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on CD4+ T Cells Defines Terminally Differentiated B Cell-Helping Effector T Cells in a B Cell-Rich Lymphoid Tissue1Laboratory of Immunology and Hematopoiesis, Department of Comparative Pathobiology, Purdue Cancer Center, Bindley Bioscience Center, and Birck Nanotechnology Center, Purdue University, West Lafayette, IN 47907
IL-7 plays important roles in development and homeostatic proliferation of lymphocytes. IL-7 uses a receptor composed of IL-7R
(CD127) and the common 
-chain (CD132) to transmit its signal. It has been unknown how CD127 is regulated during Th cell differentiation to the B cell-helping T cell lineage. In this study, we report that loss of CD127 defines terminally differentiated B cell-helping effector T cells in human tonsils. Although naive CD4+ T cells uniformly express CD127, the memory/effector (non-FOXP3+) CD4+ T cells are divided into CD127+ and CD127– cells. The CD127– T cells are exclusively localized within the germinal centers where B cells become plasma and memory B cells, whereas CD127+ T cells are found in T cell areas and the area surrounding B cell follicles. Consistently, the CD127– T cells highly express the B cell zone homing receptor CXCR5 with concomitant loss of CCR7. Compared with CD127+ memory T cells, CD127– T cells have considerably shorter telomeres, do not proliferate in response to IL-7, and are prone to cell death. The CD127– T cells produce a large amount of the B cell follicle-forming chemokine CXCL13 upon stimulation with B cells and Ags. Most importantly, they are highly efficient in helping B cells produce Igs of all isotypes in a manner dependent on CD40L and ICOS and inducing activation-induced cytidine deaminase and Ig class switch recombination. The selective loss of CD127 on the B cell-helping effector T cells would have implications in regulation and termination of Ig responses.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This work was supported, in part, from grants from the American Heart Association, National Institutes of Health-National Institute of Allergy and Infectious Diseases (AI063064), and the Crohn’s and Colitis Foundation of America (to C.H.K.).
2 Address correspondence and reprint requests to Dr. Chang H. Kim, Department of Comparative Pathobiology, Purdue University, 725 Harrison Street, West Lafayette, IN 47907. E-mail address: chkim{at}purdue.edu
3 Abbreviations used in this paper: BCL, B cell leukemia/lymphoma; GC, germinal center; PB, peripheral blood; AID, activation-induced cytidine deaminase; SEB, staphylococcal enterotoxin B; 7-AAD, 7-aminoactinomycin D; MCL, myeloid cell leukemia.
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