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  1. Article ; Online: Pathologists' perspective on the study design, analysis, and interpretation of proliferative lesions in a lifetime rodent carcinogenicity bioassay of sucralose.

    Elmore, Susan A / Rehg, Jerold E / Schoeb, Trenton R / Everitt, Jeffrey I / Bolon, Brad

    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

    2024  Volume 188, Page(s) 114524

    Abstract: Sucralose, a sugar substitute first approved for use in 1991, is a non-caloric sweetener regulated globally as a food additive. Based on numerous experimental animal studies (dating to the 1980s) and human epidemiology studies, international health ... ...

    Abstract Sucralose, a sugar substitute first approved for use in 1991, is a non-caloric sweetener regulated globally as a food additive. Based on numerous experimental animal studies (dating to the 1980s) and human epidemiology studies, international health agencies have determined that sucralose is safe when consumed as intended. A single lifetime rodent carcinogenicity bioassay conducted by the Ramazzini Institute (RI) reported that mice fed diets containing sucralose develop hematopoietic neoplasia, but controversy continues regarding the validity and relevance of these data for predicting health effects in humans. The present paper addresses the controversy by providing the perspective of experienced pathologists on sucralose-related animal toxicity and carcinogenicity data generally, and the RI carcinogenicity bioassay findings specifically, using results from publicly available papers and international regulatory authority decisions. In the authors' view, flaws in the design, methodology, data evaluation, and reporting of the RI carcinogenicity bioassay for sucralose diminish the value of the data as evidence that this agent represents a carcinogenic hazard to humans. This limitation will remain until the RI bioassay is repeated under Good Laboratory Practices and the design, data, and accuracy of the pathology diagnoses and interpretations are reviewed by qualified pathologists with experience in evaluating potential chemically-induced carcinogenic hazards.
    Language English
    Publishing date 2024-02-28
    Publishing country England
    Document type Journal Article
    ZDB-ID 782617-5
    ISSN 1873-6351 ; 0278-6915
    ISSN (online) 1873-6351
    ISSN 0278-6915
    DOI 10.1016/j.fct.2024.114524
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  2. Article ; Online: Pathologists' perspective on the study design, analysis, and interpretation of proliferative lesions in lifetime and prenatal rodent carcinogenicity bioassays of aspartame

    Elmore, Susan A. / Rehg, Jerold E. / Schoeb, Trenton R. / Everitt, Jeffrey I. / Bolon, Brad

    Food and Chemical Toxicology. 2023 Jan., v. 171 p.113504-

    2023  

    Abstract: Aspartame, an artificial sweetener commonly used as a sugar substitute, is currently authorized for use in more than 100 countries. Hundreds of studies, conducted in various countries dating back to the 1970s, have shown that aspartame is safe at real- ... ...

    Abstract Aspartame, an artificial sweetener commonly used as a sugar substitute, is currently authorized for use in more than 100 countries. Hundreds of studies, conducted in various countries dating back to the 1970s, have shown that aspartame is safe at real-world exposure levels. Furthermore, multiple human epidemiology studies have provided no indication that consumption of aspartame induces cancer. Given the continued controversy surrounding the Ramazzini Institute's (RI) studies suggesting that aspartame is a carcinogenic hazard in rodents and evaluation by the International Agency for Research on Cancer, this report aims to provide the perspective of experienced pathologists on publicly available pathology data regarding purported proliferative lesions in liver, lung, lymphoid organs, and mammary gland as well as their implications for human risk assessment as reported for three lifetime rodent carcinogenicity bioassays of aspartame conducted at the RI. In the authors' view, flaws in the design, methodology and reporting of the RI aspartame studies limit the utility of the data sets as evidence that this agent represents a carcinogenic hazard. Therefore, all three RI studies, and particularly the accuracy of their pathology diagnoses and interpretations, should be rigorously reviewed by qualified and experienced veterinary toxicologic pathologists in assessing aspartame's carcinogenic risk.
    Keywords aspartame ; carcinogenicity ; epidemiology ; experimental design ; humans ; liver ; lungs ; mammary glands ; risk ; risk assessment ; rodents ; sugars ; toxicology ; Carcinogenicity risk assessment ; Hazard identification ; Hematolymphoid tumors ; Mycoplasma pulmonis ; Ramazzini Institute
    Language English
    Dates of publication 2023-01
    Publishing place Elsevier Ltd
    Document type Article ; Online
    Note Use and reproduction
    ZDB-ID 782617-5
    ISSN 1873-6351 ; 0278-6915
    ISSN (online) 1873-6351
    ISSN 0278-6915
    DOI 10.1016/j.fct.2022.113504
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  3. Article ; Online: Is statistical re-evaluation of hemolymphoreticular neoplasms from aspartame studies valid?

    Elmore, Susan A / Rehg, Jerold E / Schoeb, Trenton R / Everitt, Jeffrey I / Bolon, Brad

    Toxicological sciences : an official journal of the Society of Toxicology

    2023  Volume 195, Issue 2, Page(s) 143–144

    Language English
    Publishing date 2023-09-21
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1420885-4
    ISSN 1096-0929 ; 1096-6080
    ISSN (online) 1096-0929
    ISSN 1096-6080
    DOI 10.1093/toxsci/kfad070
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    Zs.A 1709: Show issues Location:
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  4. Article ; Online: Pathologists' perspective on the study design, analysis, and interpretation of proliferative lesions in lifetime and prenatal rodent carcinogenicity bioassays of aspartame.

    Elmore, Susan A / Rehg, Jerold E / Schoeb, Trenton R / Everitt, Jeffrey I / Bolon, Brad

    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

    2022  Volume 171, Page(s) 113504

    Abstract: Aspartame, an artificial sweetener commonly used as a sugar substitute, is currently authorized for use in more than 100 countries. Hundreds of studies, conducted in various countries dating back to the 1970s, have shown that aspartame is safe at real- ... ...

    Abstract Aspartame, an artificial sweetener commonly used as a sugar substitute, is currently authorized for use in more than 100 countries. Hundreds of studies, conducted in various countries dating back to the 1970s, have shown that aspartame is safe at real-world exposure levels. Furthermore, multiple human epidemiology studies have provided no indication that consumption of aspartame induces cancer. Given the continued controversy surrounding the Ramazzini Institute's (RI) studies suggesting that aspartame is a carcinogenic hazard in rodents and evaluation by the International Agency for Research on Cancer, this report aims to provide the perspective of experienced pathologists on publicly available pathology data regarding purported proliferative lesions in liver, lung, lymphoid organs, and mammary gland as well as their implications for human risk assessment as reported for three lifetime rodent carcinogenicity bioassays of aspartame conducted at the RI. In the authors' view, flaws in the design, methodology and reporting of the RI aspartame studies limit the utility of the data sets as evidence that this agent represents a carcinogenic hazard. Therefore, all three RI studies, and particularly the accuracy of their pathology diagnoses and interpretations, should be rigorously reviewed by qualified and experienced veterinary toxicologic pathologists in assessing aspartame's carcinogenic risk.
    Language English
    Publishing date 2022-11-19
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 782617-5
    ISSN 1873-6351 ; 0278-6915
    ISSN (online) 1873-6351
    ISSN 0278-6915
    DOI 10.1016/j.fct.2022.113504
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 529: Show issues Location:
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  5. Book: Murine respiratory mycoplasmosis

    Davis, Jerry K. / Davidson, Maureen / Schoeb, Trenton R.

    a model to study effects of oxidants

    (Research report / Health Effects Institute ; 47)

    1991  

    Author's details [Jerry K. Davis ; Maureen Davidson and Trenton R. Schoeb]
    Series title Research report / Health Effects Institute ; 47
    Collection
    Keywords Nitrogen Dioxide / adverse effects ; Air Pollutants / adverse effects ; Respiratory Tract Infections / immunology ; Mycoplasma Infections / immunology ; Mycoplasma / immunology ; Mice, Inbred C57BL
    Language English
    Size I, 43 S. : graph. Darst.
    Publisher Health Effects Inst
    Publishing place Cambridge, Mass
    Publishing country United States
    Document type Book
    Remark Kopie erschienen im Verl. NTIS, Springfield, Va., 1992
    HBZ-ID HT007602622
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    1997 A 5878 order for loan Magazin

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  6. Article ; Online: Cutting Edge: ICOS-Deficient Regulatory T Cells Display Normal Induction of

    Landuyt, Ashley E / Klocke, Barbara J / Colvin, Tyler B / Schoeb, Trenton R / Maynard, Craig L

    Journal of immunology (Baltimore, Md. : 1950)

    2019  Volume 202, Issue 4, Page(s) 1039–1044

    Abstract: The ICOS pathway has been implicated in the development and functions of regulatory T (Treg) cells, including those producing IL-10. Treg cell-derived IL-10 is indispensable for the establishment and maintenance of intestinal immune homeostasis. We ... ...

    Abstract The ICOS pathway has been implicated in the development and functions of regulatory T (Treg) cells, including those producing IL-10. Treg cell-derived IL-10 is indispensable for the establishment and maintenance of intestinal immune homeostasis. We examined the possible involvement of the ICOS pathway in the accumulation of murine colonic Foxp3- and/or IL-10-expressing cells. We show that ICOS deficiency does not impair induction of IL-10 by intestinal CD4 T cells but, instead, triggers substantial reductions in gut-resident and peripherally derived Foxp3
    MeSH term(s) Animals ; Down-Regulation/immunology ; Forkhead Transcription Factors/immunology ; Forkhead Transcription Factors/metabolism ; Inducible T-Cell Co-Stimulator Protein/deficiency ; Inducible T-Cell Co-Stimulator Protein/immunology ; Inducible T-Cell Co-Stimulator Protein/metabolism ; Inflammation/immunology ; Inflammation/metabolism ; Interleukin-10/immunology ; Interleukin-10/metabolism ; Mice ; Mice, Knockout ; Mice, Transgenic ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism
    Chemical Substances Forkhead Transcription Factors ; Foxp3 protein, mouse ; IL10 protein, mouse ; Icos protein, mouse ; Inducible T-Cell Co-Stimulator Protein ; Interleukin-10 (130068-27-8)
    Language English
    Publishing date 2019-01-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.1801266
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    Ud II Zs.37: Show issues Location:
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  7. Article ; Online: Microbial and histopathologic considerations in the use of mouse models of inflammatory bowel diseases.

    Schoeb, Trenton R / Bullard, Daniel C

    Inflammatory bowel diseases

    2012  Volume 18, Issue 8, Page(s) 1558–1565

    Abstract: Mouse models provide powerful tools to investigate disease mechanisms and are widely used in inflammatory bowel disease research. However, it is common for reports of mouse model studies to lack potentially important information about the microbial ... ...

    Abstract Mouse models provide powerful tools to investigate disease mechanisms and are widely used in inflammatory bowel disease research. However, it is common for reports of mouse model studies to lack potentially important information about the microbial status of the mice and the method used to evaluate disease expression for statistical analysis. For example, it is common practice to state that the mice were housed under specific pathogen-free conditions but provide no further information regarding the presence or absence of organisms such as Helicobacter spp. that are known or likely to affect disease expression, thus omitting information potentially important to the expected phenotype of the mice and their responses to experimental manipulation. We therefore encourage authors to use such terms as "conventional" and "specific pathogen-free" precisely, to state the agents from which the mice are represented to be free, and to provide a brief description of the health monitoring protocol. Descriptions of histopathologic methods used to evaluate colitis in mouse models also often do not include sufficient detail to allow readers to understand and evaluate the methods; in addition, the lesions commonly are shown in photomicrographs that are too small and of too low resolution to be interpreted. Inasmuch as such methods are often the major or only source of data upon which conclusions regarding genotype or experimental treatment effects are based, the method employed should be fully described, and photomicrographs should be of adequate size and resolution to allow independent assessment.
    MeSH term(s) Animals ; Disease Models, Animal ; Inflammatory Bowel Diseases/etiology ; Inflammatory Bowel Diseases/pathology ; Mice
    Keywords covid19
    Language English
    Publishing date 2012-01-31
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1340971-2
    ISSN 1536-4844 ; 1078-0998
    ISSN (online) 1536-4844
    ISSN 1078-0998
    DOI 10.1002/ibd.22892
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    Zs.A 4530: Show issues Location:
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  8. Article ; Online: Host Genetics But Not Commensal Microbiota Determines the Initial Development of Systemic Autoimmune Disease in BXD2 Mice.

    Hong, Huixian / Alduraibi, Fatima / Ponder, David / Duck, Wayne L / Morrow, Casey D / Foote, Jeremy B / Schoeb, Trenton R / Fatima, Huma / Elson, Charles O / Hsu, Hui-Chen / Mountz, John D

    Arthritis & rheumatology (Hoboken, N.J.)

    2022  Volume 74, Issue 4, Page(s) 634–640

    Abstract: Objective: To determine the extent to which the gut microbiome influences systemic autoimmunity in a mouse model of lupus.: Methods: We generated germ-free (GF) lupus-prone BXD2 mice, which under normal conditions develop spontaneous germinal centers ...

    Abstract Objective: To determine the extent to which the gut microbiome influences systemic autoimmunity in a mouse model of lupus.
    Methods: We generated germ-free (GF) lupus-prone BXD2 mice, which under normal conditions develop spontaneous germinal centers (GCs) and high titers of serum autoantibodies. GF status was confirmed by gut bacterial culture. The autoimmune phenotypes of 6- and 12-month-old gnotobiotic GF BXD2 mice and specific pathogen-free (SPF) BXD2 mice were compared. Serum levels of autoantibodies were measured by enzyme-linked immunosorbent assay. Histologic sections of the mouse kidney and joints were evaluated. Flow cytometry was used to analyze GCs and age-associated B cells. CD4+ T cells were analyzed for PD-1+ICOS+ activated T cells, T follicular regulatory (Tfr) cells (Foxp3+CD25+ PD-1+CXCR5+), and PD-1+ICOS+ T cells expressing interleukin-17A (IL-17A) or interferon-γ (IFNγ) after stimulation with phorbol myristate acetate (PMA)/ionomycin.
    Results: In 6-month-old mice, GF status did not affect splenomegaly, GC B cells, age-associated B cells, or serum autoantibody levels, except for IgG antihistone. GF BXD2 mice exhibited a significantly higher percentage of Tfr cells compared to their SPF counterparts (P < 0.05). At 12 months of age, however, GF BXD2 mice had significantly diminished IgG autoantibody levels and a lower percentage of GC B cells and age-associated B cells (P < 0.05). Following stimulation with PMA/ionomycin, PD-1+ICOS+ CD4+ T cells expressed significantly lower IL-17A, but not IFNγ, levels in GF BXD2 mice compared to SPF BXD2 mice (P < 0.01). SPF BXD2 mice and GF BXD2 mice developed equivalent renal and joint disease with no significant differences in severity.
    Conclusion: Our results suggest a model in which genetics plays a dominant role in determining the initial development of autoimmunity. In contrast, gut microbiomes may regulate the persistence of certain aspects of systemic autoimmunity.
    MeSH term(s) Animals ; Autoantibodies ; Autoimmune Diseases/genetics ; Gastrointestinal Microbiome ; Immunoglobulin G ; Interferon-gamma ; Interleukin-17 ; Ionomycin ; Mice ; Programmed Cell Death 1 Receptor
    Chemical Substances Autoantibodies ; Immunoglobulin G ; Interleukin-17 ; Programmed Cell Death 1 Receptor ; Ionomycin (56092-81-0) ; Interferon-gamma (82115-62-6)
    Language English
    Publishing date 2022-02-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2756371-6
    ISSN 2326-5205 ; 2326-5191
    ISSN (online) 2326-5205
    ISSN 2326-5191
    DOI 10.1002/art.42008
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 24: Show issues Location:
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  9. Article ; Online: Reversing wrinkled skin and hair loss in mice by restoring mitochondrial function.

    Singh, Bhupendra / Schoeb, Trenton R / Bajpai, Prachi / Slominski, Andrzej / Singh, Keshav K

    Cell death & disease

    2018  Volume 9, Issue 7, Page(s) 735

    Abstract: Mitochondrial DNA (mtDNA) depletion is involved in mtDNA depletion syndromes, mitochondrial diseases, aging and aging-associated chronic diseases, and other human pathologies. To evaluate the consequences of depletion of mtDNA in the whole animal, we ... ...

    Abstract Mitochondrial DNA (mtDNA) depletion is involved in mtDNA depletion syndromes, mitochondrial diseases, aging and aging-associated chronic diseases, and other human pathologies. To evaluate the consequences of depletion of mtDNA in the whole animal, we created an inducible mtDNA-depleter mouse expressing, in the polymerase domain of POLG1, a dominant-negative mutation to induce depletion of mtDNA in various tissues. These mice showed reduced mtDNA content, reduced mitochondrial gene expression, and instability of supercomplexes involved in oxidative phosphorylation (OXPHOS) resulting in reduced OXPHOS enzymatic activities. We demonstrate that ubiquitous depletion of mtDNA in mice leads to predominant and profound effects on the skin resulting in wrinkles and visual hair loss with an increased number of dysfunctional hair follicles and inflammatory responses. Development of skin wrinkle was associated with the significant epidermal hyperplasia, hyperkeratosis, increased expression of matrix metalloproteinases, and decreased expression of matrix metalloproteinase inhibitor TIMP1. We also discovered markedly increased skin inflammation that appears to be a contributing factor in skin pathology. Histopathologic analyses revealed dysfunctional hair follicles. mtDNA-depleter mice also show changes in expression of aging-associated markers including IGF1R, KLOTHO, VEGF, and MRPS5. mtDNA-repleter mice showed that, by turning off the mutant POLG1 transgene expression, mitochondrial function, as well as the skin and hair pathology, is reversed to wild-type level. To our knowledge that restoration of mitochondrial functions can reverse the skin and hair pathology is unprecedented.
    MeSH term(s) Alopecia/pathology ; Amino Acid Sequence ; Animals ; Biomarkers/metabolism ; DNA Polymerase gamma/chemistry ; DNA Polymerase gamma/metabolism ; DNA, Mitochondrial/genetics ; Doxycycline/pharmacology ; Epidermis/drug effects ; Epidermis/pathology ; Hyperplasia ; Inflammation/pathology ; Matrix Metalloproteinases/metabolism ; Mice ; Mitochondria/drug effects ; Mitochondria/metabolism ; Oxidative Phosphorylation/drug effects ; Phenotype ; Reproducibility of Results ; Skin Aging/drug effects ; Skin Aging/pathology
    Chemical Substances Biomarkers ; DNA, Mitochondrial ; DNA Polymerase gamma (EC 2.7.7.7) ; POLG protein, human (EC 2.7.7.7) ; Matrix Metalloproteinases (EC 3.4.24.-) ; Doxycycline (N12000U13O)
    Language English
    Publishing date 2018-07-20
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-018-0765-9
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  10. Article: Mice expressing the variant rs1143679 allele of ITGAM (CD11b) show impaired DC-mediated T cell proliferation

    Avery, Justin T / Jimenez, Rachel V / Blake, Joseph L / Wright, Tyler T / Leόn-Ruiz, Beatriz / Schoeb, Trenton R / Szalai, Alexander J / Bullard, Daniel C

    Mammalian genome. 2019 Oct., v. 30, no. 9-10

    2019  

    Abstract: Genome-wide association studies (GWAS) and functional genomic analyses have implicated several ITGAM (CD11b) single-nucleotide polymorphisms (SNPs) in the development of SLE and other disorders. ITGAM encodes the αM chain of the β₂ integrin Mac-1, a ... ...

    Abstract Genome-wide association studies (GWAS) and functional genomic analyses have implicated several ITGAM (CD11b) single-nucleotide polymorphisms (SNPs) in the development of SLE and other disorders. ITGAM encodes the αM chain of the β₂ integrin Mac-1, a receptor that plays important roles in myeloid cell functions. The ITGAM SNP rs1143679, which results in an arginine to histidine change at amino acid position 77 of the CD11b protein, has been shown to reduce binding to several ligands and to alter Mac-1-mediated cellular response in vitro. Importantly, however, the potential contribution of this SNP variant to the initiation and/or progression of immune and inflammatory processes in vivo remains unexplored. Herein, we describe for the first time the generation and characterization of a mouse line expressing the 77His variant of CD11b. Surprisingly, we found that 77His did not significantly affect Mac-1-mediated leukocyte migration and activation as assessed using thioglycollate-induced peritonitis and LPS/TNF-α-induced dermal inflammation models. In contrast, expression of this variant did alter T cell immunity, as evidenced by significantly reduced proliferation of ovalbumin (OVA)-specific transgenic T cells in 77His mice immunized with OVA. Reduced antigen-specific T cell proliferation was also observed when either 77His splenic dendritic cells (DCs) or bone marrow-derived DCs were used as antigen-presenting cells (APCs). Although more work is necessary to determine how this alteration might influence the development of SLE or other diseases, these in vivo findings suggest that the 77His variant of CD11b can compromise the ability of DCs to induce antigen-driven T cell proliferation.
    Keywords T-lymphocytes ; alleles ; arginine ; cell movement ; cell proliferation ; genetically modified organisms ; genomics ; histidine ; immunity ; inflammation ; integrins ; ligands ; mice ; ovalbumin ; peritonitis
    Language English
    Dates of publication 2019-10
    Size p. 245-259.
    Publishing place Springer US
    Document type Article
    Note NAL-AP-2-clean
    ZDB-ID 1058547-3
    ISSN 1432-1777 ; 0938-8990
    ISSN (online) 1432-1777
    ISSN 0938-8990
    DOI 10.1007/s00335-019-09819-y
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