HIV-1 infection impairs cell cycle progression of CD4+ T cells without affecting early activation responses
SF Sieg, CV Harding… - The Journal of Clinical …, 2001 - Am Soc Clin Investig
SF Sieg, CV Harding, MM Lederman
The Journal of Clinical Investigation, 2001•Am Soc Clin InvestigFailure of CD4+ T cells to proliferate in response to antigenic stimulation is a characteristic of
HIV infection. Analysis of the proliferation defect has been hampered by an inability to
identify CD4+ cells with T cell receptor specificity for antigen. To focus only on cells that had
been stimulated through the T cell receptor, CD4+ T cells were stimulated with an anti-Vβ3
Ab that activates approximately 3–5% of peripheral blood T cells. This approach revealed
proliferation defects in cells from HIV-infected patients that were not appreciated using anti …
HIV infection. Analysis of the proliferation defect has been hampered by an inability to
identify CD4+ cells with T cell receptor specificity for antigen. To focus only on cells that had
been stimulated through the T cell receptor, CD4+ T cells were stimulated with an anti-Vβ3
Ab that activates approximately 3–5% of peripheral blood T cells. This approach revealed
proliferation defects in cells from HIV-infected patients that were not appreciated using anti …
Failure of CD4+ T cells to proliferate in response to antigenic stimulation is a characteristic of HIV infection. Analysis of the proliferation defect has been hampered by an inability to identify CD4+ cells with T cell receptor specificity for antigen. To focus only on cells that had been stimulated through the T cell receptor, CD4+ T cells were stimulated with an anti-Vβ3 Ab that activates approximately 3–5% of peripheral blood T cells. This approach revealed proliferation defects in cells from HIV-infected patients that were not appreciated using anti-CD3 Ab stimulation and provided the capacity to examine responses on a single cell basis. After anti-Vβ3 Ab stimulation, CD4+Vβ3+ cells from HIV-infected patients demonstrated defects in expression of cell cycle–associated proteins, D-type cyclins, and cyclin A. However, the expression of early activation markers, CD69 and CD25, was not significantly impaired in cells from most patients. Thus, CD4+ T cell proliferation failure in HIV disease is characterized by dysregulated activation that precludes cell cycle progression. This proliferation defect was most apparent in patients with diminished CD4+ T cell numbers and higher plasma HIV RNA levels. CD4+ T cell proliferation failure may be a key determinant of immune impairment in HIV disease.
![](/https/scholar.google.com/scholar/images/qa_favicons/ww.jci.org.png)
Showing the best result for this search. See all results