Matthew Klinker
e-mail address: mklinker@umich.edu

Mentor: David Fox, M.D. and Steven K. Lundy, Ph.D.

Research Description

While the idea that B cells could negatively regulate an immune response has only recently gained wide-spread acceptance, it is becoming clear that B cells wield greater influence than previously thought. Work in our lab has shown that one means by which B cells exert their regulation is through the direct killing of T cells via Fas/Fas ligand interaction. Importantly, this killing was shown to be antigen specific, potentially providing a means of eliminating autoreactive peripheral T cells in vivo. My current project seeks to characterize the intracellular events that result in Fas ligand expression in mouse and human B cells, and which stimuli induce these events. We are also examining the relative importance of B cell-mediated regulation in mouse models of arthritis.

Publications

Klinker MW, Schiller JJ, Magnuson VL, Wang T, Basken J, Veth K, Pearce KI, Kinnunen L, Harjutsalo V, Wang X, Tuomilehto J, Sarti C, Ghosh S; Single-nucleotide polymorphisms in the IL2RA gene are associated with age-at-diagnosis in late-onset Finnish type 1 diabetes subjects (submitted)

Jailwala P, Waukau J, Glisic S, Jana S, Ehlenbach S, Koppen M, Klinker M, Hessner M, Schiller J, Alemzadeh R, Wang X, Ghosh S. Gene expression signatures in CD4+CD25high T cells from recent-onset T1D subjects reveal evidence for increased sensitivity to apoptosis, partially mediated by IL-2 deprivation (submitted)

Glisic S, Klinker M, Waukau J, Jailwala P, Jana S, Basken J, Alemzadeh R, Hagopian W, Ghosh S. Genetic association of HLA DQB1 with CD4+CD25+high T cell apoptosis in Type 1 Diabetes. Genes and Immunity. 2009 Jun; 10(4):334-40.

Awards

Rackham Merit Fellowship