Burkitt lymphoma with a granulomatous reaction: an M1/Th1‐polarised microenvironment is associated with controlled growth and spontaneous regression

Burkitt lymphoma (BL) is an aggressive B‐cell lymphoma that, in some instances, may show a granulomatous reaction associated with a favourable prognosis and occasional spontaneous regression. In the present study, we aimed to define the tumour microenvironment (TME) in four such cases, two of which regressed spontaneously.

[1]  A. Akarca,et al.  Immune landscape in Burkitt lymphoma reveals M2-macrophage polarization and correlation between PD-L1 expression and non-canonical EBV latency program , 2020, Infectious Agents and Cancer.

[2]  K. Naresh,et al.  Role of Epstein-Barr virus in transformation of follicular lymphoma to diffuse large B-cell lymphoma: a case report and review of the literature , 2019, Haematologica.

[3]  V. Ranzani,et al.  Eomesodermin controls a unique differentiation program in human IL‐10 and IFN‐γ coproducing regulatory T cells , 2018, European journal of immunology.

[4]  J. T. Afshari,et al.  Macrophage plasticity, polarization, and function in health and disease , 2018, Journal of cellular physiology.

[5]  A. Rosenwald,et al.  The clinicopathologic spectrum of mature aggressive B cell lymphomas , 2017, Virchows Archiv.

[6]  V. A. Stewart,et al.  Regulatory T Cells in Endemic Burkitt Lymphoma Patients Are Associated with Poor Outcomes: A Prospective, Longitudinal Study , 2016, PloS one.

[7]  David C Park,et al.  Novel insights into the early histopathogenesis of immunodeficiency‐associated Burkitt lymphoma: a case report of Burkitt microlymphoma arising within HIV lymphadenitis , 2016, Histopathology.

[8]  Burton E. Barnett,et al.  Cutting Edge: B Cell–Intrinsic T-bet Expression Is Required To Control Chronic Viral Infection , 2016, The Journal of Immunology.

[9]  P. Piccaluga,et al.  The cell of origin of Burkitt lymphoma: germinal centre or not germinal centre? , 2016, Histopathology.

[10]  S. Pileri,et al.  Clonality Analysis of Immunoglobulin Gene Rearrangement by Next-Generation Sequencing in Endemic Burkitt Lymphoma Suggests Antigen Drive Activation of BCR as Opposed to Sporadic Burkitt Lymphoma , 2015, American journal of clinical pathology.

[11]  S. Pileri,et al.  Distinct Viral and Mutational Spectrum of Endemic Burkitt Lymphoma , 2015, PLoS pathogens.

[12]  M. Nussenzweig,et al.  Plasmodium Infection Promotes Genomic Instability and AID-Dependent B Cell Lymphoma , 2015, Cell.

[13]  M. Meyerson,et al.  The tumor virus landscape of AIDS-related lymphomas. , 2015, Blood.

[14]  H. Einsele,et al.  Adoptive T-cell therapy with hexon-specific Th1 cells as a treatment of refractory adenovirus infection after HSCT. , 2015, Blood.

[15]  G. Freeman,et al.  Interferon-γ-induced activation of JAK1 and JAK2 suppresses tumor cell susceptibility to NK cells through upregulation of PD-L1 expression , 2015, Oncoimmunology.

[16]  Wenyan Zhang,et al.  HIV-related Burkitt lymphoma with florid granulomatous reaction: an unusual case with good outcome. , 2014, International journal of clinical and experimental pathology.

[17]  Yong-ming Yao,et al.  Macrophage Polarization in Inflammatory Diseases , 2014, International journal of biological sciences.

[18]  B. Kempkes,et al.  Macrophage Polarisation: an Immunohistochemical Approach for Identifying M1 and M2 Macrophages , 2013, PloS one.

[19]  T. Decker,et al.  The regulation of inflammation by interferons and their STATs , 2013, JAK-STAT.

[20]  E. Vigorito,et al.  Epstein-Barr nuclear antigen 1 induces expression of the cellular microRNA hsa-miR-127 and impairing B-cell differentiation in EBV-infected memory B cells. New insights into the pathogenesis of Burkitt lymphoma , 2012, Blood Cancer Journal.

[21]  Graham M. Lord,et al.  T-bet and GATA3 orchestrate Th1 and Th2 differentiation through lineage-specific targeting of distal regulatory elements , 2012, Nature Communications.

[22]  A. Rosato,et al.  The interplay between Epstein-Barr virus and the immune system: a rationale for adoptive cell therapy of EBV-related disorders , 2010, Haematologica.

[23]  Lionel B Ivashkiv,et al.  Cross-regulation of signaling pathways by interferon-gamma: implications for immune responses and autoimmune diseases. , 2009, Immunity.

[24]  N. Shinton.  WHO Classification of Tumors of Hematopoietic and Lymphoid Tissues , 2007 .

[25]  L. Young,et al.  Epstein–Barr virus-encoded EBNA1 regulates cellular gene transcription and modulates the STAT1 and TGFβ signaling pathways , 2007, Oncogene.

[26]  H. Zebroski,et al.  Distinct memory CD4+ T-cell subsets mediate immune recognition of Epstein Barr virus nuclear antigen 1 in healthy virus carriers. , 2007, Blood.

[27]  B. Walker,et al.  Differential targeting and shifts in the immunodominance of Epstein-Barr virus--specific CD8 and CD4 T cell responses during acute and persistent infection. , 2005, The Journal of infectious diseases.

[28]  S. Pileri,et al.  Immunoglobulin gene analysis reveals 2 distinct cells of origin for EBV-positive and EBV-negative Burkitt lymphomas. , 2005, Blood.

[29]  E. Jaffe,et al.  Granulomatous reaction in Burkitt lymphoma: correlation with EBV positivity and clinical outcome. , 2005, The American journal of surgical pathology.

[30]  C. Münz.  Epstein-Barr Virus Nuclear Antigen 1 , 2004, The Journal of experimental medicine.

[31]  E. Haralambieva,et al.  Florid Granulomatous Reaction in Epstein-Barr Virus-positive Nonendemic Burkitt Lymphomas: Report of Four Cases , 2004, The American journal of surgical pathology.

[32]  R. Fåhraeus,et al.  Self-Inhibition of Synthesis and Antigen Presentation by Epstein-Barr Virus-Encoded EBNA1 , 2003, Science.

[33]  P. Kidd.  Th1/Th2 balance: the hypothesis, its limitations, and implications for health and disease. , 2003, Alternative medicine review : a journal of clinical therapeutic.

[34]  S. Stevanović,et al.  Epstein-Barr Nuclear Antigen 1-Specific CD4+ Th1 Cells Kill Burkitt’s Lymphoma Cells1 , 2002, The Journal of Immunology.

[35]  E. Bloemena,et al.  Differential Immunogenicity of Epstein-Barr Virus Latent-Cycle Proteins for Human CD4+ T-Helper 1 Responses , 2001, Journal of Virology.

[36]  Kristi Kincaid,et al.  M-1/M-2 Macrophages and the Th1/Th2 Paradigm1 , 2000, The Journal of Immunology.

[37]  R. Steinman,et al.  Human Cd4+ T Lymphocytes Consistently Respond to the Latent Epstein-Barr Virus Nuclear Antigen Ebna1 , 2000, The Journal of experimental medicine.

[38]  T. Langmann,et al.  Regulation of scavenger receptor CD163 expression in human monocytes and macrophages by pro‐ and antiinflammatory stimuli , 2000, Journal of leukocyte biology.

[39]  L. Frappier,et al.  Human CD8+ T cell responses to EBV EBNA1: HLA class I presentation of the (Gly-Ala)-containing protein requires exogenous processing. , 1997, Immunity.

[40]  P. Cresswell,et al.  Class I processing-defective Burkitt's lymphoma cells are recognized efficiently by CD4+ EBV-specific CTLs. , 1997, Journal of immunology.

[41]  Stefan Imreh,et al.  Inhibition of antigen processing by the internal repeat region of the Epstein–Barr virus nuclear antigen-1 , 1995, Nature.

[42]  E. Jaffe,et al.  Small Noncleaved Cell Lymphoma Associated with Florid Epithelioid Granulomatous Response: A Clinicopathologic Study of Seven Patients , 1993, The American journal of surgical pathology.

[43]  B. Nathwani,et al.  Hodgkin's disease occurring in monocytoid B-cell clusters. , 1991, American journal of clinical pathology.

[44]  Keith E Steele,et al.  Multiplex Immunohistochemistry for Image Analysis of Tertiary Lymphoid Structures in Cancer. , 2018, Methods in molecular biology.

[45]  S. Stevanović,et al.  Adoptive transfer of epstein-barr virus (EBV) nuclear antigen 1-specific t cells as treatment for EBV reactivation and lymphoproliferative disorders after allogeneic stem-cell transplantation. , 2013, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[46]  P. Babál,et al.  Burkitt lymphoma with unusual granulomatous reaction. A case report. , 2011, Ceskoslovenska patologie.

[47]  H. Stein,et al.  T-bet-positive and IRTA1-positive monocytoid B cells differ from marginal zone B cells and epithelial-associated B cells in their antigen profile and topographical distribution. , 2005, Haematologica.

[48]  M. Hansmann,et al.  Monocytoid B-cells occurring in Hodgkin's disease , 2004, Virchows Archiv.

[49]  R. Steinman,et al.  EBNA1-specific CD4+ T cells in healthy carriers of Epstein-Barr virus are primarily Th1 in function. , 2001, The Journal of clinical investigation.