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  1. Article ; Online: Enlarged Virchow-Robin Spaces Contributing to Ventriculomegaly in a 37-Year-Old Woman.

    Stuebe, Caren M / Gonzalez, Nancy M / Toussaint, L Gerard

    Neurology

    2023  Volume 101, Issue 23, Page(s) 1077–1078

    MeSH term(s) Female ; Humans ; Adult ; Glymphatic System ; Hydrocephalus/complications ; Hydrocephalus/diagnostic imaging ; Brain/diagnostic imaging ; Magnetic Resonance Imaging
    Language English
    Publishing date 2023-12-04
    Publishing country United States
    Document type Case Reports ; Journal Article
    ZDB-ID 207147-2
    ISSN 1526-632X ; 0028-3878
    ISSN (online) 1526-632X
    ISSN 0028-3878
    DOI 10.1212/WNL.0000000000207950
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ui II Zs.153: Show issues Location:
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  2. Article ; Online: Aerobic glycolysis enables the effector differentiation potential of stem-like CD4

    Zou, Dawei / Zhang, Xiaolong / Li, Shuang / Xiao, Xiang / Gonzalez, Nancy M / Minze, Laurie J / Li, Xian C / Chen, Wenhao

    Cellular & molecular immunology

    2024  Volume 21, Issue 5, Page(s) 527–529

    MeSH term(s) Cell Differentiation ; CD4-Positive T-Lymphocytes/immunology ; Glycolysis ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplasms/metabolism ; Humans ; Animals ; Aerobiosis ; Mice
    Language English
    Publishing date 2024-03-21
    Publishing country China
    Document type Letter ; Research Support, Non-U.S. Gov't
    ZDB-ID 2435097-7
    ISSN 2042-0226 ; 1672-7681
    ISSN (online) 2042-0226
    ISSN 1672-7681
    DOI 10.1038/s41423-024-01154-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6681: Show issues Location:
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  3. Article ; Online: Schrödinger's T Cells: Molecular Insights Into Stemness and Exhaustion.

    Gonzalez, Nancy M / Zou, Dawei / Gu, Andy / Chen, Wenhao

    Frontiers in immunology

    2021  Volume 12, Page(s) 725618

    Abstract: T cell stemness and exhaustion coexist as two key contrasting phenomena during chronic antigen stimulation, such as infection, transplant, cancer, and autoimmunity. T cell exhaustion refers to the progressive loss of effector function caused by chronic ... ...

    Abstract T cell stemness and exhaustion coexist as two key contrasting phenomena during chronic antigen stimulation, such as infection, transplant, cancer, and autoimmunity. T cell exhaustion refers to the progressive loss of effector function caused by chronic antigen exposure. Exhausted T (T
    MeSH term(s) Cell Differentiation ; Epigenesis, Genetic ; Immunotherapy/methods ; Neoplasms/immunology ; Neoplasms/therapy ; Persistent Infection/immunology ; Persistent Infection/therapy ; T-Lymphocytes/physiology
    Language English
    Publishing date 2021-08-26
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2021.725618
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: CD4

    Zou, Dawei / Yin, Zheng / Yi, Stephanie G / Wang, Guohua / Guo, Yang / Xiao, Xiang / Li, Shuang / Zhang, Xiaolong / Gonzalez, Nancy M / Minze, Laurie J / Wang, Lin / Wong, Stephen T C / Osama Gaber, A / Ghobrial, Rafik M / Li, Xian C / Chen, Wenhao

    Nature immunology

    2024  Volume 25, Issue 1, Page(s) 66–76

    Abstract: ... ...

    Abstract CD4
    MeSH term(s) Gene Expression Regulation ; Cell Differentiation ; T-Lymphocytes, Regulatory
    Language English
    Publishing date 2024-01-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-023-01682-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5294: Show issues Location:
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    Zs.MG 42: Show issues

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  5. Article ; Online: IRF4 ablation in B cells abrogates allogeneic B cell responses and prevents chronic transplant rejection.

    Wang, Guohua / Zou, Dawei / Wang, Yixuan / Gonzalez, Nancy M / Yi, Stephanie G / Li, Xian C / Chen, Wenhao / Gaber, A Osama

    The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation

    2021  Volume 40, Issue 10, Page(s) 1122–1132

    Abstract: Backgound: B cells contribute to chronic transplant rejection by producing donor-specific antibodies and promoting T cell response, but how these processes are regulated at the transcriptional level remains unclear. Herein, we investigate the role of ... ...

    Abstract Backgound: B cells contribute to chronic transplant rejection by producing donor-specific antibodies and promoting T cell response, but how these processes are regulated at the transcriptional level remains unclear. Herein, we investigate the role of transcription factor interferon regulatory factor 4 (IRF4) in controlling B cell response during chronic transplant rejection.
    Methods: We generated the Irf4
    Results: IRF4 is dynamically expressed at different stages of B cell development and is absent in germinal center (GC) B cells. However, IRF4 ablation in the B cell lineage primarily eliminates GC B cells in both naïve and NP-KLH immunized mice. In the transplantation setting, IRF4 functions intrinsically in B cells and governs allogeneic B cell responses at multiple levels, including GC B cell generation, plasma cell differentiation, donor-specific antibody production, and support of T cell response. B cell-specific IRF4 deletion combined with transient CTLA4-Ig treatment abrogates acute and chronic cardiac allograft rejection in naïve recipient mice but not in donor skin-sensitized recipients.
    Conclusions: B cells require IRF4 to mediate chronic transplant rejection. IRF4 ablation in B cells abrogates allogeneic B cell responses and may also inhibit the ability of B cells to prime allogenic T cells. Targeting IRF4 in B cells represents a potential therapeutic strategy for eliminating chronic transplant rejection.
    MeSH term(s) Animals ; B-Lymphocytes/physiology ; Disease Models, Animal ; Germinal Center/metabolism ; Graft Rejection/etiology ; Graft Rejection/prevention & control ; Graft Survival ; Haptens ; Heart Transplantation/adverse effects ; Hemocyanins ; Interferon Regulatory Factors/physiology ; Mice ; Mice, Inbred BALB C ; Mice, Knockout ; Skin Transplantation/adverse effects
    Chemical Substances 4-hydroxy-3-nitrophenylacetyl-keyhole limpet hemocyanin ; Haptens ; Interferon Regulatory Factors ; interferon regulatory factor-4 ; Hemocyanins (9013-72-3)
    Language English
    Publishing date 2021-06-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1062522-7
    ISSN 1557-3117 ; 1053-2498
    ISSN (online) 1557-3117
    ISSN 1053-2498
    DOI 10.1016/j.healun.2021.06.008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2056: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  6. Article ; Online: Urinary T cells correlate with rate of renal function loss in autosomal dominant polycystic kidney disease.

    Zimmerman, Kurt A / Gonzalez, Nancy M / Chumley, Phillip / Chacana, Teresa / Harrington, Laurie E / Yoder, Bradley K / Mrug, Michal

    Physiological reports

    2018  Volume 7, Issue 1, Page(s) e13951

    Abstract: Several innate immune response components were recognized as outcome predictors in autosomal dominant polycystic kidney disease (ADPKD) and their causative role in disease pathogenesis was confirmed in animal models. In contrast, the role of adaptive ... ...

    Abstract Several innate immune response components were recognized as outcome predictors in autosomal dominant polycystic kidney disease (ADPKD) and their causative role in disease pathogenesis was confirmed in animal models. In contrast, the role of adaptive immunity in ADPKD remains relatively unexplored. Therefore, we evaluated T cell populations in kidney and urine of ADPKD patients using flow cytometry and confocal immunofluorescence microscopy approaches. These analyses revealed ADPKD-associated overall increases in the number of intrarenal CD4 and CD8 T cells that were associated with a loss of polarity in distribution between the cortex and medulla (higher in medulla vs. cortex in controls). Also, the urinary T cell-based index correlated moderately with renal function decline in a small cohort of ADPKD patients. Together, these data suggest that similar to innate immune responses, T cells participate in ADPKD pathogenesis. They also point to urinary T cells as a novel candidate marker of the disease activity in ADPKD.
    MeSH term(s) Adult ; Aged ; Aged, 80 and over ; CD4-Positive T-Lymphocytes/pathology ; CD8-Positive T-Lymphocytes/pathology ; Female ; Humans ; Kidney/pathology ; Kidney/physiopathology ; Male ; Middle Aged ; Polycystic Kidney, Autosomal Dominant/pathology ; Polycystic Kidney, Autosomal Dominant/urine
    Language English
    Publishing date 2018-11-29
    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 2724325-4
    ISSN 2051-817X ; 2051-817X
    ISSN (online) 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.13951
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: A Comprehensive Immune Cell Atlas of Cystic Kidney Disease Reveals the Involvement of Adaptive Immune Cells in Injury-Mediated Cyst Progression in Mice.

    Song, Cheng J / Li, Zhang / Ahmed, Ummey Khalecha Bintha / Bland, Sarah J / Yashchenko, Alex / Liu, Shanrun / Aloria, Ernald J / Lever, Jeremie M / Gonzalez, Nancy M / Bickel, Marisa A / Giles, Cory B / Georgescu, Constantin / Wren, Jonathan D / Lang, Mark L / Benveniste, Etty N / Harrington, Laurie E / Tsiokas, Leo / George, James F / Jones, Kenneth L /
    Crossman, David K / Agarwal, Anupam / Mrug, Michal / Yoder, Bradley K / Hopp, Katharina / Zimmerman, Kurt A

    Journal of the American Society of Nephrology : JASN

    2022  Volume 33, Issue 4, Page(s) 747–768

    Abstract: Background: Inducible disruption of cilia-related genes in adult mice results in slowly progressive cystic disease, which can be greatly accelerated by renal injury.: Methods: To identify in an unbiased manner modifier cells that may be influencing ... ...

    Abstract Background: Inducible disruption of cilia-related genes in adult mice results in slowly progressive cystic disease, which can be greatly accelerated by renal injury.
    Methods: To identify in an unbiased manner modifier cells that may be influencing the differential rate of cyst growth in injured versus non-injured cilia mutant kidneys at a time of similar cyst severity, we generated a single-cell atlas of cystic kidney disease. We conducted RNA-seq on 79,355 cells from control mice and adult-induced conditional
    Results: Analyses of single-cell RNA-seq data of CD45
    Conclusions: Collectively, these data highlight the diversity of immune cell involvement in cystic kidney disease.
    MeSH term(s) Animals ; Cilia/metabolism ; Cysts/genetics ; Kidney/metabolism ; Mice ; Mutation ; Polycystic Kidney Diseases/metabolism
    Language English
    Publishing date 2022-02-02
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.2021030278
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3344: Show issues Location:
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  8. Article ; Online: Tissue-Resident Macrophages Promote Renal Cystic Disease.

    Zimmerman, Kurt A / Song, Cheng J / Li, Zhang / Lever, Jeremie M / Crossman, David K / Rains, Addison / Aloria, Ernald J / Gonzalez, Nancy M / Bassler, John R / Zhou, Juling / Crowley, Michael R / Revell, Dustin Z / Yan, Zhaoqi / Shan, Dan / Benveniste, Etty N / George, James F / Mrug, Michal / Yoder, Bradley K

    Journal of the American Society of Nephrology : JASN

    2019  Volume 30, Issue 10, Page(s) 1841–1856

    Abstract: Background: Mutations affecting cilia proteins have an established role in renal cyst formation. In mice, the rate of cystogenesis is influenced by the age at which cilia dysfunction occurs and whether the kidney has been injured. Disruption of cilia ... ...

    Abstract Background: Mutations affecting cilia proteins have an established role in renal cyst formation. In mice, the rate of cystogenesis is influenced by the age at which cilia dysfunction occurs and whether the kidney has been injured. Disruption of cilia function before postnatal day 12-14 results in rapid cyst formation; however, cyst formation is slower when cilia dysfunction is induced after postnatal day 14. Rapid cyst formation can also be induced in conditional adult cilia mutant mice by introducing renal injury. Previous studies indicate that macrophages are involved in cyst formation, however the specific role and type of macrophages responsible has not been clarified.
    Methods: We analyzed resident macrophage number and subtypes during postnatal renal maturation and after renal injury in control and conditional
    Results: Our data show that renal resident macrophages undergo a phenotypic switch from R2b (CD11c
    Conclusions: These data uncover an important pathogenic role for resident macrophages during rapid cyst progression.
    MeSH term(s) Animals ; Cilia/genetics ; Female ; Kidney/growth & development ; Kidney Diseases, Cystic/etiology ; Macrophages/classification ; Macrophages/physiology ; Male ; Mice ; Mutation
    Language English
    Publishing date 2019-07-23
    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 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.2018080810
    Database MEDical Literature Analysis and Retrieval System OnLINE

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