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Cai, Ling

0000-0002-8592-5269

Mayo Clinic

Sun Yat-sen University

Citations 2

History of the Rare Cancer Network and past Research
Mirimanoff, René-Olivier, Özşahin, Mahmut , Thariat, Juliette , Özyar, Enis , Schick, Ulrike , Pehlivan, Berrin , Krengli, Marco , Franzetti-Pellanda, Alessandra , Vees, Hansjörg, Scandolaro, Luciano , Belkacémi, Yazid , Villà, S. , İğdem, Şefik , Lutsyk, Myroslav, Miller, Robert C. , Mirimanoff, R.O., Cai, Ling , Thariat, Juliette

Rare Tumors | November 7, 2014 | Volume: 6 | Issue: 3 | Pages: 86-90

10.4081/rt.2014.5462 Get It

Approximately, twenty years ago, the Rare Cancer Network (RCN) was formed in Lausanne, Switzerland, to support the study of rare malignancies. The RCN has grown over the years and now includes 130 investigators from twenty-four nations on six continents. The network held its first international symposium in Nice, France, on March 21-22, 2014. The proceedings of that meeting are presented in two companion papers. This manuscript reviews the history of the growth of the RCN and contains the abstracts of fourteen oral presentations made at the meeting of prior RCN studies. From 1993 to 2014, 74 RCN studies have been initiated, of which 54 were completed, 10 are in progress or under analysis, and 9 were stopped due to poor accrual. Forty-four peer reviewed publications have been written on behalf of the RCN.
CD40 Mediates Downregulation of CD32B on Specific Memory B Cell Populations in Rheumatoid Arthritis
Zhang, Xiaoyu , Burch, Erin, So, Edward , Hubbard, Fleesie, Matteson, Eric L. , Strome, Scott E. , Cai, Ling

The Journal of Immunology | May 18, 2013 | Volume: 190 | Issue: 12 | Pages: 6015-6022

10.4049/jimmunol.1203366 Get It

Abstract Altered B cell function is important in the pathogenesis of rheumatoid arthritis (RA). In this report, we show that patients with active RA have an increased frequency of CD32B low/neg cells in the CD27+IgD− memory B cell subset and that these changes are associated with phenotypic and functional B cell activation. Studies using PBMCs from healthy donors revealed that downregulation of CD32B on B cells is mediated by CD40–CD40L interactions and is potentiated by IL-4 and inhibited by both IL-10 and IL-21. These findings appear physiologically relevant because CD4 T cell expression of CD40L correlated with the frequency of CD32B low/neg cells in the CD27+IgD− memory B subset in patients with RA. Our data support a model in which high levels of CD40L, present on circulating T cells in patients with RA, causes B cell activation and CD32B downregulation, resulting in secondary protection of memory B cells from CD32B-mediated cell death.