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Introduction Traditional approaches to stress management are difficult to learn and to implicate in daily life. Emerging technologies like virtual reality (VR) have become a target of extensive study for recreational and medical purposes. The autonomic nervous system (ANS) plays a crucial role in stress response, post-stress relaxation, and recovery. This study aimed to assess the effect of modified VR intervention on short-term heart rate variability (HRV) and perceived anxiety levels in healthy volunteers affected by moderate stress. The stressors included mental arithmetic tasks. Material and Methods The study involved healthy adults, of both sexes, aged 20 to 60 years, without history of cardiovascular diseases, essential abnormalities on ECG, and with normal or moderate level of situational anxiety. The VR gadgets used in the study were commercially available BoboVR X1 headsets, one with modification for medical applications (Pure Purr technology) and one with none (sham technology). The investigational (Pure Purr) headset with an audio-visual sequence was modified by adding a binaural effect and was synchronised with the tract of respiratory movements and the frequency of heart rate. To track changes in the ANS, participants underwent both electrocardiography (ECG) and measurement of HRV. Results The findings showed a significant increase in parasympathetic activity after 5-minute exposure to the investigational device compared to stress, as shown by high-frequency HRV (499.8 ms2 and 340.5 ms2, p < 0.001). RMSSD for a modified headset was higher (p = 0.02) compared to a sham headset with no modifications (RMSSD difference of 12.3% (2.6% to 23.1%)). The LF/HF ratio, however, was lower (difference of 14.5% (2.6% to 23.1%), p = 0.04). Conclusions These findings suggest that a medical device with pre-installed Pure Purr software had a significant effect on the recovery of the ANS in healthy volunteers affected by moderate stress.

Immune checkpoint inhibitors (ICI) used for cancer immunotherapy were shown to boost the existing anti-tumor immune response by preventing the inhibition of T cells by tumor cells. Antibodies targeting two negative immune checkpoint pathways, namely cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), programmed cell death protein 1 (PD-1), and programmed cell death-ligand 1 (PD-L1), have been approved first for patients with melanoma, squamous non-small cell lung cancer (NSCLC), and renal cell carcinoma. Clinical trials are ongoing to verify the efficiency of these antibodies for other cancer types and to evaluate strategies to block other checkpoint molecules. However, a number of patients do not respond to this treatment possibly due to profound immunosuppression, which is mediated partly by myeloid-derived suppressor cells (MDSC). This heterogeneous population of immature myeloid cells can strongly inhibit anti-tumor activities of T and NK cells and stimulate regulatory T cells (Treg), leading to tumor progression. Moreover, MDSC can contribute to patient resistance to immune checkpoint inhibition. Accumulating evidence demonstrates that the frequency and immunosuppressive function of MDSC in cancer patients can be used as a predictive marker for therapy response. This review focuses on the role of MDSC in immune checkpoint inhibition and provides an analysis of combination strategies for MDSC targeting together with ICI to improve their therapeutic efficiency in cancer patients.

The immune system has many sophisticated mechanisms to balance an extensive immune response. Distinct immunosuppressive cells could protect from excessive tissue damage and autoimmune disorders. Tumor cells take an advantage of those immunosuppressive mechanisms and establish a strongly immunosuppressive tumor microenvironment (TME), which inhibits antitumor immune responses, supporting the disease progression. Myeloid-derived suppressor cells (MDSC) play a crucial role in this immunosuppressive TME. Those cells represent a heterogeneous population of immature myeloid cells with a strong immunosuppressive potential. They inhibit an antitumor reactivity of T cells and NK cells. Furthermore, they promote angiogenesis, establish pre-metastatic niches, and recruit other immunosuppressive cells such as regulatory T cells. Accumulating evidences demonstrated that the enrichment and activation of MDSC correlated with tumor progression, recurrence, and negative clinical outcome. In the last few years, various preclinical studies and clinical trials targeting MDSC showed promising results. In this review, we discuss different therapeutic approaches on MDSC targeting to overcome immunosuppressive TME and enhance the efficiency of current tumor immunotherapies.