Escape mechanisms of murine leukemias from immunological defenses
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Escape mechanisms of murine leukemias from immunological defenses by Alice Lin-Tsing Yu

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Published .
Written in English


Book details:

Edition Notes

Statementby Alice Lin-Tsing Yu.
Classifications
LC ClassificationsMicrofilm 50851 (Q)
The Physical Object
FormatMicroform
Paginationix, 120 leaves.
Number of Pages120
ID Numbers
Open LibraryOL1826313M
LC Control Number89893274

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This review examines the diversity of mechanisms used by fungi to escape immune responses, and specifically explores the observation that these mechanisms range from clear virulence traits to more opportunistic consequences of fungal environmental growth and survival strategiesCited by: 4.   Mechanisms of tumor immune escape: role of MSC. Several mechanisms are responsible for the ability of tumor cells to escape from the immune system-mediated control. Both soluble factors and cell-to-cell interactions are involved, some cell populations as myeloid-derived suppressor cells (MDSC) and regulatory T cells (Treg) can amplify tumor by: Molecular mechanisms underlying MHC-I changes in cancer immune escape. The role of STAT3 in cancer immune escape. The TME has high levels of activated STAT3 .   Several adaptive immune mechanisms promote parasite replication and disease. 15 The progression of murine L. major infection has been correlated with the expansion of Th2 cells and the production of IL-4, IL-5, and IL In susceptible mice, IL-4 production within the first day of infection was shown to downregulate IL receptor β-chain.

  The immune response to a murine myeloid leukemia (cell line C) was studied in vitro and in vivo. Natural killer (NK) cells and CD8+ cytotoxic T ly.   Tumor escape mechanisms have focused mainly on mutations of immune and apoptotic pathway genes. However, data obtained over the past few years suggest that epigenetic silencing in cancer may be as frequent a cause of gene inactivation as are mutations. A “Fas counterattack” mechanism of immune escape has emerged in colon (), melanoma (), and liver cancer cells, which are Fas-resistant but express tumor cells resist the FasL assault from T cells but express their own FasL which may delete anti-tumor T cells by Fas-mediated apoptosis (Fig. 1).Hence, cancer cells can advance beyond the defensive measure of Fas resistance, to the.   Intracellular bacteria such as Anaplasma spp. and Mycobacterium spp. pose a risk to human and animal populations worldwide. The main function of immune response cells is to eliminate invading pathogens. However, pathogens can deregulate host cell function and turn defense cells into suitable hosts. Intracellular bacterial have a smaller genome, compared to the host cell, thus requiring.

  2. Host defense mechanisms against HPV. While the majority of the human population acquires HPV infections, only about 10% to 15% of infected individuals establish life-long persistent infection, and only a subset of which has the potential to progress to invasive cancer (Schiffman et al., ). This suggests that, for a majority of HPV.   As illustrated in the review’s text, tumor acidity acts as a broad immune escape mechanism by which cancer cells, simultaneously wipe out the activity of all antitumor immune effectors (including T cells, NK cells and crucial antigen-presenting cells such as dendritic cells), at the same time favoring the accrual and conversion of regulatory.   The great escape: acquired mechanisms of immune evasion in cancer. Multiple immunotherapeutic approaches have potently targeted T-cell responses (T) against cancer cells (C) in the clinical setting (1); however, a substantial subset of initial responders acquire novel immunogenomic means of immune escape and relapse. Molecular mechanisms used by tumors to escape immune recognition: Immunogenetherapy and the cell biology of major histocompatibility complex class I Nicholas P. Restifo, Yutaka Kawakami, Franco Marincola, Peter Shamamian, Akash Taggarse, Fernando Esquivel, Steven A. Rosenberg.