## 4 Discussion  
Currently, HSPs are under intensive investigation. In clinical models heat shock proteins, alone or in a complex with tumour-derived peptides, have been shown to elicit an anti-tumour response in cancer patients. HSPs can act as common tumour-specific antigens as well as adjuvants that facilitate the uptake, processing and presentation of antigens. Due to their immunogenic properties, they are used in autologous tumour-derived HSP peptide-based vaccines [1]. \(\gamma\delta\) T cells represent a small subset of the T cells in peripheral blood. Despite this, they are considered to be good candidates for effective antitumor therapy [4]. \(\gamma\delta\) T cells  
Figure 2: Decreased concentration of CD3 + HLA/DR+ \(\gamma\delta\) T cells among patients at disease presentation compared to the concentration of the lymphocytes after induction. \begin{table}
\begin{tabular}{c c c c c c c c c} \hline \hline
**Research Group** & \multicolumn{4}{c}{**Research Group after Chemotherapy**} & \multicolumn{4}{c}{**Control Group**} \\
**Chemotherapy** & & & & & & & & \\ \hline \multirow{3}{*}{CD3 + \(\gamma\delta\) T cells} & CD3 + \(\gamma\delta\) T cells & CD4 + \(\gamma\delta\) T cells & CD8 + \(\gamma\delta\) T cells & CD3 + \(\gamma\delta\) T cells & CD4 + \(\gamma\delta\) T cells & CD8 + \(\gamma\delta\) T cells & T cells & CD8 + \(\gamma\delta\) T cells & T cells \\ \hline \hline CD3 + \(\gamma\delta\) T cells & 0.87 & & & & 0.08 * & & & \\ \hline CD3 + HLA/DR + \(\gamma\delta\) T cells & 0.029 & & & & 0.026 & & & \\ \hline CD4 + \(\gamma\delta\) T cells & & & 0.57 & & & & 0.51 * & \\ \hline CD8 + \(\gamma\delta\) T cells & & & 0.39 & & & & 0.93 * \\ \hline \hline \end{tabular}  
* results not described in the main text.  
\end{table} 
Table 3: The results of statistical tests regarding the comparison of \(\gamma\delta\) T cells in two time points in the research group (Wilcoxon test) and between the research and study group ([PERSON] test). can recognize a wide variety of structurally different ligands including phosphoantigens, aminobisphosphonates, alkylamines and several self-proteins such as HSPs, that can be detected without a presentation by other cells or molecules [12]. Activated (CD3+ HLA/DR+) \(\gamma\delta\) T cells secrete cytokines, which influence the tumour microenvironment and involve IFN-\(\gamma\) inhibiting tumour growth, blocking angiogenesis and macrophage stimulation [4]. In the 90s the correlation between HSPs and \(\gamma\delta\) T cells was extensively studied following the report demonstrating that murine \(\gamma\delta\) T cells could be stimulated with HSP65 from mycobacterial extracts, which results in the induction of cytotoxic immune response against affected host cells. It has been reported that a similar mechanism can also take part in the elimination of cancer cells [13, 14]. [PERSON] et al. showed that V\(\gamma\)9V82 T cells recognize HSPs on oral tumour cells and [PERSON] et al. on oesophageal tumour targets [15, 16]. Increased cytotoxicity of \(\gamma\delta\) T lymphocytes has been demonstrated relative to cell lines expressing HSPs [17]. Despite years of research, the specific mechanisms of interaction remain enigmatic, while the targeting of \(\gamma\delta\) T cells by HSPs seems to be a forgotten direction because potent non-peptide phosphoantigens rather than HSPs have been found to be the essential stimulatory components of mycobacterial extracts for human V\(\gamma\)9V82 [18]. The most popular trend in cancer immunotherapy based on \(\gamma\delta\) T cells is focused on the stimulation of cells by the systemic administration of phosphoantigens, nitrogen-containing bisphosphonates (N-bis) or synthetic phosphoagonist bromohydrin pyrophosphate (BrH-PP). Despite the proven safety of \(\gamma\delta\) T cells immunotherapy, its clinical benefit remains an issue.