NK1.1⁺ CD4⁺ CD8‐ thymocytes with specific lymphokine secretion

Abstract

CD4+8- or CD4-8+ thymocytes have been regarded as direct progenitors of peripheral T cells. However, recently, we have found a novel NK1.1+ subpopulation with skewed T cell antigen receptor (TcR) V beta family among heat-stable antigen negative (HSA-) CD4+8- thymocytes. In the present study, we show that these NK1.1+ CD4+8- thymocytes, which represent a different lineage from the major NK1.1- CD4+8- thymocytes or CD4+ lymph node T cells, vigorously secrete interleukin (IL)-4 and interferon (IFN)-gamma upon stimulation with immobilized anti-TcR-alpha beta antibody. On the other hand, neither NK1.1- CD4+8- thymocytes nor CD4+ lymph node T cells produced substantial amounts of these lymphokines. A similar pattern of lymphokine secretion was observed with the NK1.1+ CD4+T cells obtained from bone marrow. The present findings elucidate the recent observations that HSA- CD4+8- thymocytes secrete a variety of lymphokines including IFN-gamma, IL-4, IL-5 and IL-10 before the CD4+8- thymocytes are exported from thymus. Our evidence indicates that NK1.1+ CD4+8- thymocytes are totally responsible for the specific lymphokine secretions observed in the HSA- CD4+8- thymocytes.

Retracted: α‐GalCer ameliorates listeriosis by accelerating infiltration of Gr‐1+ cells into the liver

“…Although lysosomal glycosphingolipid, isoglobotrihexosylceramide has been reported as a possible endogenous ligand for iNKT cells [28,33], a recent study argues against this possibility [34]. iNKT cells are abundant in the liver and rapidly secrete large amounts of immunoregulatory cytokines such as IFN-g and IL-4 after stimulation through their TCR [35][36][37][38][39][40]. Administration of a-GalCer to mice causes rapid release of various cytokines from iNKT cells, which participate in the regulation of various diseases, including tumor rejection and prevention of autoimmune diseases [41][42][43][44][45][46].…”

Effects of non-major histocompatibility antigens on acute graft-versus-host reaction after allogeneic bone marrow transplantation

“…8,9 It seemed that mismatch at the Mls-1 locus However, BMT mice prepared with a combination of both class I and non-MHC Ag mismatches showed signs between donors and recipients resulted in significant modification of acute GVHR. [10][11][12][13][14][15][16] We report different immunoof clinical GVHR and various cytokines were produced by the spleen cells at an early stage (4 days) after BMT.…”

“…Spleen and thymus cells were stained as (Kyowa Hakko Kogyo, Tokyo, Japan) were cocultured on described elsewhere. [10][11][12] Briefly, in the case of V␤6 staina 96-well flat-bottom culture plate (Falcon; Becton Dickining, cells were first reacted with anti-V␤6 moAb (44-22-son, NJ, USA) as described previously. 9 After 72 h of incu-1).…”

“…8,9 It seemed that mismatch at the Mls-1 locus However, BMT mice prepared with a combination of both class I and non-MHC Ag mismatches showed signs between donors and recipients resulted in significant modification of acute GVHR. [10][11][12][13][14][15][16] We report different immunoof clinical GVHR and various cytokines were produced by the spleen cells at an early stage (4 days) after BMT.logical characteristics seen among donor T cells from various BMT chimeras where MHC and/or minor Ag are Although no clinical GVHR was detected in BMT chimeras prepared with a non-MHC mismatched but MHC matched or mismatched. The Mls-1 disparity significantly modified T cell responses and augmented or altered the matched combination, large amounts of various cytokines were secreted by spleen cells.…”

IL‐18 time‐dependently modulates Th1/Th2 cytokine production by ligand‐activated NKT cells

“…NKT cells as well as CD4 + T cells are potent producers of both IFN-c and IL-4 by TCR/CD3 cross-linking [1,2]. NKT cells also produce these cytokines upon stimulation by the synthetic ligand a-galactosylceramide (a-GalCer) [3].…”