CD4 T Cells Treated with gp120 Acquire a CD45R0+/CD45RA+ Phenotype

Sergey A Trushin1, 2, Gary D Bren1, Andrew D Badley*, 1, 2
1 Division of Infectious Diseases, Mayo Clinic, Rochester, MN 55905, USA
2 Program in Translational Immunovirology and Biodefense, Mayo Clinic, Rochester, MN 55905, USA

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© Trushin et al.; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http: // which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Division of Infectious Diseases, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA; Tel: 507-266-5065; Fax: 507-284-3757; E-mail:


HIV-infected patients exhibit quantitative and qualitative defects in CD4 T cells, including having increased numbers of CD4+CD45R0+/CD45RA+ T cells, although it remains unclear how these cells arise. Here we demonstrate that gp120 treatment of activated but not resting primary human CD4 T cells decreases number of cells with single positive CD45R0+/CD45RA- effector memory phenotype while proportionally increasing the subset of cells with double positive CD45R0+/CD45RA+ mixed phenotype. We found that double positive CD45R0+/CD45RA+CD4 T cells preferentially undergo apoptosis while single positive CD45R0+/CD45RA- and CD45R0-/CD45RA+ do not. Blocking gp120-CD4 interaction with sCD4 or inhibition Lck activity reverses gp120 induced increase in double positive CD45R0+/CD45RA+CD4 T cells and subsequently diminishes the apoptosis of double positive CD45R0+/CD45RA+ cells. Altogether these data indicate that gp120 ligation of the CD4 receptor increases the number of double positive CD45R0+/CD45RA+ CD4 T cells which subsequently undergo apoptosis in a CD4 dependent manner.