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  1. Article ; Online: Immune and epithelial determinants of age-related risk and alveolar injury in fatal COVID-19.

    Chait, Michael / Yilmaz, Mine M / Shakil, Shanila / Ku, Amy W / Dogra, Pranay / Connors, Thomas J / Szabo, Peter A / Gray, Joshua I / Wells, Steven B / Kubota, Masaru / Matsumoto, Rei / Poon, Maya Ml / Snyder, Mark E / Baldwin, Matthew R / Sims, Peter A / Saqi, Anjali / Farber, Donna L / Weisberg, Stuart P

    JCI insight

    2022  Volume 7, Issue 11

    Abstract: Respiratory failure in COVID-19 is characterized by widespread disruption of the lung's alveolar gas exchange interface. To elucidate determinants of alveolar lung damage, we performed epithelial and immune cell profiling in lungs from 24 COVID-19 ... ...

    Abstract Respiratory failure in COVID-19 is characterized by widespread disruption of the lung's alveolar gas exchange interface. To elucidate determinants of alveolar lung damage, we performed epithelial and immune cell profiling in lungs from 24 COVID-19 autopsies and 43 uninfected organ donors ages 18-92 years. We found marked loss of type 2 alveolar epithelial (T2AE) cells and increased perialveolar lymphocyte cytotoxicity in all fatal COVID-19 cases, even at early stages before typical patterns of acute lung injury are histologically apparent. In lungs from uninfected organ donors, there was also progressive loss of T2AE cells with increasing age, which may increase susceptibility to COVID-19-mediated lung damage in older individuals. In the fatal COVID-19 cases, macrophage infiltration differed according to the histopathological pattern of lung injury. In cases with acute lung injury, we found accumulation of CD4+ macrophages that expressed distinctly high levels of T cell activation and costimulation genes and strongly correlated with increased extent of alveolar epithelial cell depletion and CD8+ T cell cytotoxicity. Together, our results show that T2AE cell deficiency may underlie age-related COVID-19 risk and initiate alveolar dysfunction shortly after infection, and we define immune cell mediators that may contribute to alveolar injury in distinct pathological stages of fatal COVID-19.
    MeSH term(s) Acute Lung Injury/pathology ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Alveolar Epithelial Cells/pathology ; Autopsy ; COVID-19 ; Humans ; Lung/pathology ; Middle Aged ; Young Adult
    Language English
    Publishing date 2022-06-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.157608
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Preconditioning thermal therapy: flipping the switch on IL-6 for anti-tumour immunity.

    Mikucki, Maryann E / Fisher, Daniel T / Ku, Amy W / Appenheimer, Michelle M / Muhitch, Jason B / Evans, Sharon S

    International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group

    2013  Volume 29, Issue 5, Page(s) 464–473

    Abstract: Cancer immunotherapy aims to generate long-lived, tumour-specific adaptive immunity to limit dysregulated tumour progression and metastasis. Tumour vasculature has emerged as a critical checkpoint controlling the efficacy of immunotherapy since it is the ...

    Abstract Cancer immunotherapy aims to generate long-lived, tumour-specific adaptive immunity to limit dysregulated tumour progression and metastasis. Tumour vasculature has emerged as a critical checkpoint controlling the efficacy of immunotherapy since it is the main access point for cytotoxic T cells to reach tumour cell targets. Therapeutic success has been particularly challenging to achieve because of the local, cytokine-rich inflammatory milieu that drives a pro-tumourigenic programme supporting the growth and survival of malignant cells. Here, we focus on recent evidence that systemic thermal therapy can switch the activities of the inflammatory cytokine, interleukin-6 (IL-6), to a predominantly anti-tumourigenic function that promotes anti-tumour immunity by mobilising T cell trafficking in the recalcitrant tumour microenvironment.
    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes/immunology ; Humans ; Hyperthermia, Induced ; Immunotherapy, Adoptive ; Interleukin-6/immunology ; Neoplasms/immunology ; Neoplasms/therapy ; Tumor Microenvironment/immunology
    Chemical Substances Interleukin-6
    Language English
    Publishing date 2013-07-17
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 632526-9
    ISSN 1464-5157 ; 0265-6736
    ISSN (online) 1464-5157
    ISSN 0265-6736
    DOI 10.3109/02656736.2013.807440
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  3. Article ; Online: Immune Adjuvant Activity of Pre-Resectional Radiofrequency Ablation Protects against Local and Systemic Recurrence in Aggressive Murine Colorectal Cancer.

    Ito, Fumito / Ku, Amy W / Bucsek, Mark J / Muhitch, Jason B / Vardam-Kaur, Trupti / Kim, Minhyung / Fisher, Daniel T / Camoriano, Marta / Khoury, Thaer / Skitzki, Joseph J / Gollnick, Sandra O / Evans, Sharon S

    PloS one

    2015  Volume 10, Issue 11, Page(s) e0143370

    Abstract: Purpose: While surgical resection is a cornerstone of cancer treatment, local and distant recurrences continue to adversely affect outcome in a significant proportion of patients. Evidence that an alternative debulking strategy involving radiofrequency ... ...

    Abstract Purpose: While surgical resection is a cornerstone of cancer treatment, local and distant recurrences continue to adversely affect outcome in a significant proportion of patients. Evidence that an alternative debulking strategy involving radiofrequency ablation (RFA) induces antitumor immunity prompted the current investigation of the efficacy of performing RFA prior to surgical resection (pre-resectional RFA) in a preclinical mouse model.
    Experimental design: Therapeutic efficacy and systemic immune responses were assessed following pre-resectional RFA treatment of murine CT26 colon adenocarcinoma.
    Results: Treatment with pre-resectional RFA significantly delayed tumor growth and improved overall survival compared to sham surgery, RFA, or resection alone. Mice in the pre-resectional RFA group that achieved a complete response demonstrated durable antitumor immunity upon tumor re-challenge. Failure to achieve a therapeutic benefit in immunodeficient mice confirmed that tumor control by pre-resectional RFA depends on an intact adaptive immune response rather than changes in physical parameters that make ablated tumors more amenable to a complete surgical excision. RFA causes a marked increase in intratumoral CD8+ T lymphocyte infiltration, thus substantially enhancing the ratio of CD8+ effector T cells: FoxP3+ regulatory T cells. Importantly, pre-resectional RFA significantly increases the number of antigen-specific CD8+ T cells within the tumor microenvironment and tumor-draining lymph node but had no impact on infiltration by myeloid-derived suppressor cells, M1 macrophages or M2 macrophages at tumor sites or in peripheral lymphoid organs (i.e., spleen). Finally, pre-resectional RFA of primary tumors delayed growth of distant tumors through a mechanism that depends on systemic CD8+ T cell-mediated antitumor immunity.
    Conclusion: Improved survival and antitumor systemic immunity elicited by pre-resectional RFA support the translational potential of this neoadjuvant treatment for cancer patients with high-risk of local and systemic recurrence.
    MeSH term(s) Adaptive Immunity/drug effects ; Adjuvants, Immunologic/pharmacology ; Animals ; Antigens/metabolism ; CD8-Positive T-Lymphocytes/immunology ; Catheter Ablation ; Cell Proliferation/drug effects ; Colorectal Neoplasms/immunology ; Colorectal Neoplasms/pathology ; Colorectal Neoplasms/surgery ; Cytokines/metabolism ; Female ; Lymph Nodes/drug effects ; Lymph Nodes/pathology ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Models, Biological ; Neoplasm Invasiveness ; Neoplasm Recurrence, Local/pathology ; Neoplasm Recurrence, Local/prevention & control ; Survival Analysis ; Tumor Microenvironment/drug effects
    Chemical Substances Adjuvants, Immunologic ; Antigens ; Cytokines
    Language English
    Publishing date 2015-11-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0143370
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Tumor-induced MDSC act via remote control to inhibit L-selectin-dependent adaptive immunity in lymph nodes.

    Ku, Amy W / Muhitch, Jason B / Powers, Colin A / Diehl, Michael / Kim, Minhyung / Fisher, Daniel T / Sharda, Anand P / Clements, Virginia K / O'Loughlin, Kieran / Minderman, Hans / Messmer, Michelle N / Ma, Jing / Skitzki, Joseph J / Steeber, Douglas A / Walcheck, Bruce / Ostrand-Rosenberg, Suzanne / Abrams, Scott I / Evans, Sharon S

    eLife

    2016  Volume 5

    Abstract: Myeloid-derived suppressor cells (MDSC) contribute to an immunosuppressive network that drives cancer escape by disabling T cell adaptive immunity. The prevailing view is that MDSC-mediated immunosuppression is restricted to tissues where MDSC co-mingle ... ...

    Abstract Myeloid-derived suppressor cells (MDSC) contribute to an immunosuppressive network that drives cancer escape by disabling T cell adaptive immunity. The prevailing view is that MDSC-mediated immunosuppression is restricted to tissues where MDSC co-mingle with T cells. Here we show that splenic or, unexpectedly, blood-borne MDSC execute far-reaching immune suppression by reducing expression of the L-selectin lymph node (LN) homing receptor on naïve T and B cells. MDSC-induced L-selectin loss occurs through a contact-dependent, post-transcriptional mechanism that is independent of the major L-selectin sheddase, ADAM17, but results in significant elevation of circulating L-selectin in tumor-bearing mice. Even moderate deficits in L-selectin expression disrupt T cell trafficking to distant LN. Furthermore, T cells preconditioned by MDSC have diminished responses to subsequent antigen exposure, which in conjunction with reduced trafficking, severely restricts antigen-driven expansion in widely-dispersed LN. These results establish novel mechanisms for MDSC-mediated immunosuppression that have unanticipated implications for systemic cancer immunity.
    MeSH term(s) Adaptive Immunity ; Animals ; Cell Line, Tumor ; Disease Models, Animal ; Female ; Gene Expression Regulation, Neoplastic ; Immune Tolerance ; L-Selectin/biosynthesis ; Lymph Nodes/immunology ; Lymphocytes/immunology ; Lymphocytes/metabolism ; Male ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; Myeloid-Derived Suppressor Cells/physiology ; Neoplasms/immunology ; Neoplasms/physiopathology ; RNA Interference ; Transplantation, Heterologous
    Chemical Substances L-Selectin (126880-86-2)
    Language English
    Publishing date 2016-12-08
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.17375
    Database MEDical Literature Analysis and Retrieval System OnLINE

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