B淋巴细胞是免疫系统的重要组成部分，发育过程中经历多个前体细胞阶段，成熟后进入淋巴结等外周淋巴器官，在接触外源性病原体后，在滤泡T辅助细胞的帮助下，逐步分化并在B淋巴滤泡内形成生发中心B细胞，并最终分化成能产生大量保护性抗体的浆细胞，来消灭病原菌。生发中心B细胞分化异常和许多人类疾病相关，其中包括自身免疫性疾病以及B细胞淋巴瘤。我们实验室深入研究：生发中心B细胞发育、分化以及恶变的转录和表观遗传学机制；B细胞淋巴瘤的免疫治疗。目前，我们的主要研究手段包括小鼠遗传学模型，经典免疫学，分子生物学和二代测序等。

1.  Zhang H, Dai D, Hu Q, Yang F, Xue Y, Li F, Shen N, Zhang M, Huang C(通讯作者）.Bach2 attenuates IL-2R signaling to control Treg homeostasis and Tfr development.Cell Reports,2021,35(6):109096.  [Link]

2.  Zhou XR, Li X, Liao LP, Han J, Huang J, Li JC, Tao HR, Fan SJ, Chen ZF, Li Q, Chen SJ, Ding H, Yang YX, Zhou B, Jiang HL, Chen KX, Zhang YY, Huang CX(共同通讯）, Luo C.P300/CBP inhibition sensitizes mantle cell lymphoma to PI3Kδ inhibitor idelalisib.Acta Pharmacol Sin . ,2021,s41401-021-00643-2.  [Link]

3.  Peng C, Hu Q, Yang F, Zhang H, Li F, Huang C (通讯).BCL6-Mediated Silencing of PD-1 Ligands in Germinal Center B Cells Maintains Follicular T Cell Population..J Immunol,2019,202(3):704-713.  [Link]

4.  Deng S,, Hu Q, Zhang H, Yang F, Peng C, Huang C (通讯).HDAC3 inhibition up-regulates PD-L1 expression in B-cell lymphomas and augments the efficacy of anti-PD-L1 therapy..Molecular Cancer Therapeutic ,2019,18(5):900-908.  [Link]

5.  Peng H, Yang F, Hu Q, Sun J, Peng C, Zhao Y, Huang C（通讯）.The ubiquitin-specific protease USP8 directly deubiquitinates SQSTM1/p62 to suppress its autophagic activity..Autophagy,2019,Jul 1:1-11.  [Link]

6.  Zhang H, Hu Q, Zhang M, Yang Fang, Peng C, Zhang Z, Huang C(通讯）.Bach2 deficiency leads to spontaneous expansion of IL-4-producing T follicular helper cells and autoimmunity.Frontier In Immunology,2019,.  [Link]

7.  Sun J, Hu Q, Peng H , Peng C, Zhou L, Lu J, Huang C (通讯作者）.ubiquitin-specific protease USP8 deubiquitinates and stabilizes Cx43. Journal of Biology Chemistry.Journal of Biology Chemistry,2018,293(21):8275-8284 .  [Link]

8.  Chen J, Jian X, Deng S, Ma Z, Shou X, Shen Y, Zhao Y, Huang C (共同通讯) & Shi Y.Identification of recurrent USP48 and BRAF mutations in Cushing’s disease.Nature Communication,2018,9(1):3171.  [Link]

9.  Yu X, Lao Y, Teng XL, Li S, Zhou Y, Wang F, Guo X, Deng S, Chang Y, Wu X, Liu Z, Chen L, Lu LM, Cheng J, Li B, Su B, Jiang J, Li HB, Huang C (共同通讯), Yi J, Zou Q.SENP3 maintains the stability and function of regulatory T cells via BACH2 deSUMOylation..Nature Communication,2018,9(1):3157.  [Link]

10.  Zhang Q, Peng C, Song J, Zhang Y, Chen J, Song Z, Shou X, Ma Z, Peng H, Jian X, He W, Ye Z, Li Z, Wang Y, Ye H, Zhang Z, Shen M, Tang F, Chen H, Shi Z, Chen C, Chen Z, Shen Y, Wang Y, Lu S, Zhang J, Li Y, Li S, Mao Y, Zhou L, Yan H, Shi Y, Huang C (共同通讯), Zhao Y.Germline Mutations in CDH23, Encoding Cadherin-Related 23, Are Associated with Both Familial and Sporadic Pituitary Adenomas.Am J Hum Genet,2017,100(5):817-823.  [Link]

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12.  Huang C (共同通讯), Melnick A#.Mechanisms of action of BCL6 during germinal center B cell development.Science China Life sciences,2015,58(12): 1226-1232.  [Link]

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14.  Huang C, Gonzalez DG, Cote CM, Jiang Y, Hatzi K, Teater M, Dai K, Hla T, Haberman AM, Melnick A.The BCL6 RD2 Domain Governs Commitment of Activated B Cells to Form Germinal Centers.Cell Reports,2014,8(5):1497-508.  [Link]

15.  Huang C, Hatzi K, Melnick AM.Lineage-specific functions of Bcl6 in immunity and inflammation are mediated through distinct biochemical mechanisms.Nature Immunology ,2013,14(4): 380-8.  [Link]

16.  Swaminathan S, Huang C, Geng H, Chen Z, Harvey R, Kang H, Carina Ng, Titz B, Hurtz C, Sadiyah F, Melnick AM, Müschen M.BACH2 mediates negative ion and p53-dependent tumor suppression at the pre-B cell receptor checkpoint.Nature Medicine ,2013,19(8):1014-22.  [Link]

17.  Cubedo E, Gentles AJ, Huang C, Natkunam, Y, Melnick A; Lossos IS.Identification of LMO2 transcriptome and interactome in diffuse large B-cell lymphoma.Blood,2012,119(23): 5478-5491.  [Link]

18.  Sun Z, Huang C, He J, Lamb, Kristy L Kang X Shen WH Yin, Y.PTEN C-terminal deletion causes genomic instability and tumor development.Cell Reports,2014,13;6(5):844-54.  [Link]

19.  Hatzi K, Jiang Y, Huang C, Garrett-Bakelman F, Gearhart MD, GElemento O, Melnick A.A hybrid mechanism of action for BCL6 in B cells defined by formation of functionally distinct complexes at enhancers and promoters.Cell Reports,2013,15;4(3):578-88.  [Link]