Quantitation of the Host Cell Infiltration Kinetics of the Nonimmunogenic Colon 26 Tumor by Multiparameter Flow Cytometry

Sneed, Rosie A.; Stevenson, Anita P.; Stewart, Carleton C.

doi:10.1002/jlb.46.6.547

Cited by 5 publications

(1 citation statement)

References 16 publications

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“…Flow cytometric analysis of tumor-infiltrating immune cells and in vivo depletion after immunotherapy revealed several marked differences between TC-1/dB2m and TC-1/A9 tumors: i) TC-1/dB2m tumors contained more pDCs, CD4 + T, Treg, and γδ T cells, but fewer TAMs and NK cells. However, this observation should be interpreted with caution, as infiltration of tumors with immune cells is a dynamic process with specific kinetics of individual subpopulations (8,(31)(32)(33), which hampers a direct comparison among tumors induced by different cells. Although we strived to analyze tumors of similar size, the composition of the cell infiltrate may be affected by the markedly different growth of TC-1-, TC-1/A9-and TC-1/dB2m-induced tumors.…”

Section: Discussionmentioning

confidence: 99%

Establishment and characterization of a mouse tumor cell line with irreversible downregulation of MHC class I molecules

et al. 2019

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In the majority of human tumors, downregulation of major histocompatibility complex class I (MHC-I) expression contributes to the escape from the host immune system and resistance to immunotherapy. Relevant animal models are therefore needed to enhance the efficacy of cancer immunotherapy. As loss of β-2 microglobulin expression results in irreversible downregulation of surface MHC-I molecules in various human tumors, the β-2 microglobulin gene (B2m) was deactivated in a mouse oncogenic TC-1 cell line and a TC-1/dB2m cell line that was negative for surface MHC-I expression was derived. Following stimulation with interferon γ, MHC-I heavy chains, particularly the H-2D b molecules, were found to be expressed at low levels on the cell surface, but without β-2 microglobulin. B2m deactivation in TC-1/dB2m cells led to reduced proliferation and tumor growth. These cells were insensitive to DNA vaccination and only weakly responsive to combined immunotherapy with a DNA vaccine and the ODN1826 adjuvant. In vivo depletion demonstrated that NK1.1 + cells were involved in both reduced tumor growth and an antitumor effect of immunotherapy. The number of immune cells infiltrating TC-1/dB2m-induced tumors was comparable with that in tumors developing from TC-1/A9 cells characterized by reversible MHC-I downregulation. However, the composition of the cell infiltrate was different and, most importantly, infiltration with immune cells was not increased in TC-1/dB2m tumors after immunotherapy. Therefore, the TC-1/dB2m cell line represents a clinically relevant tumor model that may be used for enhancement of cancer immunotherapy.

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Section: Discussionmentioning

confidence: 99%

Establishment and characterization of a mouse tumor cell line with irreversible downregulation of MHC class I molecules

et al. 2019

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Role of macrophages in the host response to Lewis lung peritoneal carcinomatosis

Barth

Morahan

1994

Cancer Immunol Immunother

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Lewis lung (3LL) peritoneal carcinomatosis elicits a complex host response in the peritoneal compartment. The response was delayed, showing few inflammatory cells through day 6 after lethal challenge with 3LL cells. Responses began in about half the mice on day 7 and had appeared in all mice by day 11. On day 7, some mice still showed no detectable 3LL growth in the pertioneal lavage fluid, and no differences in the peritoneal cell populations as compared with the control group. Other tumor-bearing mice, however, had evidence of 3LL cells and hemorrhagic ascites in the peritoneal compartment, with increased numbers of peritoneal macrophages (PM) and polymorphonuclear neutrophils (PMN). By day 11, all tumor-bearing mice had 3LL growth and hemorrhagic ascites. On days 7-11, there was a major influx of macrophages with a later influx of PMN between days 11 and 14. Two distinct PM populations were detected on day 7 in mice that showed detectable 3LL peritoneal carcinomatosis: resident PM, which did not express the Mac-2 antigen, and recruited PM, which were Mac-2+. At least some resident PM remained in the peritoneal compartment through day 14. Analysis of the kinetics of the cytotoxic capabilities of PM from tumor-bearing mice showed that by day 7 macrophages were able to kill the B16 melanoma tumor target, but not the 3LL target. The PM, however, were able to be activated further to kill the 3LL target by treatment in vitro with lipopolysaccharide and interferon gamma. No inhibition of PM tumoricidal activity could detected in the peritoneal wash of tumor-bearing mice. A lack of activation of PM from 3LL tumor-bearing mice may be involved in progression of peritoneal carcinomatosis.

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Chapter 39 Cell Preparation for the Identification of Leukocytes

Stewart

1990

Flow Cytometry

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Quantitation of the Host Cell Infiltration Kinetics of the Nonimmunogenic Colon 26 Tumor by Multiparameter Flow Cytometry

Cited by 5 publications

References 16 publications

Establishment and characterization of a mouse tumor cell line with irreversible downregulation of MHC class I molecules

Establishment and characterization of a mouse tumor cell line with irreversible downregulation of MHC class I molecules

Role of macrophages in the host response to Lewis lung peritoneal carcinomatosis

Chapter 39 Cell Preparation for the Identification of Leukocytes

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