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Lei Jin , M.Sc , Ph.D.
Assistant Professor

Phone: 518-262-0053


2004 - Ph.D. from Tufts University
1998 - M.Sc from Fudan University

Current Research

 A majority of infectious microorganisms (pathogens) either colonize or cross mucosal surfaces to enter the host. In order for the immune system to function properly and fight these pathogens, it must first be able to detect the presence of pathogens. This detection arm of the immune system surveys the inside and outside of cells for the presence of pathogens. Once a pathogen is detected, an alarm response is triggered which involves the production of immune proteins called cytokines and interferons from infected cells. These proteins aid the elimination of the pathogen by the immune system. A key part of the detection arm of the immune system that operates inside cells has recently been identified, namely the protein MPYS, also known as STING, MITA and TMEM173. In order to more fully understand how MPYS actually works, and how it contributes to eliminating pathogens, MPYS-deficient mice have been generated. These mice will be used to explore how a mammal copes with pathogen infections in the absence of MPYS and also to work out a better mucosal vaccine strategy to protect the host. The knowledge generated from this project will significantly advance our understanding of the mammalian immune response to pathogens, and ultimately lead to better health care.

Research Interests

  • Host Defense Against Bacterial Infection;
  • Innate Immune Signaling;
  • Adjuvant Development

Research Summary


PubMed Publications

  1. Sialic acid binding domains of CD22 are required for negative regulation of B cell receptor signaling. Jin L, McLean PA, Neel BG, Wortis HH. J Exp Med. 2002 May 6;195(9):1199-205.

  2. MHC class II structural requirements for the association with Igalpha/beta, and signaling of calcium mobilization and cell death. Jin L, Stolpa JC, Young RM, Pugh-Bernard AE, Refaeli Y, Cambier JC. Immunol Lett. 2008 Mar 15;116(2):184-94. Epub 2007 Dec 26.

  3. MPYS, a novel membrane tetraspanner, is associated with major histocompatibility complex class II and mediates transduction of apoptotic signals. Jin L, Waterman PM, Jonscher KR, Short CM, Reisdorph NA, Cambier JC. Mol Cell Biol. 2008 Aug;28(16):5014-26. Epub 2008 Jun 16

  4. Cellular reactive oxygen species inhibit MPYS induction of IFNbeta. Jin L, Lenz LL, Cambier JC. PLoS One. 2010 Dec 10;5(12):e15142.

  5. Identification and characterization of a loss-of-function human MPYS variant. Jin L, Xu LG, Yang IV, Davidson EJ, Schwartz DA, Wurfel MM, Cambier JC. Genes Immun. 2011 Jun;12(4):263-9. Epub 2011 Jan 20

  6. MPYS is required for IFN response factor 3 activation and type I IFN production in the response of cultured phagocytes to bacterial second messengers cyclic-di-AMP and cyclic-di-GMP. Jin L, Hill KK, Filak H, Mogan J, Knowles H, Zhang B, Perraud AL, Cambier JC, Lenz LL. J Immunol. 2011 Sep 1;187(5):2595-601. Epub 2011 Aug 3.

  7. VISA is required for B cell expression of TLR7. Xu LG, Jin L, Zhang BC, Akerlund LJ, Shu HB, Cambier JC. J Immunol. 2012 Jan 1;188(1):248-58. Epub 2011 Nov 21.

  8. SMIP-016 in action: CD37 as a death receptor. Jin L, Cambier JC. Cancer Cell. 2012 May 15;21(5):597-8.