Host Resistance to<i>Listeria monocytogenes</i>Infection Is Enhanced but Resistance to<i>Staphylococcus aureus</i>Infection Is Reduced in Acute Graft-versus-Host Disease in Mice

Miura, Tomisato; Mizuki, Daisuke; Sasaki, Sanae; Hasegawa, Suguru; Sashinami, Hiroshi; Nakane, Akio

doi:10.1128/iai.68.7.4340-4343.2000

Cited by 8 publications

(6 citation statements)

References 39 publications

(21 reference statements)

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“…This is consistent with observations made in other models in which Listeria-associated apoptosis has been observed in hepatocytes but not in macrophages (including Kupffer cells) and in neutrophil-depleted mouse models, in which apoptosis was detectable in hepatocytes (2,35). In our hands, apoptosis of hepatocytes from lethally infected wild-type animals was more frequent than in studies by Miura et al (28). These differences may reflect the different mouse strains studied.…”

Section: Discussioncontrasting

confidence: 63%

Listeria monocytogenesInfection in Caspase-11-Deficient Mice

2002

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Caspase-11 (Cas11) is a cysteine protease involved in programmed cell death and cytokine maturation. Through activation of Cas1 (interleukin-1beta [IL-1beta]-converting enzyme), Cas11 is directly involved in the maturation of IL-1beta and IL-18. Apoptosis is mediated through Cas3. Given the role of apoptosis and cytokine signaling during the innate immune response in intracellular infection, we examined Cas11-deficient (Cas11(-/-)) mice during infection with Listeria monocytogenes. Cas11(-/-) and wild-type C57BL/6 mice were equally susceptible to intravenous infection with L. monocytogenes, resulting in similar bacterial burdens in tissue and similar survival rates. By contrast, enhanced susceptibility was observed in control mice on a mixed genetic 129/C57BL/DBA2 background. Cas11(-/-) and wild-type mice infected with Listeria had similar hepatic microabscess formation in terms of histologic appearance, size, and number. Apoptosis of L. monocytogenes-infected hepatocytes in vivo and in vitro in primary culture was not altered by the absence of Cas11. Serum IL-18 and IL-1beta levels were similar in Cas11(-/-) mice and controls. Endotoxin (lipopolysaccharide [LPS])-challenged Cas11(-/-) mice were deficient in the production of gamma interferon. IL-1beta responses in Cas11(-/-) were normal with intravenous administration of LPS but decreased with intraperitoneal administration. Our findings suggest that Cas11 deficiency does not impair the immune response to infection with L. monocytogenes. Apoptosis and maturation of IL-18 and IL-1beta were normal despite Cas11 deficiency. LPS-induced proinflammatory pathways are altered by the absence of Cas11. While Cas11-mediated Cas1 and Cas3 activation is crucial for cytokine maturation and apoptosis during inflammation, alternative pathways allow normal inflammatory and apoptotic responses during infection with L. monocytogenes.

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Section: Discussioncontrasting

confidence: 63%

Listeria monocytogenesInfection in Caspase-11-Deficient Mice

2002

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“…It has been described in the literature that the 4T1 cell line elaborates a variety of immune suppressive molecules similar to the clinical situation, including PGE-2 [Mitsuhashi et al, 2004], TGF-b [Muraoka et al, 2002;Kobie et al, 2003], and other factors [Danna et al, 2004]. Additionally, it is known that the BALB/c strain possesses a Th2 propensity as noted by susceptibility to Listeria [Miura et al, 2000] and prolonged allograft survival [Wang et al, 2003] in contrast to other strains, due in part to upregulated production of the Th1 inhibiting enzyme arginase [Mills et al, 2000]. Due to the central role of BORIS in maintaining the oncogenic phenotype [Loukinov et al, 2002;Hong et al, 2005;Vatolin et al, 2005], we sought to determine the feasibility of inducing a relevant anti-4T1 response to this transcription factor by immunization.…”

Section: Resultsmentioning

confidence: 97%

Antitumor efficacy of DNA vaccination to the epigenetically acting tumor promoting transcription factor BORIS and CD80 molecular adjuvant

Loukinov

Ghochikyan

Mkrtichyan

et al. 2006

J of Cellular Biochemistry

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Cancer testis (CT) antigens are promising candidates for tumor vaccines due to their immunogenicity and tissue-restricted expression. Recently, we identified a novel cancer testis gene, BORIS, whose expression is restricted to male testis after puberty and is strictly absent in non-malignant female tissue. BORIS encodes a DNA-binding protein that shares 11 zing finger (ZF) with transcription factor CTCF and differs at the N- and C-termini. CTCF has been implicated in epigenetic regulation of imprinting, X chromosome inactivation, repression, and activation of cancer testis antigens. BORIS expression has been documented in cancers of diverse histological origin, including, but not limited to breast, prostate, ovary, gastric, liver, endometrial, glia, colon, and esophagus. Interestingly, BORIS induces demethylation and subsequent expression of many cancer-testis genes, including MAGE-A1 and NY-ESO-1, indicating that it is expressed very early in malignancy and might be an attractive candidate for immunotherapy. In this study we tested BORIS as a vaccine in a very aggressive, highly metastatic, and poorly immunogenic murine model of mammary carcinoma. Immunizations with a DNA encoding the mutant form of murine BORIS antigen (pmBORIS lacking DNA-binding function) significantly prolonged survival, and inhibited tumor growth in BALB/c mice inoculated with 4T1 cells. Priming with pmBORIS mixed with molecular adjuvant and boosting with adenoviral vector expressing mBORIS was generally more effective, suggesting that the vaccination protocol could be further optimized. This is the first report demonstrating the feasibility of vaccination with a cancer associated epigenetic regulator for the induction of tumor inhibition.

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“…3 d after infection, animals that had received the PIP antibody had either higher (P = 0.0005 for liver and P = 0.1816 for spleen) or lower L. monocytogenes organ bur dens (P = 0.0227 for liver and P = 0.0059 for spleen; Fig. S3, n-p), as has been described previously (Miura et al, 2000). In contrast, antiBTLA-treated mice controlled infection similarly to both control groups, indicating an intact innate immune response (Fig.…”

mentioning

confidence: 60%

Defining the Role of BTLA in Breast Cancer Immunosurveillance and Selective Targeting of the BTLA-HVEM-LIGHT Costimulatory System

Gillanders¹,

Murphy²

2011

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATE May 2011 REPORT TYPE Annual DATES COVERED PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBERWashington University St. Louis, MO 63130 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTES ABSTRACTNone provided. SUBJECT TERMSNone provided. this balance, and recent work has uncovered critical roles for CTLA4 and PD-1 in restraining immune responses in chronic viral infection and malignancy. We recently cloned B-and T-lymphocyte attenuator (BTLA), the third inhibitory receptor of the CD28 family expressed on lymphocytes. Using BTLA-deficient mice and monoclonal antibodies specific for BTLA that we generated, we have studied several in vivo models of infection and autoimmunity, showing the importance of BTLA in regulating immune responses. Several lines of evidence suggest that inhibitory molecules such as CTLA-4 and PD-1 limit cancer immunosurveillance. OBJECTIVE/HYPOTHESIS:The hypothesis of this application is that BTLA contributes to the inhibition of breast cancer immunosurveillance, and selective targeting of the BTLA-LIGHT-HVEM costimulatory system can enhance breast cancer immunity. SPECIFIC AIMS:(1) Define the role of BTLA in breast cancer immunosurveillance.(2) Determine if inhibitory molecules of the CD28 receptor family function as redundant immunologic checkpoints in breast cancer immunosurveillance.(3) Develop novel therapeutics to successfully dissociate T cell costimulation and inhibition in the BTLA-LIGHT-HVEM costimulatory system. PROGRESS:The award was in the format of a Synergistic Idea Award to William E. Gillanders, M.D., a breast cancer surgeon, and Kenneth Murphy, M.D., Ph.D., a basic immunologist. The current reporting period represents the second year of a two year award. Of note, Dr. Gillanders has requested a no-cost extension to continue the studies proposed.The research proposed in Sp...

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Host Resistance toListeria monocytogenesInfection Is Enhanced but Resistance toStaphylococcus aureusInfection Is Reduced in Acute Graft-versus-Host Disease in Mice

Cited by 8 publications

References 39 publications

Listeria monocytogenesInfection in Caspase-11-Deficient Mice

Listeria monocytogenesInfection in Caspase-11-Deficient Mice

Antitumor efficacy of DNA vaccination to the epigenetically acting tumor promoting transcription factor BORIS and CD80 molecular adjuvant

Defining the Role of BTLA in Breast Cancer Immunosurveillance and Selective Targeting of the BTLA-HVEM-LIGHT Costimulatory System

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