Abstract
The aim of the study was to investigate the relationship between PD‐1 expression on the surface of CD4+ T cells and prognosis of patients with diffuse large B‐cell lymphoma (DLBCL). Sixty patients who were newly diagnosed with DLBCL and 39 healthy controls were enrolled. In CD4+ T cells of DLBCL patients, the median MFI of PD‐1 were 541.5 (range: 348.25–758.75), significantly higher than 250 (range: 211–326) in healthy controls (P < 0.001). The ZAP70, PI3K, and NFAT mRNA expression levels of patients were 0.47, 0.47, and 0.62 times, respectively, of those of the healthy controls (P < 0.05). In patients with the percentage of PD‐1 on CD4+ T cells ≥30.25%, their EFS and OS were significantly lower than patients with PD‐1+ CD4+ T cells <30.25% (P < 0.05). The possible explanation is that high PD‐1 expression on CD4+ cells of DLBCL patients may impair T‐cell function and thus contribute to poor prognosis. There was no relationship between PD‐1 surface expression on CD4+ T cells and PD‐1 expression within the biopsy of tumor microenvironments from DLBCL patients.
Highlights
Diffuse large B-cell lymphoma (DLBCL) is the most common form of non-Hodgkin’s lymphoma, accounting for 36.2% of all cases in China [1]
According to the international prognostic index (IPI) score, 26.67% of patients were at low risk (IPI ≤ 1), while medium and high-risk patients accounted for 73.33% of all cases
Recent studies have indicated that anti-PD-1 antibody therapy were effective for patients with refractory and relapsed Hodgkin’s lymphoma, advanced multiple myeloma, and melanoma [12,13,14]
Summary
Diffuse large B-cell lymphoma (DLBCL) is the most common form of non-Hodgkin’s lymphoma, accounting for 36.2% of all cases in China [1]. The most widely used therapy is R-CHOP (rituximab + cyclophosphamide + doxorubicin + vindesine + prednisone) and 50–60% of DLBCL patients achieve complete remission, 30–40% of patients still relapse (~10% of patients with refractory) [2]. PD-1 expression is very low in resting cells, but after cell activation, PD-1 is widely expressed on T lymphocytes, B lymphocytes, NK cells, NK/T cells, and macrophages. PD-1 is an inhibitory molecule of the B7 family and PD-1 overexpression can cause inactivation of T cells via phosphatase SHP1 and SHP2 recruitment, which inhibits the zeta chain accessory protein kinase (ZAP70)/nuclear factor of activated T (NFAT) pathway [3]. PD-1 directly inhibits phosphatidylinositol 3-kinase (PI3K) and the corresponding downstream Akt activity, thereby inhibiting T lymphocyte
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