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  • 1
    Online Resource
    Online Resource
    Protective function and durability of mouse lymph node-resident memory CD8+ T cells
    eLife Sciences Publications, Ltd ; 2021
    In:  eLife Vol. 10 ( 2021-06-18)
    Details
    In: eLife, eLife Sciences Publications, Ltd, Vol. 10 ( 2021-06-18)
    Abstract: Protective lung tissue-resident memory CD8 + T cells (Trm) form after influenza A virus (IAV) infection. We show that IAV infection of mice generates CD69 + CD103 + and other memory CD8 + T cell populations in lung-draining mediastinal lymph nodes (mLNs) from circulating naive or memory CD8 + T cells. Repeated antigen exposure, mimicking seasonal IAV infections, generates quaternary memory (4M) CD8 + T cells that protect mLN from viral infection better than 1M CD8 + T cells. Better protection by 4M CD8 + T cells associates with enhanced granzyme A/B expression and stable maintenance of mLN CD69 + CD103 + 4M CD8 + T cells, vs the steady decline of CD69 + CD103 + 1M CD8 + T cells, paralleling the durability of protective CD69 + CD103 + 4M vs 1M in the lung after IAV infection. Coordinated upregulation in canonical Trm-associated genes occurs in circulating 4M vs 1M populations without the enrichment of canonical downregulated Trm genes. Thus, repeated antigen exposure arms circulating memory CD8 + T cells with enhanced capacity to form long-lived populations of Trm that enhance control of viral infections of the mLN.
    Type of Medium: Online Resource
    ISSN: 2050-084X
    URL: Article
    DOI: 10.7554/eLife.68662
    Language: English
    Publisher: eLife Sciences Publications, Ltd
    Publication Date: 2021
    detail.hit.zdb_id: 2687154-3
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  • 2
    Online Resource
    Online Resource
    p53 Hinders CRISPR/Cas9-Mediated Targeted Gene Disruption in Memory CD8 T Cells In Vivo
    The American Association of Immunologists ; 2020
    In:  The Journal of Immunology Vol. 205, No. 8 ( 2020-10-15), p. 2222-2230
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 205, No. 8 ( 2020-10-15), p. 2222-2230
    Abstract: CRISPR/Cas9 technology has revolutionized rapid and reliable gene editing in cells. Although many cell types have been subjected to CRISPR/Cas9-mediated gene editing, there is no evidence of success in genetic alteration of Ag-experienced memory CD8 T cells. In this study, we show that CRISPR/Cas9-mediated gene editing in memory CD8 T cells precludes their proliferation after Ag re-encounter in vivo. This defect is mediated by the proapoptotic transcription factor p53, a sensor of DNA damage. Temporarily inhibiting p53 function offers a window of opportunity for the memory CD8 T cells to repair the DNA damage, facilitating robust recall responses on Ag re-encounter. We demonstrate this by functionally altering memory CD8 T cells using CRISPR/Cas9-mediated targeted gene disruption under the aegis of p53siRNA in the mouse model. Our approach thus adapts the CRISPR/Cas9 technology for memory CD8 T cells to undertake gene editing in vivo, for the first time, to our knowledge.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.2000654
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2020
    detail.hit.zdb_id: 1475085-5
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  • 3
    Online Resource
    Online Resource
    Monocyte-Derived CD11c+ Cells Acquire Plasmodium from Hepatocytes to Prime CD8 T Cell Immunity to Liver-Stage Malaria
    Elsevier BV ; 2019
    In:  Cell Host & Microbe Vol. 25, No. 4 ( 2019-04), p. 565-577.e6
    Details
    In: Cell Host & Microbe, Elsevier BV, Vol. 25, No. 4 ( 2019-04), p. 565-577.e6
    Type of Medium: Online Resource
    ISSN: 1931-3128
    URL: Article
    DOI: 10.1016/j.chom.2019.02.014
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
    detail.hit.zdb_id: 2276339-9
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  • 4
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    Online Resource
    Inefficient Recovery of Repeatedly Stimulated Memory CD8 T Cells after Polymicrobial Sepsis Induction Leads to Changes in Memory CD8 T Cell Pool Composition
    The American Association of Immunologists ; 2023
    In:  The Journal of Immunology Vol. 210, No. 2 ( 2023-01-15), p. 168-179
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 210, No. 2 ( 2023-01-15), p. 168-179
    Abstract: Long-lasting sepsis-induced immunoparalysis has been principally studied in primary (1°) memory CD8 T cells; however, the impact of sepsis on memory CD8 T cells with a history of repeated cognate Ag encounters is largely unknown but important in understanding the role of sepsis in shaping the pre-existing memory CD8 T cell compartment. Higher-order memory CD8 T cells are crucial in providing immunity against common pathogens that reinfect the host or are generated by repeated vaccination. In this study, we analyzed peripheral blood from septic patients and show that memory CD8 T cells with defined Ag specificity for recurring CMV infection proliferate less than bulk populations of central memory CD8 T cells. Using TCR-transgenic T cells to generate 1° and higher-order (quaternary [4°]) memory T cells within the same host, we demonstrate that the susceptibility and loss of both memory subsets are similar after sepsis induction, and sepsis diminished Ag-dependent and -independent (bystander) functions of these memory subsets equally. Both the 1° and 4° memory T cell populations proliferated in a sepsis-induced lymphopenic environment; however, due to the intrinsic differences in baseline proliferative capacity, expression of receptors (e.g., CD127/CD122), and responsiveness to homeostatic cytokines, 1° memory T cells become overrepresented over time in sepsis survivors. Finally, IL-7/anti–IL-7 mAb complex treatment early after sepsis induction preferentially rescued the proliferation and accumulation of 1° memory T cells, whereas recovery of 4° memory T cells was less pronounced. Thus, inefficient recovery of repeatedly stimulated memory cells after polymicrobial sepsis induction leads to changes in memory T cell pool composition, a notion with important implications in devising strategies to recover the number and function of pre-existing memory CD8 T cells in sepsis survivors.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.2200676
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2023
    detail.hit.zdb_id: 1475085-5
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  • 5
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    Online Resource
    Severity of Sepsis Determines the Degree of Impairment Observed in Circulatory and Tissue-Resident Memory CD8 T Cell Populations
    The American Association of Immunologists ; 2021
    In:  The Journal of Immunology Vol. 207, No. 7 ( 2021-10-01), p. 1871-1881
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 207, No. 7 ( 2021-10-01), p. 1871-1881
    Abstract: Sepsis reduces the number and function of memory CD8 T cells within the host, contributing to the long-lasting state of immunoparalysis. Interestingly, the relative susceptibility of memory CD8 T cell subsets to quantitative/qualitative changes differ after cecal ligation and puncture (CLP)–induced sepsis. Compared with circulatory memory CD8 T cells (TCIRCM), moderate sepsis (0–10% mortality) does not result in numerical decline of CD8 tissue-resident memory T cells (TRM), which retain their “sensing and alarm” IFN-γ–mediated effector function. To interrogate this biologically important dichotomy, vaccinia virus–immune C57BL/6 (B6) mice containing CD8 TCIRCM and skin TRM underwent moderate or severe (∼50% mortality) sepsis. Severe sepsis led to increased morbidity and mortality characterized by increased inflammation compared with moderate CLP or sham controls. Severe CLP mice also displayed increased vascular permeability in the ears. Interestingly, skin CD103+ CD8 TRM, detected by i.v. exclusion or two-photon microscopy, underwent apoptosis and subsequent numerical loss following severe sepsis, which was not observed in mice that experienced moderate CLP or sham surgeries. Consequently, severe septic mice showed diminished CD8 T cell–mediated protection to localized skin reinfection. Finally, the relationship between severity of sepsis and demise in circulatory versus tissue-embedded memory CD8 T cell populations was confirmed by examining tumor-infiltrating and nonspecific CD8 T cells in B16 melanoma tumors. Thus, sepsis can differentially affect the presence and function of Ag-specific CD8 T cells that reside inside tissues/tumors depending on the severity of the insult, a notion with direct relevance to sepsis survivors and their ability to mount protective memory CD8 T cell–dependent responses to localized Ag re-encounter.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.2001142
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2021
    detail.hit.zdb_id: 1475085-5
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