| Summary: | Xu Wang,1,2,* Shuai Lu,1,2,* Yankai Xiao,1,2 Ling Xu,2,3 Lingling Zhou,1,2 Junyan Hu,2 Bo Li,1,2 Chengwu Zeng,1,2 Yangqiu Li1–3 1Key Laboratory for Regenerative Medicine of Ministry of Education, Jinan University, Guangzhou, 510632, People’s Republic of China; 2Institute of Hematology, Jinan University, Guangzhou, 510632, People’s Republic of China; 3Department of Hematology, First Affiliated Hospital, Jinan University, Guangzhou, 510632, People’s Republic of China *These authors contributed equally to this work Background: T cell immunodeficiency is a common feature in patients with different kinds of hematological disease such as T cell non-Hodgkin lymphoma (T-NHL), B cells NHL (B-NHL), NK/T cell NHL (NK/T-CL) and acute myeloid leukemia (AML). In our recent research, we found that significantly lower expression levels in MALT1 and NF-κB were related to suppression of T cell activation. Therefore, this study was conducted to further investigate the role of downregulating MALT1 in the development of immunodeficiency in T cells.Methods: We induced activation inhibition in CD3+ T cells by MALT1 knockdown. Then we characterized the gene expression profile after MALT1 suppression by microarray analysis.Result: The differentially expressed genes were ZAP-70, p65, MDM2, ATM, NFATC2 which participate in the NF-κB, p53, and NFAT pathways in CD3+ T cells after MALT1 downregulation.Conclusion: MALT1 suppression may contribute to immunodeficiency in T cells via suppression of T cell activation and proliferation pathways. These data may help to explain some of the characteristics of immunodeficiency of T cells. Keywords: CD3+ T-cells, MALT1, immunodeficiency, T-cell activation, microarray
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