Biomedical Sciences (BMS) Graduate Program
Admissions | Academic Program | Faculty | Events | Campuses & Facilities | The Bay Area | BMS Intranet | Students | Home

 

back to
BMS Faculty Directory
Mark Anderson, MD, PhD
The Genetic Control of Autoimmune Disease
phone
(415) 514-1683
email
additional
websites

secondary
research affiliation


The main research interest of our laboratory group is to examine the genetic control of autoimmune disease to gain a better understanding of the mechanisms by which immune tolerance is broken. Recently, we generated a mouse model of a human autoimmune disease called APECED, which is classically manifested by an autoimmune attack directed at multiple endocrine organs. This disease is inherited in a monogenic autosomal recessive fashion and the causative gene was identified and is called Aire (for autoimmune regulator). Aire knockout mice, like their human counterparts, develop an autoimmune disease that is targeted to multiple organs. Interestingly, we can ascribe one of the primary defects in these mice to the thymus gland. Specifically, it appears that Aire helps protect against autoimmunity by helping direct the ectopic transcription of multiple self-antigens in thymic medullary epithelial cells. Studies in our laboratory are ongoing on this interesting model of autoimmune disease looking in greater detail how this defect results in the breaking of immune tolerance and what genes may interact with the Aire gene to protect against or worsen autoimmunity. In addition to these ongoing studies, our laboratory is also interested in developing other models of autoimmune disease by using transgenic, knockout, and knock-in approaches.


Selected Publications

[1] J.J. DeVoss, and M.S. Anderson, Lessons on immune tolerance from the monogenic disease APS1. Current Opinion in Genetics & Development 2007 In Press

J. DeVoss, Y. Hou, K. Johannes, W. Lu, G.I. Liou, J. Rinn, H. Chang, R. Caspi, L. Fong, and M.S. Anderson, Spontaneous autoimmunity prevented by thymic expression of a single self-antigen 10.1084/jem.20061864. J. Exp. Med. 203 (2006) 2727-2735.

W. Jiang*, M.S. Anderson*, Bronson, R., Mathis, D., and Benoist, C.  “Modifier loci condition the autoimmunity induced by aire-deficiency”  Journal of Experimental Medicine 2005 Sep 19, 202:805-815. *Co-first author.

 
M.S. Anderson, E. Venanzi, Z. Chen, S. Berzins, C. Benoist,  and D. Mathis.  "The cellular mechanism of aire control of T cell tolerance"  Immunity 2005 Aug; 23:227-239.

Anderson MS, Bluestone JA. 2005. THE NOD MOUSE: A Model of Immune Dysregulation. Annu Rev Immunol 23: 447-85.

Su MA,
Anderson MS. Aire: an update. Curr Opin Immunol. 2004 Dec;16(6):746-52.

Anderson MS
. Autoimmune endocrine disease. Curr Opin Immunol. 2002 Dec;14(6):760-4.

Anderson MS
, Venanzi ES, Klein L, Chen Z, Berzins SP, Turley SJ, von Boehmer H, Bronson R, Dierich A, Benoist C, Mathis D. Projection of an immunological self shadow within the thymus by the aire protein. Science. 2002 Nov 15;298(5597):1395-401.


information last updated May 2007

Featured Paper
Anderson Lab
Lessons on immune tolerance from the monogenic disease APS1. Current Opinion in Genetics & Development 2007 In Press
Download Paper
Featured Paper
Anderson Lab
Spontaneous autoimmunity prevented by thymic expression of a single self-antigen 10.1084/jem.20061864. J. Exp. Med. 203 (2006) 2727-2735.
Download Paper


Copyright © University of California San Francisco | Image Credits