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TBET‐expressing Th1 CD4 + T cells accumulate in chronic lymphocytic leukaemia without affecting disease progression in Eµ‐TCL1 mice
Author(s) -
Roessner Philipp M.,
Hanna Bola S.,
Öztürk Selcen,
Schulz Ralph,
Llaó Cid Laura,
Yazdanparast Haniyeh,
Scheffold Annika,
Colomer Dolors,
Stilgenbauer Stephan,
Lichter Peter,
Seiffert Martina
Publication year - 2020
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/bjh.16316
Subject(s) - adoptive cell transfer , immunology , biology , bone marrow , chronic lymphocytic leukemia , population , cancer research , t cell , leukemia , medicine , immune system , environmental health
Summary Chronic lymphocytic leukaemia (CLL) is associated with alterations in T cell number, subset distribution and function. Among these changes, an increase in CD4 + T cells was reported. CD4 + T cells are a heterogeneous population and distinct subsets have been described to exert pro‐ and anti‐tumour functions. In CLL, controversial reports describing the dominance of IFNγ‐expressing Th1 T cells or of IL‐4‐producing Th2 T cells exist. Our study shows that blood of CLL patients is enriched in Th1 T cells producing high amounts of IFNγ. Moreover, we observed that their frequency remains relatively stable in CLL patients over a time course of five years. Furthermore, we provide evidence for an accumulation of Th1 T cells in the Eµ‐TCL1 mouse model of CLL. As TBET (encoded by Tbx21) is a crucial transcription factor for Th1 polarization, we generated Tbx21 −/− bone marrow chimaeric mice which showed a lower number of IFNγ‐producing Th1 T cells, and used them for adoptive transfer of Eµ‐TCL1 leukaemia. Disease development in these mice was, however, comparable to that in wild‐type controls, excluding a major role for TBET‐expressing Th1 cells in Eµ‐TCL1 leukaemia. Collectively, our data highlight that Th1 T cells accumulate in CLL but reducing their number has no impact on disease development.