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La prise en charge des lymphomes T cutanés primitifs tels que le mycosis fongoïde (MF) et le syndrome de Sézary (SS) reste difficile. Le récepteur type 2 du facteur de nécrose tumorale α (TNFR2), dont le rôle est de favoriser la prolifération cellulaire, semble une cible prometteuse pour le développement de thérapies ciblées. En effet, dans certains contextes tumoraux, TNFR2 peut être exprimé sur les cellules tumorales leur octroyant ainsi un avantage de survie. Notre objectif était d’évaluer l’expression de TNFR2 chez un grand nombre de patients atteints de lymphome T périphérique, y compris SS et MF, afin de distinguer les candidats à une stratégie thérapeutique ciblant le TNFR2.

The immunosuppressive phenylalanine oxidase interleukin 4-induced gene 1 (IL4I1), primarily produced by antigen-presenting cells, inhibits T-cell proliferation and promotes the generation of Foxp3+regulatory T cells in vitro.Highly expressed by tumour-associated macrophages from human cancers, IL4I1 has a potential role in immune evasion from the anti-tumour immune response. We have reviewed single-nucleotide polymorphisms (SNPs) and mutations described for the exon 4 of the IL4I1 isoform 1, which is expressed in lymphoid tissue. Two of them were expressed in an exogenous system to analyse their effect on the enzymatic activity. The N92D SNP leads to a hyperactive enzyme, while the R102G mutation is hypomorphic. Moreover, we show that IL4I1 activity is not only directed against phenylalanine, as initially described, but also at a lower level against arginine. These data pave the way to more extensive analyses of the mutational state of IL4I1 in pathological conditions such as cancer, where its participation in immune system dysfunctions may have therapeutic implications.