GLORIA

GEOMAR Library Ocean Research Information Access

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • The American Association of Immunologists  (3)
  • 2010-2014  (3)
Material
Publisher
  • The American Association of Immunologists  (3)
Language
Years
  • 2010-2014  (3)
Year
Subjects(RVK)
  • 1
    Online Resource
    Online Resource
    The American Association of Immunologists ; 2013
    In:  The Journal of Immunology Vol. 190, No. 1_Supplement ( 2013-05-01), p. 132.39-132.39
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 190, No. 1_Supplement ( 2013-05-01), p. 132.39-132.39
    Abstract: Human invariant NKT cells (iNKT cells) are a novel lymphocyte population characterized by an invariant T-cell receptor (Vα24/Vβ11). iNKT cells activated with αGalCer and IL-2 have been shown to produce large amounts of cytokines such as IFN-γ and also have potent killing activity against various tumor cell lines. One major hurdle to studying the anti-tumor activity of iNKT cells is they don’t recognize antigens presented by classical MHC molecules and their tumor antigen specificity is unknown. Therefore, we expressed the MHC class I restricted TIL 1383I TCR into iNKT cells to better study their biology and anti-tumor activity. The 1383I TCR is a high affinity TCR that recognizes the melanoma antigen tyrosinase presented by HLA-A2. In this study, we report the production and function of the TIL 1383I TCR transduced human iNKT cells. iNKT cells were activated and expanded from normal PBMCs by stimulating them with αGalCer in the presence of IL-2 and IL-15. The iNKT cells were isolated using iNKT magnetic beads and transduced using retroviral vectors encoding the TIL 1383I TCR. The TIL 1383I TCR transduced iNKT expression was measured by flow cytometry (FACS) and their anti-tumor activity by intracellular cytokine staining. The TIL 1383I TCR transduced iNKT cells specifically produced IFN-γ in response to tyrosinase peptide loaded T2 cells and HLA-A2+/tyrosinase+ human melanomas. These results indicate that iNKT cells can be engineered to recognize normal tumor antigens.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2013
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 184, No. 1 ( 2010-01-01), p. 127-133
    Abstract: Although B and T lymphocyte attenuator (BTLA) was originally identified as an inhibitory coreceptor selectively expressed on Th1 cells and B cells, recent studies have revealed that BTLA is expressed on a variety of cells, including macrophages, dendritic cells, and NK cells, and modulates their functions. However, the role of BTLA in the regulation of NKT cell function remains unknown. In this study, we found that BTLA was expressed on NKT cells at the levels similar to those on T cells and that BTLA-deficient (BTLA−/−) NKT cells produced larger amounts of IL-4 and IFN-γ upon α-glactosylceramide stimulation as compared with wild-type (WT) NKT cells. In vivo, BTLA−/− mice produced larger amounts of IL-4 and IFN-γ upon Con A injection and were more susceptible to Con A-induced hepatitis than WT mice. In addition, the augmentation of Con A-induced hepatitis in BTLA−/− mice was not observed in BTLA/NKT-double deficient mice. Moreover, NKT−/− mice reconstituted with BTLA−/− NKT cells were significantly more susceptible to Con A-induced hepatitis as compared with NKT −/− mice reconstituted with WT NKT cells. These results suggest that BTLA functions as the inhibitory coreceptor of NKT cells and plays a critical role in the prevention of NKT cell-mediated liver injury.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2010
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 188, No. 9 ( 2012-05-01), p. 4654-4662
    Abstract: The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that mediates a variety of biological effects by binding to environmental pollutants, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or dioxin). Although numerous animal studies have demonstrated the harmful effects of dioxins, it remains controversial whether dioxins pose a risk to human health. Enhanced lytic replication of EBV is a risk factor for the development of autoimmune diseases and cancers. This study evaluated the possibility that ligand-activated AhR reactivates EBV. EBV reactivation and AhR transactivation were evaluated with luciferase assays. Saliva samples were collected from 19 patients with primary Sjögren’s syndrome (SS). Control saliva samples were obtained from 10 healthy individuals and nine patients with severe dry mouth. TCDD enhanced BZLF1 transcription, which mediates the switch from the latent to the lytic form of EBV infection in EBV-positive B cell lines and in a salivary gland epithelial cell line. Moreover, TCDD-induced increases in BZLF1 mRNA and EBV genomic DNA levels were confirmed in the B cell lines. Saliva from SS patients activated the transcription of both CYP1A1 and BZLF1. Additionally, there was a positive correlation between CYP1A1 and BZLF1 promoter activities. AhR ligands elicited the reactivation of EBV in activated B cells and salivary epithelial cells, and these ligands are involved in SS. Our findings reveal novel aspects of the biological effects of dioxin and the AhR-dependent pathogenesis of autoimmune diseases.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    RVK:
    RVK:
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2012
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...