Appointments
 
Professor of Microbiology and Immunology

 
Weill Cornell \r\nPhysician
   

Ding, Aihao
 (212) 746-4551  (212) 758-8536

Ding, A., C. F. Nathan, and D. Stuehr. (1988) Release of reactive nitrogen intermediates and reactive oxygen intermediates from mouse peritoneal macrophages. J. Immunol. 141:2407.

Ding, A., F. Porteu, E. Sanchez and C. Nathan. (1990) Shared actions of endotoxin and taxol on TNF receptor and TNF release. Science 248:370.

Xie, Q.-W., H. J. Cho, J. Calaycay, R. A. Mumford, K. M. Swiderek, T. D. Lee, A. Ding, T. Troso, and C. Nathan.(1992) Cloning and characterization of inducible nitric oxide synthase from mouse macrophages. Science 256:225.

Jin, F.-Y., C. F. Nathan, D. Razioch, and A. Ding. (1997) Secretory leukocyte protease inhibitor: a macrophage product induced by and antagonistic to bacterial lipopolysaccharide. Cell, 88:417.

Byrd, C. A., W. Bornmann, H. Erdjument-Bromage, P. Tempst, N. Pavletich, C. F. Nathan and A. Ding. (1999) Lipopolysaccharide-mimetic effects of taxol mediated by a heat shock protein. Proc. Natl. Acad. Sci. USA, 96:5645.

Byrd-Leifer, C. A., E. F. Block, K. Takeda, S. Akira and A. Ding. (2001) The role of MyD88 and TLR4 in the LPS-mimetic activity of Taxol. Eur.J. Immunol. 31:2448.

Nathan, C. and A. Ding. (2001) TREM-1: A new regulator of innate immunity in sepsis syndrome. Nature Med. 7:530-532.

Zhu, J., C. Nathan, W. Jin, D. Sim, G. S. Ashcroft, S. M. Wahl, L. Lacomis, H. Erdjument-Bromage, P. Tempst, C. D. Wright and A. Ding. (2002) Conversion of proepithelin to epithelins: roles of SLPI and elastase in host defense and wound repair. Cell 111:867.40.

Odaka, C., T. Mizuochi, J. Yang and A. Ding. (2003) Murine macrophages produce secretory leukocyte protease inhibitor during clearance of apoptotic cells: implications for resolution of the inflammatory response. J. Immunol., 171:1507-1514.

Shi, S., C. Nathan, D. Schnappinger, J. Drenkow, M. Fuortes, E. Block, A. Ding, T.R. Gingeras, G. Schoolnik, S. Akira, K. Takeda and S. Ehrt. (2003) MyD88 primes macrophage for full-scale activation by interferon-? yet mediates few responses to Mycobacterium tuberculosis. J. Exp. Med., 198:987-997.

Yang, J., J Zhu and A. Ding (2005) Suppression of macrophage responses to bacterial lipopolysaccharide (LPS) by secretory leukocyte protease inhibitor (SLPI) is independent of its anti-protease function. Biochim. Biophys. Acta., 1745:310-317.

Ding, A., H Yu, J Yang, S Shi and S Ehrt. (2005) Induction of macrophage-derived SLPI by Mycobacterium tuberculosis depends on TLR2 but not MyD88. Immunology, 116:381-389.

Sun D. and A. Ding (2006) MyD88 mediates stabilization of cytokine and chemokine mRNAs induced by interferon-g. Nat. Immunol., 7:375-381.

Cohn E., C. Nathan, D. Radzioch, H. Yu, Z. Xiang, and A. Ding (2006) Abrupt expression of TLR4 in TLR4-deficient macrophages imposes a selective disadvantage: genetic evidence for TLR4-dependent responses to endogenous, non-microbial stimuli, J. Immunol., 167:1185-1194.


Xu.W, B. He, A. Chiu, M. Buldys, M. Shen, A. Ding, D.M. Knowles, P. Santini, and A. Cerutti. (2007) Epithelial cells trigger frontline immunoglobulin class switching through an SLPI-regulated pathway: a tail from the crypt. Nat. Immunol., 8:294-303.


Kim, Y., P. Zhou, L. Qian, J.-Z. Chuang, J. Lee, C. Li, C. Iadecola, C. Nathan and A. Ding. (2007) MyD88-5 links mitochondria, microtubules and JNK3 in neurons and regulates neuronal survival. J. Exp. Med., 204:2063-2074.




   
   
 
 
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