Accelerated progression of Hodgkin’s-like lymphomas in golli deficient SJL mice

• Golli KO SJL mice have an accelerated progression of Hodgkin’s like lymphoma.
• CD44highCD62Llow effector/memory CD4+ T cells are accumulated in golli KO lymphoma.
• Upregulation of regulatory cytokines in golli KO lymphoma infiltrated CD4+ T cells.
• Increased Treg cell surface molecules on golli KO lymphoma infiltrated CD4+ T cells.
• Increased IL-10 producing cells in golli KO mice prior to the onset of lymphoma.
• Increased FoxP3+ Treg cells in golli KO mice prior to the onset of lymphoma.
• Higher conversion of FoxP3+ Treg cells from golli KO T cells in vitro.

Spontaneously occurring lymphomas in SJL mice have many pathological features similar to Hodgkin’s lymphoma in humans. The malignant growth of the tumor cells is dependent on the support of host FoxP3+CD4+ regulatory T cells (Tregs). In this study, we report that the ablation of golli protein, a negative regulator of CRAC (calcium release activated calcium) channel, in SJL mice results in an accelerated progression of Hodgkin’s-like lymphoma which is accompanied by a facilitated conversion of FoxP3+ Treg cells. Our results suggest that golli protein might affect the progression of Hodgkin’s-like lymphomas through regulating the induction of Treg cells.