Translational Biomedicine

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Letter to Editor - (2017) Volume 8, Issue 2

Role of IgG Plasma Cells in the Change of Protein C System in Ulcerative Colitis

Lin XH1, Wang HC2#, Guo JL3,Yang JN1, Li YX1, Dai ZF1,Yang RL1, Zhang JJ4,Yang DS5, Wang B1, Hu JH4, Ren XQ4* and Cheng GC3

1Department of Clinical Laboratory, Translational Medicine Center, Huaihe Hospital Affiliated to Henan University, China

2Department of Nephrology, First Affiliated Hospital of Henan University, China

3Department of Cardiovascular Medicine, Huaihe Hospital Affiliated to Henan University, China

4Department of General Surgery, Huaihe Hospital Affiliated to Henan University,China

5Department of Gastroenterology, Huaihe Hospital Affiliated to Henan University, China

#equally contributed

*Corresponding Author:

Ren XQ
Department of General Surgery, Huaihe
Hospital Affiliated to Henan University
115 Ximen Street, Kaifeng City
Henan Province, China.
Tel: 0086-371-23906758
Fax: 0086-371-23906058
E-mail: [email protected]

Received date: June 12, 2017; Accepted date: June 25, 2017; Published date: June 29, 2017

Citation: Lin XH, Wang HC, Guo JL, et al. Role of IgG Plasma Cells in the Change of Protein C System in Ulcerative Colitis. Transl Biomed. 2017, 8:2. doi: 10.21767/2172-0479.100116

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Letter to Editor

Ulcerative colitis (UC), one type of inflammatory bowel disease, often involving part or all of the colon segment, and the damage generally confined to the colon mucosa [1]. Our previous experimental results indicated that the imbalance of regulatory function of protein C system (PCS) may be one of the most important pathogenesis in the patients with UC. Macrophages from colonic mucosa act on the mucous microvascular endothelial cells through secretion of proinflammatory cytokines, and further causing the inhibition of PCS [2]. While the initiator of PCS inhibition by macrophages is still unclear.

Overactivation of humoral immunity is closely related to UC pathogenesis process [3], and lamina propria lymphocytes (mainly activated B lymphocytes) are suggested to be the source of increased immunoglobulin and antibody [4]. Our research revealed that plenty of plasma cells accumulated in the colonic mucosa in UC mice, flow cytometry experiments further confirmed the infiltration of CD54+CD38+ plasma cells, and the phenotype of the plasma cells was IgG type. These results are consistent with the recent studies which draw the conclusion that the number of IgG type plasma cells was elevated in the inflammatory tissues of some autoimmune diseases [5]. The above results indicate that the number of IgG plasma cells is related to the disease activity and play an important role in the pathological process of UC.

Next, we explore if the elevated plasma cells associated with macrophages -induced PCS change. Our earlier experiment also found infiltration of excess macrophages [2], as well as enhancement of IgG immune complexes (IgG-IC) in UC (unpublished), meanwhile, some studies indicated that CXCR4+ IgG plasma cells result in the pathological process of UC through CD14+ macrophages stimulated by FcγRs [5]. In order to explore how increased IgG plasma cells act on macrophages, and whether the elevated IgG-IC mediate the interaction of plasma cells with macrophages, IgG-IC was mimicked in vitro to simulate isolated colon macrophages, and the expressions and levels of proinflammatory cytokines such as TNF-α and IL-6 in the supernatant of macrophages were detected. We found that both TNF-α and IL-6 expressions and levels were increased obviously. Therefore, we speculate that IgG plasma cells increase, and initiate the inhibition of PCS in the pathogenesis of UC, possibly by the secretion of IgG antibody, and formation of IgG-IC, further action on the macrophages. IgG type plasma cells might represent a promising target for the treatment of UC.


This work was supported by the National Natural Science Foundation of China (No.81500430 to Dr. Xu Hong LIN, and No. U1304802 to Dr. Xu Hong LIN).



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  2. Lin XH, Wang HC, Wei DD, Wang B, Ge QX, et al. (2015) Study of the change and role of protein C system in ulcerate colitis. Sheng Li Xue Bao 67:214-224.
  3. Jinno Y,Ohtani H,Nakamura S, Oki M,Maeda K,et al. (2006) Infiltration of CD19+ plasma cells with frequent labeling of Ki-67 in corticosteroid-resistant active ulcerative colitis. Virchows Arch 448:412-421.
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  5. Uo M,Hisamatsu T,Miyoshi J,Kaito D,Yoneno K, et al. (2013) Mucosal CXCR4+ IgG plasma cells contribute to the pathogenesis of human ulcerative colitis through FcgammaR-mediated CD14 macrophage activation. Gut 62:1734-1744.