Natural killer T cells are required for the development of a superantigen-driven T helper type 2 immune response in mice (original) (raw)
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Infection and Immunity, 2006
NKT cells are a heterogeneous population characterized by the ability to rapidly produce cytokines, such as interleukin 2 (IL-2), IL-4, and gamma interferon (IFN-␥) in response to infections by viruses, bacteria, and parasites. The bacterial superantigen staphylococcal enterotoxin B (SEB) interacts with T cells bearing the V3, -7, or -8 T-cell receptors, inducing their expansion and cytokine secretion, leading to death in some cases due to cytokine poisoning. The majority of NKT cells bear the V7 or -8 T-cell receptor, suggesting that they may play a role in regulating this response. Using mice lacking NKT cells (CD1d ؊/؊ and J␣18 ؊/؊ mice), we set out to identify the role of these cells in T-cell expansion, cytokine secretion, and toxicity induced by exposure to SEB. We find that V8 ؉ CD4 ؉ T
1998
Updated information and services can be found at: These include: REFERENCES http://iai.asm.org/content/66/11/5082#ref-list-1 at: This article cites 41 articles, 19 of which can be accessed free CONTENT ALERTS more» articles cite this article), Receive: RSS Feeds, eTOCs, free email alerts (when new http://journals.asm.org/site/misc/reprints.xhtml Information about commercial reprint orders: http://journals.asm.org/site/subscriptions/ To subscribe to to another ASM Journal go to: on October 16, 2014 by guest http://iai.asm.org/ Downloaded from on October 16, 2014 by guest http://iai.asm.org/ Downloaded from INFECTION AND IMMUNITY, 0019-9567/98/$04.00ϩ0
Cellular Immunology, 1989
The induction of enhanced natural cytotoxicity from human peripheral mononuclear cells by staphylococcal enterotoxin B (SEB) was examined. The activated killer cytotoxicity (AKC) was maximum at 16 hr with 1 m&ml SEB. The precursor and effector cells of AKC were determined to be primarily CD5 negative, CD8 negative, CD 16 positive cells. Monocytes and interleukin-1 played no role' in the generation of AKC. However, a major role for interleukin-2 (IL-2) in AKC was shown by the inhibition of AKC when anti-IL-2 antibody or cyclosporin was added to the induction cultures. SEB rapidly induced the production of IL-2 from glass nonadherent cells by 6 hr and reached peak levels by 24 hr ( 162 U/ml). IL-2 induced by SEB in these induction cultures was preferentially produced by CD16 positive cells. Even though interferony (IFN-7) production was induced in these cultures, no role for IFN could be shown in SEE induced AKC. 8 1989 Academic ~m.s, hc.
Infection and Immunity, 2009
http://iai.asm.org/content/77/2/707 Updated information and services can be found at: These include: REFERENCES http://iai.asm.org/content/77/2/707#ref-list-1 at: This article cites 52 articles, 14 of which can be accessed free CONTENT ALERTS more» articles cite this article), Receive: RSS Feeds, eTOCs, free email alerts (when new http://journals.asm.org/site/misc/reprints.xhtml Information about commercial reprint orders: http://journals.asm.org/site/subscriptions/ To subscribe to to another ASM Journal go to:
European Journal of Immunology, 1999
Radiation chimeras, generated by transplantation of SCID bone marrow into C3H/HeJ mice, show lethal susceptibility to staphylococcal enterotoxin B (SEB), thus constituting a valid murine model for SEB shock. This SEB sensitivity is due to the ability of the irradiated host to restore residual T cell populations, since the SCID donor bone marrow is unable to generate T cells. SCID bone marrow transplanted into irradiated nude mice does not generate SEB-sensitive chimeras, as a consequence of the inability of the recipient nude mice to develop mature T cells. Thymectomy of normal recipient mice prior to bone marrow transplantation does not affect the development of susceptibility to SEB, suggesting that postthymic, residual T cells of the host probably mediate this SEB sensitivity. In vivo depletion experiments show that CD4 + T cells are required for the SEB-triggered shock, while CD8 + cells suppress it. A further examination of the T helper subpopulations in the SEB-sensitive mice reveals a prevalence of CD4 + CD45RB dim cells over CD4 + CD45RB bright cells. This T helper balance was statistically significant when correlated with SEB-induced mortality. Our model provides a possible explanation for the SEB resistance of normal mice: they have a prevalence of CD4 + CD45RB dim over CD4 + CD45RB bright cells.
Frontiers in immunology, 2018
Toxic shock syndrome (TSS) is capable of inducing life-threatening fever, rash, and systemic organ failure, though the specific mechanisms behind these symptoms remain poorly understood. Staphylococcal enterotoxin B (SEB) and other superantigens have shown to be important factors in TSS, capable of promoting cross-linking between T cell receptors and major histocompatibility complexes which results in overwhelming T cell activation, proliferation, and cytokine production. The resulting proinflammatory cytokine cascade, often referred to as the "cytokine storm," seems to be critical to the development of disease. Interestingly, clinical studies have shown that children exhibit less severe TSS-associated morbidity than adults, though the mechanism behind this phenomenon has not been addressed. Indeed, despite the fact that most novel antigen exposure occurs early in life, be it from environmentally acquired pathogens or routine vaccination, normal pediatric T cell immune fun...
European Journal of Immunology, 1998
Upon primary activation, T helper (Th) cell populations express different cytokines transiently and with different kinetics. Stimulation of naive murine splenic Th cells with the bacterial superantigen Staphylococcus aureus enterotoxin B (SEB) in vitro results in expression of IL-2, IFN-+ and IL-10 with fast, intermediate and slow kinetics, respectively. This first report of a functional analysis of cells separated alive according to cytokine expression shows that these cytokines are not produced by different Th cell subpopulations, but can be expressed sequentially by individual Th cells. Th cells, activated with SEB for 1 day and isolated according to expression of IL-2, using the cellular affinity matrix technology, upon continued stimulation with SEB later secrete most of the IFN-+ and IL-10. Likewise, after 2 days of SEB culture, cells expressing IFN-+ , separated according to specific surface-associated IFN-+ as detected by magnetofluorescent liposomes, 1 day later secrete IL-10. Thus, individual Th1 cells can contribute to the control of their own IFN-+ expression by sequential expression of first IL-2, supporting their proliferation, and later IL-10, down-regulating the production of IFN-+ -inducing monokines and limiting the pro-inflammatory effects of IFN-+ .
Proceedings of the National Academy of Sciences, 1992
The role of the CD4 molecule in activation of T-helper cells was examined by investigating the effect of an anti-CD4 monoclonal antibody (Leu3a) in conventional peptide antigen-specific cloned T-helper cells that are also reactive to staphylococcal enterotoxin B (SEB). These T-helper cell clones are CD4+/CD45RO+/T-cell antigen receptor «-chain variable region 12-positive and can respond to nominal peptide antigens and SEB by proliferation in the presence of class II major histocompatibility complex-expressing accessory cells. Al-
International Immunology, 1997
The mechanisms involved in the maintenance of staphylococcal enterotoxin B (SEB)-induced T cell anergy are poorly understood. Here, we demonstrate that CD4 ⍣ T cell anergy induced by SEB treatment is under partial B cell control. This effect is not mediated by anti-SEB antibodies or any in vitro B cell-produced suppresser factor. At day 13 after SEB immunization, T cells from B cell-deficient mice proliferate upon in vitro stimulation with SEB. These results suggest that SEB-induced T cell anergy is reversible and that B cells have an important function in anergy maintenance in CD4 ⍣ T cells, both in vivo and in vitro.