky GA and Kahn ML:
  Regulation of blood and lymphatic vascular separation by signaling proteins SLP-76 and Syk.
  Science 2003, 299: 247-251.
• Mócsai A, Zhou M, Meng F, Tybulewicz VL, Lowell CA:
  Syk is required for integrin signaling in neutrophils.
  Immunity 2002, 16: 547-558.