NDLI: HIV-1 gp120 Accelerates Fas-Mediated Activation-Induced Human Lamina Propria T Cell Apoptosis

Content Provider	Springer Nature Link
Author	Boirivant, Monica Viora, Marina Giordani, Luciana Luzzati, Alma L. Pronio, Anna Maria Montesani, Chiara Pugliese, Orsola
Copyright Year	1998
Abstract	Intestinal mucosa represents an important portal of entry of HIV and a site of virus reservoir and active replication. Recently, in HIV patients, an early depletion of intestinal lamina propria T lymphocytes (LPT) has been described. HIV-1 gp120 has been demonstrated to promote apoptosis in noninfected isolated peripheral blood T cells, therefore we investigated whether gp120 modulates apoptosis of normal human intestinal lamina propria T cells. Purified T cells were obtained by immunomagnetic negative selection from human lamina propria mononuclear cells isolated from surgical specimens by enzymatic procedure. Cells were incubated with or without recombinant gp120 (10 μg/ml) and cultured either in the absence of any stimulus or in the presence of plate-bound anti-CD3 Ab (OKT3) or soluble anti-CD2 Ab (T11$_{2}$ + T11$_{3}$). Apoptosis was assessed by flow cytometric analysis after propidium iodide staining. We demonstrated that preincubation of normal LPT cells with HIV-1 gp120 accelerates the apoptosis observed during CD2-pathway stimulation of LPT cells. This process is mediated by Fas/Fas ligand interaction and related to an increased induction of Fas ligand mRNA by gp120. Therefore HIV-1 gp120 could contribute to the depletion of noninfected LPT cells inducing a premature cell death.
Starting Page	39
Ending Page	47
Page Count	9
File Format	PDF
ISSN	02719142
Journal	Journal of Clinical Immunology
Volume Number	18
Issue Number	1
e-ISSN	15732592
Language	English
Publisher	Kluwer Academic Publishers-Plenum Publishers
Publisher Date	1998-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Immunology Medical Microbiology Internal Medicine Infectious Diseases
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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