Immune response of cdT cells in Schistosome japonicum–infected C57BL/6 mouse liver H. XIE, 1,† D. CHEN, 2,† L. LI, 3,† X. YU, 3 C. WU, 4,5 H. GU, 6 X. TANG, 7 A. PENG 8 & J. HUANG 3 1 Functional Experiment Centre, Guangzhou Medical University, Guangzhou, China, 2 Department of Laboratory Medicine, Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China, 3 Department of Pathogenic Biology and Immunology, institute of immunology, Guangzhou Medical University, Guangzhou, China, 4 Institute of Immunology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China, 5 Key Laboratoryof Tropical Disease Control Research of Ministry of Education, Sun Yat-sen University, Guangzhou, China, 6 Department of Pharmacology, Vanderbilt University, Nashville, TN, USA, 7 Department of Infectious Diseases, Affiliated No.8 Guangzhou Peoples Hospital, Guangzhou Medical University, Guangzhou, China, 8 Clinical laboratory, Traditional Chinese Medicine Hospital of Guangdong province, Guangzhou, China SUMMARY Systematic evaluation of the role of cdT cells during the Schistosoma japonicum infection has not been reported, despite the fact that cdT cells contribute to many infectious diseases in innate immunity. Therefore, the aim of this study was to observe the properties of cdT cells in the liver of C57BL/6 mice infected by S. japonicum. In this report, using immuno-fluorescent histological analysis, cdT cells were found around hepatic granulomatous. Moreover, the flow cytometry results revealed that the percentage of hepa- tic cdT cells increased significantly after S. japonicum infec- tion. More interestingly, a subset of CD3 À cdTCR + cells were found and markedly increased after infection. Further- more, expression of activation markers (CD25 and CD69) and cytokine profiles were detected in these hepatic CD3 + cdTCR + and CD3 À cdTCR + cells. The significantly higher level of CD69, IL-4 and IL-17 were observed in CD3 + cdTCR + cells after infection, suggesting that CD3 + cdTCR + cells instead of CD3 À cdTCR + cells might play a predominant role during the infection. Finally, our results indicated that the expression of NKG2D on CD3 + cdTCR + cells was higher than that on CD3 À cdTCR + cells. Collectively, cdT cells could play an important role in the liver of C57BL/6 mouse during japonicum infection. Keywords cytokines , NKG2D, Schistosoma japonicum, cdT cell INTRODUCTION Schistosomiasis is a chronic parasitic disease caused by extracellular parasite Schistosoma, such as Schistosoma japonicum, and widespread in vertebrates including humans (1). A key feature of the immune response in S. japonicum-infected mice is triggered by parasite eggs that are gradually deposited in host tissues, particularly in the liver (2, 3). Infection of S. japonicum, a multicellular parasite which has an extremely diverse repertoire of anti- gens, induces the production of bulk cytokines to induce immune cells that play important roles in the immune response to infection (1). The main adaptive immune response against schistosomes is mediated by MHC class II-restricted CD4 + T cells (4). Moreover, cdT cells, CD1- restricted NKT cells and CD8 + T-cell responses are also induced, although their effects are less clear (5). T cells are subdivided into two large populations distin- guished by their surface expression of ab and cd T-cell receptors (TCR) (6). T cells undergo extensive DNA rear- rangements at the a, b, c and d TCR loci aiming to express functional TCR chains and make a selection between two developmental programs during the DN3 stage. Thus, two distinct characteristics and functions of T-cell subsets are generated (7, 8). Cells with the ab TCR generally express CD4 or CD8 lineage markers and mostly fall into helper or effector/cytotoxic subsets. Whereas cd cells in humans usually do not express these lineage mark- ers. They usually do not require conventional antigen pre- sentation in the context of MHC (8). In fact, the ab and cdT-cell populations recognize different types of antigens. Correspondence: Jun Huang, Department of Pathogenic Biology and Immunology, Guangzhou Medical College, 510182 Guangz- hou, China (e-mail: hj165@sina.com) and Anping Peng, Clinical laboratory, Traditional Chinese Medicine Hospital of Guangdong province, 510120 Guangzhou, China (e-mail: penganping @21cn.com). † These authors share equal first authorship. Received: 8 April 2014 Accepted for publication: 29 July 2014 © 2014 John Wiley & Sons Ltd 658 Parasite Immunology, 2014, 36, 658–667 DOI: 10.1111/pim.12135