TY - JOUR AB - Initially, identified as a Hodgkin lymphoma marker, CD30 was subsequently detected on a subset of human B cells within and around germinal centers (GCs). While CD30 expression is typically restricted to a few B cells, expansion of CD30-expressing B cells occurs in certain immune disorders and during viral infections. The role of CD30 in B cells remains largely unclear. To address this gap in knowledge, we established a conditional CD30-knockin mouse strain. In these mice, B-cell-specific CD30 expression led to a normal B-cell phenotype in young mice, but most aged mice exhibited significant expansion of B cells, T cells and myeloid cells and increased percentages of GC B cells and IgG1-switched cells. This may be driven by the expansion of CD4+ senescence-associated T cells and T follicular helper cells, which partially express CD30-L (CD153) and may stimulate CD30-expressing B cells. Inducing CD30 expression in antigen-activated B cells accelerates the GC reaction and augments plasma cell differentiation, possibly through the posttranscriptional upregulation of CXCR4. Furthermore, CD30 expression in GC B cells promoted the expansion of IgG1-switched cells, which displayed either a GC or memory-like B-cell phenotype, with abnormally high IgG1 levels compared with those in controls. These findings shed light on the role of CD30 signaling in GC B cells and suggest that elevated CD30+ B-cell numbers lead to pathological lymphocyte activation and proliferation. AU - Wang, Y. AU - Rambold, U. AU - Fiedler, P. AU - Babushku, T. AU - Tapken, C.L. AU - Hoefig, K.P. AU - Hofer, T.P. AU - Adler, H. AU - Yildirim, A.Ö. AU - Strobl, L.J. AU - Zimber-Strobl, U. C1 - 72047 C2 - 56518 CY - 5 Dongdan Santiao, Dongchen District, Being, 100005, Peoples R China TI - CD30 influences germinal center B-cell dynamics and the expansion of IgG1-switched B cells. JO - Cell. Mol. Immunol. PB - Chin Society Immunology PY - 2024 SN - 1672-7681 ER - TY - JOUR AU - Adler, B.* AU - Adler, H. C1 - 60988 C2 - 50011 CY - Macmillan Building, 4 Crinan St, London N1 9xw, England SP - 967-968 TI - Type I interferon signaling and macrophages: A double-edged sword? JO - Cell. Mol. Immunol. VL - 19 IS - 9 PB - Nature Publishing Group PY - 2022 SN - 1672-7681 ER - TY - JOUR AU - Vincent-Fabert, C.* AU - Saintamand, A.* AU - David, A.* AU - Alizadeh, M.* AU - Boyer, F.* AU - Arnaud, N.* AU - Zimber-Strobl, U. AU - Feuillard, J.* AU - Faumont, N.* C1 - 55120 C2 - 46233 CY - 5 Dongdan Santiao, Dongchen District, Being, 100005, Peoples R China SP - 412-414 TI - Reproducing indolent B-cell lymphoma transformation with T-cell immunosuppression in LMP1/CD40-expressing mice. JO - Cell. Mol. Immunol. VL - 16 IS - 4 PB - Chin Society Immunology PY - 2019 SN - 1672-7681 ER - TY - JOUR AB - The chemokine receptor CCR7 and its ligands CCL19 and CCL21 guide the homing and positioning of dendritic and T cells in lymphoid organs, thereby contributing to several aspects of adaptive immunity and immune tolerance. In the present study, we investigated the role of CCR7 in the pathogenesis of collagen-induced arthritis (CIA). By using a novel anti-human CCR7 antibody and humanized CCR7 mice, we evaluated CCR7 as a target in this autoimmune model of rheumatoid arthritis (RA). Ccr7-deficient mice were completely resistant to CIA and presented severely impaired antibody responses to collagen II (CII). Selective CCR7 expression on dendritic cells restored arthritis severity and anti-CII antibody titers. Prophylactic and therapeutic treatment of humanized CCR7 mice with anti-human CCR7 mAb 8H3-16A12 led to complete resistance to CIA and halted CIA progression, respectively. Our data demonstrate that CCR7 signaling is essential for the induction of CIA and identify CCR7 as a potential therapeutic target in RA. AU - Moschovakis, G.L.* AU - Bubke, A.* AU - Friedrichsen, M.* AU - Ristenpart, J.* AU - Back, J.W.* AU - Falk, C.S.* AU - Kremmer, E. AU - Förster, R.* C1 - 53927 C2 - 45149 CY - Macmillan Building, 4 Crinan St, London N1 9xw, England SP - 791-799 TI - The chemokine receptor CCR7 is a promising target for rheumatoid arthritis therapy. JO - Cell. Mol. Immunol. VL - 16 IS - 10 PB - Nature Publishing Group PY - 2018 SN - 1672-7681 ER - TY - JOUR AB - It is well accepted that CD8+ T cells play a pivotal role in providing protection against infection with intracellular pathogens and some tumors. In many cases protective immunity is maintained for long periods of time (immunological memory). Over the past years, it has become evident that in order to fulfill these multiple tasks, distinct subsets of effector and memory T cells have to be generated. Until today, however, little is known about the underlying mechanisms of subset differentiation and the timing of lineage fate decisions. In this context, it is of special importance to determine at which level of clonal expansion functional and phenotypical heterogeneity is achieved. Different models for T cell subset diversification have been proposed; these differ mainly in the time point during priming and clonal expansion (prior, during, or beyond the first cell division) when differentiation programs are induced. Recently developed single-cell adoptive transfer technology has allowed us to demonstrate that individual precursor cell still bears the full plasticity to develop into a plethora different T cell subsets. This observation targets the shaping of T cell subset differentiation towards factors that are still operative beyond the first cell division. These findings have important implications for vaccine development, as the modulation of differentiation patterns towards distinct subsets could become a powerful strategy to enhance the efficacy and quality of vaccines. AU - Stemberger, C.* AU - Neuenhahn, M.* AU - Buchholz, V.R.* AU - Busch, D.H. C1 - 850 C2 - 26551 SP - 399-405 TI - Origin of CD8⁺ effector and memory T cell subsets. JO - Cell. Mol. Immunol. VL - 4 IS - 6 PY - 2007 SN - 1672-7681 ER - TY - JOUR AB - It is well accepted that CD8+ T cells play a pivotal role in providing protection against infection with intracellular pathogens and some tumors. In many cases protective immunity is maintained for long periods of time (immunological memory). Over the past years, it has become evident that in order to fulfill these multiple tasks, distinct subsets of effector and memory T cells have to be generated. Until today, however, little is known about the underlying mechanisms of subset differentiation and the timing of lineage fate decisions. In this context, it is of special importance to determine at which level of clonal expansion functional and phenotypical heterogeneity is achieved. Different models for T cell subset diversification have been proposed; these differ mainly in the time point during priming and clonal expansion (prior, during, or beyond the first cell division) when differentiation programs are induced. Recently developed single-cell adoptive transfer technology has allowed us to demonstrate that individual precursor cell still bears the full plasticity to develop into a plethora different T cell subsets. This observation targets the shaping of T cell subset differentiation towards factors that are still operative beyond the first cell division. These findings have important implications for vaccine development, as the modulation of differentiation patterns towards distinct subsets could become a powerful strategy to enhance the efficacy and quality of vaccines. AU - Stemberger, C.* AU - Neuenhahn, M.* AU - Buchholz, V.R.* AU - Busch, D.H. C1 - 4230 C2 - 25033 SP - 399-405 TI - Origin of CD8+ Effector and Memory T Cell Subsets. JO - Cell. Mol. Immunol. VL - 4 IS - 6 PB - Chin. Society of Immunology PY - 2007 SN - 1672-7681 ER -