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While it is obviously impossible to explain all discrepant reports, we previously found that certain levels of TIGIT and PD-1 expression are characteristic features of lymphatic infiltrations in a wide range of inflamed and cancerous tissue [ 10 ].

We have recently shown that highest physiological TIGIT and PD-1 expression was found in follicular T helper cells residing at the periphery of germinal centers in lymph nodes and tonsils [ 10 ].

Given this consistently high expression levels and because of the easiness to identify follicular T cells, we have used these cells as a reference to compare the variable TIGIT and PD-1 expression of T cells located in other tissue areas. The much less variable expression levels of CD3 in our cancers argue against relevant fixation related variations in tissue immunoreactivity as a possible reason for the observed interindividual TIGIT expression differences.

Biological reasons for the variable expression might include modulation of the immune environment by the Hodgkin and Reed-Sternberg HRS cells or the lymphocytic background itself. Hence, it is tempting to speculate that also the level of TIGIT expression may be influenced by regulatory molecules in a similar way as known from PD That highest TIGIT and PD-1 levels in our current study were also found in a HL subtype with a characteristic follicular architecture suggests an important function of these receptors in dense meshworks of leucocytes.

Highest levels of TIGIT and PD-1 in tightly packed lymphocytic rosettes surrounding the neoplastic cells fits well to the concept of compensatory downregulation of excessive inflammatory reactions through immune checkpoint upregulation [ 34 , 35 ]. Our fluorescent measurement revealed that the TIGIT and PD-1 expression in individual T cells could reach 2 to 4-fold higher levels than those found in normal human tonsils. Another feature of HL is that the tumor cells have developed mechanisms to escape the excessive immune-cell infiltration of the host.

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For example, the cellular landscape of HL is characterized by a paucity of specific cytotoxic T cells and natural killer NK cells [ 37 ]. Much hope is, therefore, put on novel therapeutic strategies modulating the immune system and its response to the disease, particularly in heavily treated relapsed or refractory HL where effective therapies are lacking. After promising results were reported from a first clinical trial [ 5 ] using the PD-1 inhibitor nivolumab in chemotherapy refractory HL, a number of follow up studies have confirmed the potential of immune checkpoint therapy in this disease [ 38 — 41 ].

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Combining immunotherapies is another option to increase response rates. For example, combination of anti-PD-1 and anti-CTLA4 drugs has demonstrated additive efficacy in melanomas, non-small-cell lung cancer and renal cell carcinoma [ 6 , 42 , 43 ].

These findings identify HL as a disease entity where it could be interesting to determine whether TIGIT inhibitors alone or in combination with other immunotherapies and anti-CD30 treatment might be effective. My Profile Logout.

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