Immune Microenvironment of Primary and Recurrent Craniopharyngiomas: A Study of the Differences and Clinical Significance

Abstract

Objective: This study explored the differences between the immune microenvironments of primary and recurrent craniopharyngiomas (CPs). In addition, we investigated the relationship between the immune microenvironment and clinical characteristics of CP.

Methods: We collected 52 specimens from 26 patients with CPs. For each patient, specimens for both primary and recurrent CPs were obtained. We performed an immunohistochemical analysis of these specimens to determine the distributions of M2 macrophages, CD8+ T cells, programmed cell death 1 ligand 1 (PD-L1), and Ki67.

Results: In recurrent CP specimens, the distributions of M2 macrophages, Ki67, and PD-L1 increased compared with primary CP specimens (P = 0.019, P = 0.0084, and P = 0.0319, respectively). Moreover, the distributions of M2 macrophages, CD8+ T cells, and PD-L1 in papillary CPs were higher than those observed in adamantinomatous craniopharyngiomas (ACPs) (P = 0.0317, P = 0.0359, and P < 0.0001, respectively). In the adult ACP group, M2 macrophages, CD8+ T cells, and PD-L1 were more abundant/expressed than in the child ACP group (P = 0.0159, P = 0.0215, and P < 0.0088, respectively). A positive correlation was found between M2 macrophages and CD8+ T cells (r = 0.4079; P = 0.0027). Correspondingly, M2 macrophages and CD8+ T cells were both positively correlated with PD-L1 (r = 0.4564; P = 0.0007 and r = 0.3987; P = 0.0034, respectively). The observed high expression of M2 macrophages in primary CPs suggests a shortened time for tumor recurrence (P = 0.0131).

Conclusions: The microenvironment of recurrent CP varies from that of primary CP. The abundance of M2 macrophages in primary CP may indicate a risk of early recurrence. Therefore, it is recommended to increase the frequency of follow-up examinations in these patients.

Keywords: CD8+ T cell; Craniopharyngioma; Immune microenvironment; Ki67; M2 macrophages; Programmed cell death 1 ligand 1.