Fas(CD95)/FasL interactions required for programmed cell death after T-cell activation

Article Abstract:

Experimental studies to identify gene products associated with apoptosis due to receptor crosslinking of T-cell hybridomas indicates that Fas ligand is induced and regulated by the receptor crosslinking and the cell-death program is activated by the engagement of Fas by Fas ligand. A soluble Fas-immunoglobulin fusion protein selectively inhibits cell death, while it does not prevent cell activation. Activation-stimulated T-cell death is explained by the death-gene products (Fas and Fas ligand) and their interaction.

T cells

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Protection against Fas-dependent Th1-mediated apoptosis by antigen receptor engagement in B cells

Article Abstract:

The study of the cytotoxic CD4+ Th1-cells induced cell death in B-cells reveals that the B cells are capable of regulating their lifetime and destruction. The cell-death occurs by the process of triggering a Fas-dependent apoptotic pathway by the Th1-cells in the B cells. Extreme levels of sensitivity is exhibited by the CD40-ligand-stimulated B cells towards the pathway triggering while the anti-Ig M-stimulated B cells resisted any influence by the triggering.

Antigens

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Sensitization of T cells to CD95-mediated apoptosis by HIV-1 Tat and gp120

Article Abstract:

The HIV-1 Tat and gp120 speed up the physiological process of activation-induced, CD95-mediated T-cell apoptosis, which may be a pathway to the depletion of CD4+ T-cell in AIDS. The T-cell-receptor- and CD4(gp120)-induced apoptosis are highly sensitive toward the HIV-1 Tat through the upregulation of CD95 ligand expression. The infected and non-infected cells are affected by the Tat.

Physiological aspects, AIDS (Disease), CD4 lymphocytes

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