Methylcholanthrene causes increased thymocyte apoptosis (Q77114962)

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3 December 2019

title

Methylcholanthrene causes increased thymocyte apoptosis (English)

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3 December 2019

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1

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3 December 2019

author name string

G Browne

series ordinal

2

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3 December 2019

C R Petzold

series ordinal

3

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publication date

1 July 1998

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3 December 2019

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volume

128

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issue

2

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page(s)

151-167

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Tumor necrosis factor: function, release and clearance.

3 December 2019

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Loss of a unique tumor antigen by cytotoxic T lymphocyte immunoselection from a 3-methylcholanthrene-induced mouse sarcoma reveals secondary unique and shared antigens

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Fluorathene induces programmed cell death and alters growth of immature B cell populations in bone marrow cultures

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Perinatal thymocyte antigen expression and postnatal immune development altered by gestational exposure to tetrachlorodibenzo-p-dioxin (TCDD)

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Signaling for death of lymphoid cells

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p53 is required for radiation-induced apoptosis in mouse thymocytes

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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) kills glucocorticoid-sensitive thymocytes in vivo

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2,3,7,8-Tetrachlorodibenzo-p-dioxin kills immature thymocytes by Ca2 -mediated endonuclease activation

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Selective events in T cell development

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bcl-2 inhibits multiple forms of apoptosis but not negative selection in thymocytes

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Dexamethasone, beta-estradiol, and 2,3,7,8-tetrachlorodibenzo-p-dioxin elicit thymic atrophy through different cellular targets

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3-Methylcholanthrene induces differential inhibition of humoral and cell mediated immune responses in mice of different ages

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bcl-2 transgene inhibits T cell death and perturbs thymic self-censorship

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Identifiers

DOI

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3 December 2019

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