Expression of SOCS1 and SOCS3 genes in human graft-versus-host disease after allogeneic hematopoietic stem cell transplantation.
- Author:
Tae Hyang LEE
1
;
Ji Yoon LEE
;
Sohye PARK
;
Seung Hwan SHIN
;
Seung Ah YAHNG
;
Jae Ho YOON
;
Sung Eun LEE
;
Byung Sik CHO
;
Yoo Jin KIM
;
Seok LEE
;
Chang Ki MIN
;
Dong Wook KIM
;
Jong Wook LEE
;
Woo Sung MIN
;
Chong Won PARK
;
Hee Je KIM
Author Information
- Publication Type:Original Article
- Keywords: Suppressor of cytokine signaling proteins; Graft vs. host disease; Quantitative real-time polymerase chain reaction; Allogeneic transplantation
- MeSH: Anemia, Aplastic; Graft vs Host Disease; Hematopoietic Stem Cell Transplantation; Hematopoietic Stem Cells; Humans; Interferon-gamma; Interleukins; Leukemia, Myelogenous, Chronic, BCR-ABL Positive; Leukocytes; Myelodysplastic Syndromes; Polymerase Chain Reaction; Real-Time Polymerase Chain Reaction; Reverse Transcription; Siblings; Suppressor of Cytokine Signaling Proteins; T-Lymphocytes; Tissue Donors; Transplantation, Homologous; Unrelated Donors
- From:Blood Research 2013;48(1):16-23
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND: Suppressor of cytokine signaling genes (SOCS) are regarded as pivotal negative feedback regulators of cytokine signals, including the interferon-gamma (IFN-gamma), granulocyte-colony stimulating factor, and interleukin families, released by T cells. A detailed understanding of the involvement of SOCS genes in graft-versus-host disease (GVHD) is critical to effectively manage GVHD, yet their expression patterns among recipients remain largely unexplored. METHODS: Expression levels of SOCS1 and SOCS3 were determined by real-time quantitative reverse transcription PCR (qRT-PCR) in patients with acute GVHD (aGVHD) and chronic GVHD (cGVHD), in a severity-dependent manner, after allogeneic hematopoietic stem cell transplantation (HSCT). A total of 71 recipients with AML (N=40), ALL (N=12), myelodysplastic syndromes (MDS; N=10), chronic myelogenous leukemia (CML; N=2), severe aplastic anemia (SAA; N=5), or others (N=2), who received allogeneic HSCT from human leukocyte antigen-identical siblings or unrelated donors between 2009 and 2011, were included in the present study. RESULTS: Overall, the expression levels of SOCS1 decreased in recipients with grade II to IV aGVHD and cGVHD when compared to normal donors and non-GVHD recipients. Interestingly, the expressions of SOCS1 decreased significantly more in cGVHD than in aGVHD recipients (P=0.0091). In contrast, SOCS3 expressions were similarly reduced in all the recipients. CONCLUSION: This is the first study to show that SOCS1 and SOCS3 are differentially expressed in recipients following allogeneic HSCT, suggesting a prognostic correlation between SOCS genes and the development of GVHD. This result provides a new platform to study GVHD immunobiology and potential diagnostic and therapeutic targets for GVHD.
