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Published on: June 23, 2011
Different proliferative response of human and chimpanzee lymphocytes after contact with human immunodeficiency virus
A M Di Rienzo1, G Furlini, R Olivier
1Department of Retroviruses, Institut Pasteur, Paris.
Insights
Recombinant gp120 protein induces T cell anergy, a state of unresponsiveness, in human lymphocytes. This gp120-induced anergy, which halts cell cycle progression, was not observed in chimpanzee lymphocytes, suggesting its role in human immunodeficiency virus (HIV) pathogenesis.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- T cell functional defects are characteristic of human immunodeficiency virus (HIV) infection.
- Indirect mechanisms contributing to CD4+ T cell depletion are suspected.
- Lymphocyte unresponsiveness to HIV particles or proteins is documented but poorly understood.
Purpose of the Study:
- To investigate the role of recombinant gp120 in inducing T cell anergy.
- To characterize the effects of gp120-induced anergy on lymphocyte proliferation and cell cycle progression.
- To compare the response of human and chimpanzee lymphocytes to gp120.
Main Methods:
- Incubation of human T helper lymphocytes with recombinant gp120 and various stimuli (IL-2, IL-4, IL-6, anti-CD2, anti-CD3, PMA).
- Assessment of lymphocyte proliferative responses.
- Analysis of cell cycle phase distribution in anergic versus control cells.
- Incubation of chimpanzee lymphocytes with gp120 and assessment of proliferation.
Main Results:
- Recombinant gp120 induced anergy in human T helper lymphocytes, inhibiting responses to multiple stimuli.
- Anergic cells exhibited altered cell cycle distribution, indicating a pre-mitotic block.
- Chimpanzee lymphocytes preincubated with gp120 did not display anergy.
Conclusions:
- gp120 is capable of inducing T cell anergy in humans.
- Anergy may contribute to CD4+ T cell depletion and pathogenesis in HIV infection.
- The absence of gp120-induced anergy in chimpanzees may explain their resistance to immunodeficiency.
Abstract:
T cell functional defects are a common aspect of human immunodeficiency virus (HIV) infection. Moreover, it has been suggested that indirect mechanisms are involved in CD4+ cell depletion. Unresponsiveness to proliferative stimuli of lymphocytes incubated with HIV particles or with viral proteins is well documented. Nevertheless, drawing a clear picture of the anergy phenomenon is difficult because of several unresolved and controversial questions. Here we report that recombinant gp120 induces anergy in T helper lymphocytes cultured with different stimuli. The proliferative responses to interleukin (IL)-2, IL-4, IL-6, anti-CD2, anti-CD3 and phorbol 12-myristate 13-acetate are inhibited. Moreover, anergic cells show a different distribution in cell cycle phases as compared to control cells, leading us to suggest that the progression in the cell cycle is hampered and that a pre-mitotic block takes place. Furthermore, since chimpanzees are susceptible to HIV-1 infection without showing immunodeficiency signs, we analyzed the proliferation of chimpanzee lymphocytes without observing anergy in cells preincubated with gp120. Taken together, these results support the hypothesis that anergy plays an important role in HIV infection in vivo.
