Interleukln-2 inhibits lymphocyte apoptosis in PBMC from HIV-INFECTED patients by blocking down-modulation of Bcl-2

Y. Adachi, N. Ovaizu, S. Than, T. W. McCloskev, Savita G Pahwa

Research output: Contribution to journalArticle

Abstract

H1V+ patients. We have previously reported that peripheral blood mononuclear cells(PBMC) from HIV-infected patients underwent marked spontaneous apoptosis in vitro. In this study, we examined the effect of IL-2 upon culture-induced apoptosis in PBMC from HIV infected patients by flow cy tome try. Here, we report that addition of IL-2 resulted in the reduction of spontaneous apoptosis in patient cells in both CD3+ and CD19lymphocytes. Interestingly, we observed that Bcl-2 expression in patient PBMC decreased rapidly upon in vitro culture while that in PBMC of healthy volunteers was relatively unaffected. The most significant decrease in Bcl-2 expression was noted in the apoptotic cell population. The apoptosis-inhibitory effect of IL-2 was found to be associated with the blocking of this cultureinduced down-modulation of Bcl-2 in patient PBMC. These data provide an experimental rationale for IL-2 therapy in slowing disease progression probably via its ability to block accelerated apoptosis in HIV infection.

Original languageEnglish
JournalFASEB Journal
Volume10
Issue number6
StatePublished - Dec 1 1996
Externally publishedYes

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Lymphocytes
mononuclear leukocytes
Blood Cells
Blood
lymphocytes
apoptosis
Modulation
HIV
Interleukin-2
Apoptosis
interleukin-2
HIV infections
disease course
in vitro culture
HIV Infections
volunteers
Cells
Disease Progression
Healthy Volunteers
cells

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

Interleukln-2 inhibits lymphocyte apoptosis in PBMC from HIV-INFECTED patients by blocking down-modulation of Bcl-2. / Adachi, Y.; Ovaizu, N.; Than, S.; McCloskev, T. W.; Pahwa, Savita G.

In: FASEB Journal, Vol. 10, No. 6, 01.12.1996.

Research output: Contribution to journalArticle

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