Abstract
Invasive nonfunctioning pituitary adenomas (NFPAs) grow rapidly and the mechanisms are unclear. Among many complex mechanisms, the role of immunity in the development of NFPAs has not been fully explored. Here, we analyzed the clinical features 146 NFPA patients who underwent trans-sphenoidal surgery or craniotomy and examined the effects of immune tolerance in invasiveness of NFPA patients using fluorescence-activated cell sorting and immunohistochemical methods. We found patients with invasive NFPAs had more visual deficits and defective fields, higher tumor size, and lower white blood cell count compared with patients with noninvasive NFPAs. Additionally, compared with patients with noninvasive NFPAs, patients with invasive NFPAs had conspicuously lower CD3−CD56+ natural killer (NK) cells and significantly higher levels of CD3+CD8+CD28-T cells (CD8+ Tregs) and interleukin-10 (IL-10) in peripheral blood. Moreover, patients with invasive NFPAs had lower infiltrated CD56+ cells, less infiltrated CD28+ cells, and significantly greater IL-10 expression. These results demonstrated that low CD56+ cells infiltration and CD28+ cells infiltration, as well as high IL-10 expression in pituitary tumor tissues, were related with increased invasiveness of NFPAs. Levels of CD3−CD56+ NK cells, CD8+ Tregs and IL-10 in the peripheral blood could be feasible diagnostic markers for invasive NFPAs.
Highlights
Pituitary adenomas (PAs) account for 10–25% of all intracranial neoplasms [1]
Visual deficits and visual field defects are the most common symptoms in all patients with nonfunctioning pituitary adenomas (NFPAs), they were more common in patients with invasive NFPAs than in patients with noninvasive NFPAs
Our findings indicated that the reduction of natural killer (NK) cells was related with increased invasiveness of NFPAs and may be a useful biomarker of invasive NFPAs As a common subset of tregs, CD8+ tregs that render antigen presenting cells (APC), mainly dendritic cells (DCs), tolerant through cell-cell contact, can secrete IL-10, transforming growth factor (TGF)-β, IFN-γ, CCL4, and directly kill CD4+ effector T cells and APCs
Summary
Pituitary adenomas (PAs) account for 10–25% of all intracranial neoplasms [1]. They are derived from intracranial adenohypophyseal cells and often presented as neurological deficits ( visual impairment), pituitary dysfunction, parasellar compartment invasion and sphenoid sinuses [2]. The majority of PAs are histologically benign, 25–55% of PAs often invade surrounding structures and exhibit malignant behaviors [3, 4]. Neurosurgery resection remains the initial treatment of choice for most PAs. curative radical surgery of invasive PAs remains difficult. Approximately 10–20% PAs are unable to produce active hormone and classified as nonfunctioning pituitary adenomas (NFPAs) [5].
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