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Comparison of gene expression between natural ligand treatment and agonistic antibody treatment in a CD30+ cell line

ABSTRACT: CD30 receptor (TNFRSF8) is highly expressed in some types of lymphoma. CD30 is successfully used as a target for antibody-drug conjugate to treat CD30+ lymphoma. The agonistic activity of the anti-CD30 antibody likely contributes to tumor cell killing. However, not all antibodies exhibit agonistic activity. We found that potent agonistic antibodies recognize the N-terminus epitope cluster that is distantly located from the ligand binding site of CD30. This study compared gene expression profiles between CD30 natural ligand and agonistic antibody T104 treatment in a CD30+ ALCL Karpas 299 cell line.

ORGANISM(S): Homo sapiens

PROVIDER: GSE59174 | GEO | 2025/08/10

REPOSITORIES: GEO

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Gene expression in CD30+ L540 cell line induced by different anti-CD30 antibodies that bind to different epitopes

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Homo sapiens

Project description:Comparison of gene expression between natural ligand treatment and agonistic antibody treatment in a CD30+ cell line

| PRJNA254536 | ENA

Essential role for CD30-Transglutaminase 2 axis in memory Th1 and Th17 cell generation.

Project description:Memory helper T (Th) cells are crucial for secondary immune responses against infectious microorganisms but also drive the pathogenesis of chronic inflammatory diseases. Therefore, it is of fundamental importance to understand how memory T cells are generated. However, the molecular mechanisms governing memory Th cell generation remain incompletely understood. Here, we identified CD30 as a molecule heterogeneously expressed on effector Th1 and Th17 cells, and CD30hi effector Th1 and Th17 cells preferentially generated memory Th1 and Th17 cells. We found that CD30 mediated signal induced Transglutaminase-2 (TG2) expression, and that the TG2 expression in effector Th cells is essential for memory Th cell generation. In fact, Cd30-deficiency resulted in the impaired generation of memory Th1 and Th17 cells, which can be rescued by overexpression of TG2. Furthermore, transglutaminase-2 (Tgm2)-deficient CD4 T cells failed to become memory Th cells. As a result, T cells from Tgm2-deficient mice displayed impaired antigen-specific antibody production and attenuated Th17-mediated allergic responses. Our data indicate that CD30-induced TG2 expression in effector Th cells is essential for the generation of memory Th1 and Th17 cells, and that CD30 can be a marker for precursors of memory Th1 and Th17 cells.

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