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  • The American Association of Immunologists  (4)
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  • The American Association of Immunologists  (4)
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  • 1
    Online Resource
    Online Resource
    Real-time tracking ATAK cells in vivo (52.1)
    The American Association of Immunologists ; 2011
    In:  The Journal of Immunology Vol. 186, No. 1_Supplement ( 2011-04-01), p. 52.1-52.1
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 186, No. 1_Supplement ( 2011-04-01), p. 52.1-52.1
    Abstract: Background: Activated Targeted Killer (ATAK) cells are a cellular immunotherapy which protects neutropenic mice from invasive candidiasis and aspergillosis. However,the lifespan and distribution of ATAK cells into organs has not been determined in vivo. Methods: ATAK cells were stably transfected with a luminescence reporter system. Neutropenic mice were imaged by IVIS after administration of coelentrazine substrate. RT-PCR was used to confirm the luminescence results. Results: On day 1 after ATAK cell administration, livers, kidneys, and spleens were infiltrated by the ATAK cells. By day 3, cells had infiltrated more significantly into the spleen, and also spread into the lungs. By day 5, cell signal began to wane. By day 8, the day after neutrophil recovery, there was no detectable signal. By RT-PCR, viable cells were detected at 6 hours and 3 days after treatment. By day 5, no mRNA was detected. Mouse immunity to ATAK cells was detectable by ELISA and flow cytometry post-neutrophil recovery. Discussion: ATAK cells are viable and circulate widely into visceral organs in neutropenic mice, commensurate with their ability to protect mice from tissue invasive fungal infections. Hence the cells can provide protection during the critical neutropenic period yet the risk of engraftment is minimized by host-versus-graft affect after marrow recovery.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.186.Supp.52.1
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2011
    detail.hit.zdb_id: 1475085-5
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  • 2
    Online Resource
    Online Resource
    ATAK Cells Require Intact Cytochrome Oxidase Activity to Kill Fungi (38.18)
    The American Association of Immunologists ; 2010
    In:  The Journal of Immunology Vol. 184, No. 1_Supplement ( 2010-04-01), p. 38.18-38.18
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 184, No. 1_Supplement ( 2010-04-01), p. 38.18-38.18
    Abstract: Invasive fungal infections cause high mortality rates in neutropenic patients. We developing an immunotherapy based on activation of HL-60 cells into Activated Targeted Killer (ATAK) cells. We have shown that ATAK cells phagocytize and kill C. albicans in vitro, and protect neutropenic mice from invasive candidiasis and aspergillosis. However, the mechanism by which ATAK cells kill fungi were unclear. Because we have recently found that gp91phox deficient mice were hypersusceptible to invasive candidiasis, we used siRNA to suppress gp91-phox expression in ATAK cells to define impact of suppression of NADPH-superoxide formation on fungal killing. We use a lentivirus to stably transfect a gp91-phox-targeting siRNA construct into HL-60 cells. Stable transfectants had significantly suppressed mRNA level (by RT-PCR) and protein expression (by western blot) of gp91-phox. To confirm functional suppression, we compared the superoxide production in wild-type ATAK cells and gp91-phox-/- cells by DHR123 staining and flow cytometry. We found the gp91-phox -/-cells had markedly reduced superoxide generation. In in vitro killing assays, gp91-phox-/- ATAK cells had marked reductions in their killing of C. albicans relative to wild type cells. Finally, gp91-phox deficient ATAK cells were unable to protect neutropenic mice from invasive candidiasis or invasive aspergillosis. Thus, ATAK cell fungal killing and in vivo efficacy requires intact superoxide production by the NADPH-oxidase system.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.184.Supp.38.18
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2010
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
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    Online Resource
  • 3
    Online Resource
    Online Resource
    Passive immunization with CotH3 antibodies protects neutropenic mice from lethal mucormycosis through enhancing macrophage killing (MPF6P.660)
    The American Association of Immunologists ; 2015
    In:  The Journal of Immunology Vol. 194, No. 1_Supplement ( 2015-05-01), p. 202.18-202.18
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 194, No. 1_Supplement ( 2015-05-01), p. 202.18-202.18
    Abstract: Mucormycosis is a fatal fungal infection caused commonly by Rhizopus. We recently identified R. oryzae CotH3 as a surface protein which mediates invasion of host cells. CotH3 is present in other fungi that cause mucormycosis. Previously, we found polyclonal anti-CotH3 antibodies (CotH3-Abs) to block host cell invasion by R. oryzae and protect diabetic ketoacidotic mice from mucormycosis. Because neutropenic patients are also predisposed to mucormycosis, we used a cyclophosphamide/cortisone acetate injected mice to detect if CotH3-Abs protect against mucormycosis. Mice were infected intratracheally with R. oryzae, Mucor, Lichtheimia, Apophysomyces, Rhizomucor, or Cunninghamella prior to treating with CotH3-Abs (0.3mg, 0.1mg or 0.03mg) at different times post infection (4, 16, or 48h). All treatment doses showed enhanced survival of mice infected with R. oryzae vs. placebo-treated mice when used 16h post infection (p & lt;0.005). The 0.03mg dose given 16h post infection demonstrated better survival outcome vs. higher doses. Protection was time dependent with higher survival of mice receiving CotH3-Abs at earlier time points post infection. Further, CotH-Abs prolonged survival of mice infected with each of the other tested organisms. Finally, CotH3-Abs reduced tissue fungal burden in target organs and dramatically enhanced mouse macrophage killing via enhancing lysosomal synthesis. Our studies warrant further development of CotH3-Abs as a novel therapy for mucormycosis.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.194.Supp.202.18
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2015
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
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    Online Resource
  • 4
    Online Resource
    Online Resource
    Th17 Cells Are Not Required for Host Defense Against Murine Disseminated Candidiasis, But Are Required for Vaccine-Mediated Protection (132.10)
    The American Association of Immunologists ; 2009
    In:  The Journal of Immunology Vol. 182, No. 1_Supplement ( 2009-04-01), p. 132.10-132.10
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 182, No. 1_Supplement ( 2009-04-01), p. 132.10-132.10
    Abstract: Background: We are developing a vaccine based on the recombinant N-terminus of the candidal adhesin, Als3p (rAls3p-N), which results in significant protection against disseminated candidiasis. Vaccine protection requires upstream T lymphocytes and downstream functional phagocytes. We therefore sought to determine the role of Th17 cells in vaccine-mediated protection. Methods: We compared Th1 (CD4+IFN- ƒ×+), Th17 (CD4+IL-17+), and Th1/17 (CD4+IFN- ƒ×+IL-17+) cell frequencies in mice vaccinated with rAls3p-N + Al(OH)3 or Al(OH)3 adjuvant alone. We also compared vaccine efficacy in IL-17 deficient, CCR6 (cell surface marker of Th17 cells) deficient, or congenic wild type control mice infected via the tail-vein with C. albicans. Results: Vaccination increased Th1, Th17, and Th1/Th17 frequencies in mice. Splenocytes from vaccinated mice stimulated with rAls3p-N ex vivo produced significantly higher levels of IFN- ƒ×, IL-17, and KC than splenocytes from control mice. IL-17 and CCR6 deficient mice were not more susceptible to disseminated candidiasis than control mice. However, vaccine efficacy was abrogated in both IL-17 and CCR6 deficient mice. Conclusion: Th17 cells are not required for host defense against disseminated candidiasis in unvaccinated mice. However, the rAls3p-N vaccine stimulates Th17 and Th1/17 cells, and Th17 cells are required for vaccine efficacy in mice.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.182.Supp.132.10
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2009
    detail.hit.zdb_id: 1475085-5
    Location Call Number Limitation Availability
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    Online Resource
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