Publication date: Available online 13 October 2017
Source:Clinical Immunology
Author(s): Masataka Umeda, Tomohiro Koga, Kunihiro Ichinose, Takashi Igawa, Tomohito Sato, Ayuko Takatani, Toshimasa Shimizu, Shoichi Fukui, Ayako Nishino, Yoshiro Horai, Yasuko Hirai, Shin-ya Kawashiri, Naoki Iwamoto, Toshiyuki Aramaki, Mami Tamai, Hideki Nakamura, Kazuo Yamamoto, Norio Abiru, Tomoki Origuchi, Yukitaka Ueki, Atsushi Kawakami
The cell-surface glycoprotein CD52 is widely expressed in lymphocytes. CD4+CD52hi T cells are functioning suppressor CD4+T cells. We investigated the role of the immune regulation of CD4+CD52 T cells in systemic lupus erythematosus (SLE). CD4+CD52lo T cells were increased in SLE patients, in positive correlation with SLEDAI, anti-ds-DNA antibody, and IgG concentration. Circulating follicular helper-like T cells (Tfh-like cells) were also increased in SLE, in positive correlation with CD4+CD52lo T cells. Chemokine receptor 8 (CCR8) expression in CD4+CD52lo T cells was increased. In vitro experiments using CD4 T cells of SLE patients showed that thymus and activation-regulated chemokine (TARC), a ligand of CCR8, contributed to the development of CD4+CD52hi T cells into CD4+CD52lo T cells. Our findings suggest that CD4+CD52lo T-cell upregulation is involved in the production of pathogens by autoantibodies, and TARC may contribute to the development of SLE through an aberrant induction of CD4+CD52lo T cells.
http://ift.tt/2gaQqZF
Medicine by Alexandros G. Sfakianakis,Anapafseos 5 Agios Nikolaos 72100 Crete Greece,00302841026182,00306932607174,alsfakia@gmail.com,
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