Background:  Autologous hematopoietic stem cell transplantation (HSCT) recipients, despite a prolonged period of CD4⁺ T-cell deficiency present low rates of opportunistic infections compared with HIV-infected patients with similar immune-deficit levels. We correlated T-cell phenotype and function in HIV-infected patients and autologous HSCT recipients with comparable CD4⁺ T-cell count.

Methods:  We cross-sectionally studied 5 HIV-infected patients with CD4⁺ median value of 230 cells/mL naïve to ART and free from opportunistic infections; and 5 neoplastic patients receiving autologous HSCT 9 months before observation with actual CD4 median value of 255 cells/mL in absence of opportunistic infections and neoplasia’s relapse. T-cell phenotype (CD45RA, CCR7), intracellular cytokine expression, and lymphocyte proliferative responses were measured. Mann-Whitney test was used for statistical analysis.

Results:  HIV⁺ patients and autologous HSCT recipients were both characterized by a low percentage of naïve and central memory CD4⁺ T cells and a compensative expansion of effector memory (CD45RA^–CCR7^–) CD4 T cells. This phenotypic pattern was associated mainly with interferon-gamma (IFN-g) production and reduced interleukin-2 (IL-2) expression of CD4⁺ T cells in both populations. As for CD8⁺ T-cell distribution, autologous HSCT recipients displayed significantly lower levels of effector memory cells (p <0.05) and the highest levels of effector (CD45RA⁺CCR7^–) CD8⁺ cells (p = 0.05), with a naïve population more represented than the HIV-infected patients. This translates in higher IFN-g⁺CD8⁺ expression in autologous HSCT patients, while HIV⁺ subjects showed higher expression of tumor necrosis factor-alpha (TNF-a) CD8⁺ cells. Analysis of stimulation index revealed low levels of proliferative response for PHA and FLU stimulation in autologous HSCT recipients, comparable to HIV⁺ patients.

Conclusions:  The CD4⁺ T-cell count deficiency in autologous HSCT recipients is associated with a skewed representation of naïve and CM cells and cytokine and proliferative defects, indicating an ineffective T-helper response lasting for almost 9 months after transplantation. The increase in late effector CD8⁺ T cells concordant with a more efficient cytokine production, observed in HSCT recipients, suggest a rapid recovery of CD8⁺ efficient response and a possible role for these cells in preventing actual infections.