1,721,047 research outputs found
The significance of leucocyte phenotype: a report from the November Meeting of the British Society for Immunology. London, U.K., November 12-13, 1987.
No full texta detailed report a critical assessementt of data presented at the meeting has been provide
Cell-cell and cell-matrix adhesion structures may influence the growth pattern of chronic lymphoid malignancies
No full textNo abstract availabl
CD30 and type 2 T helper (Th2) responses [published erratum appears in J Leukoc Biol 1995 Jun;57(6):978] [see comments]
No full textCD30 is one of the members of the tumor necrosis factor receptor superfamily, originally described as a marker of Reed-Sternberg and Hodgkin's cells in Hodgkin's lymphoma. CD30 appears to be preferentially expressed on, and its soluble form (sCD30) released by, CD4+ and CD8+ T cell clones capable of producing T helper 2 (Th2)-type cytokines. In noneoplastic conditions, CD30+ T cells are barely detectable in vivo; however, a few allergen-specific CD4+CD30+ T cells inducible to the production of Th2-type cytokines could be sorted out from the circulation of allergic subjects after allergen exposure. Moreover, high numbers of CD30+ T cells were found in the lymph node of a patient suffering from Omenn's syndrome, a rare congenital Th2-mediated immunodeficiency disorder. More importantly, high serum levels of sCD30 were observed in some conditions in which a pathogenetic role for Th2 cells has been suggested, such as Omenn's syndrome, atopy, systemic lupus erythematosus, and after infection with measles virus or human immunodeficiency virus. Thus, detection of CD30+ T cells and/or of increased levels of sCD30 may reflect the presence of immune responses or immune alterations characterized by the prevalent activation of Th2-like cells
Immunohistological analysis of Tac antigen expression in tissues involved by Hodgkin's disease
No full textHRS cells in tissue sections of lymph node involved by Hodhkin diseasehave been shown to express the TAC peptide of IL2-receptor molecul
Identification of malignant plasma cell precursors in the bone marrow of multiple myeloma.
No full textPrecursors of plasma cells were studied in the bone marrow of 28 patients with multiple myeloma, plasma cell leukemia, and benign monoclonal gammopathy. Pre-B and B cell populations were analyzed with anti-B monoclonal antibodies corresponding to the clusters standardized at the Leucocyte Typing Workshops in Paris and Boston (CD9, CD10, CD19-22, CD24). In advanced forms of plasma cell malignancies, such as cases of multiple myeloma in stages II and III and of plasma cell leukemia, some cells of lymphoid morphology expressed common acute lymphoblastic leukemia antigen (CALLA, CD10) and HLA-DR, but contained no detectable terminal deoxynucleotidyl transferase enzyme. These CALLA+ cells were absent in benign monoclonal gammopathies. In multiple myeloma, the CALLA+ cells were negative for surface and cytoplasmic immunoglobulins (Ig), and, unlike CALLA+, terminal deoxynucleotidyl transferase (TdT+) pre-B cells in the normal bone marrow also failed to react with antibodies to B cell-associated antigens such as CD9, CD19, CD22, and CD24. The CALLA+, Ig- cells could be regarded as preplasmacytic since, after having been separated and stimulated with the phorbol ester 12-0-tetradecanoyl-phorbol-13 acetate in vitro, they transformed into plasma cells and synthesized the same heavy and light chains as myeloma cells
Hyaline-vascular type of Castleman's disease (angiofollicular lymph node hyperplasia) with monotypic plasma cells. An immunohistochemical study with monoclonal antibodies
No full textA case of angiofollicular lymph node hyperplasia (Castleman's disease) characterized by monotypic (IgG+, lambda+) plasmacytosis is described. Fresh tissue was available and a thorough immunohistochemical analysis of lymphoid and non-lymphoid cells was performed on cryostat sections. Although lymphoid follicles were numerous and exhibited some abnormal features they did not appear part of the monoclonal cell proliferation. Follicular lymphocytes were mixtures of Kappa+ and lambda+ cells. Vessels penetrating within these abnormal follicles expressed reduced levels of FVIII and Leu-M5 antigens and exhibited thicker layer of collagen type IV. The analysis of T-cell subsets showed a normal (3:1) T4/T8 ratio. This case extends to the mixed variant of hyaline-vascular Castleman's disease, the neoplastic potential previously associated to the plasma cell variant of the disease
An erythroid specific nuclear factor binding to the proximal CACCC box of the beta-globin gene promoter
Full text linkLPR mice with Toll-IL-1 Receptor 8 deficiency are prone to develop B-cell lymphomas
No full textPURPOSE: The association among autoimmunity, chronic inflammation and malignancy has been described and confirmed by epidemiological studies. Notwithstanding these achievements, the molecular mechanisms underlying this association are still unknown. Several evidences suggest that patients suffering from different autoimmune diseases are prone to develop B-cell Non-Hodgkin’s Lymphomas. We investigated the role of Tir8 gene, already known to be associated with autoimmunity, in the development of lymphoma. Indeed, the ability to dampen signaling from IL-1R and TLR family members confers TIR8/SIGIRR the ability to act as regulator of inflammation, cancer-related inflammation and autoimmunity.
METHODS: B6lpr/lpr and B6lpr/lpr/Tir8−/− mice were followed up to 16 month of age and the mortality was reported. Histopathological and immunohistochemical analysis were performed on different tissues and organs of the mice. IgH gene rearrangement was investigate by Southern blot and PCR on gDNA from different organs of the mice. Transplantation in SCID mice of cells from B6lpr/lpr and B6lpr/lpr/Tir8−/− mice was performed.
RESULTS: Both strains developed Diffuse Large B-Cell Lymphoma (DLBCL) during their late age, but in B6lpr/lpr/Tir8−/− mice DLBCL occurred earlier and were more aggressive, with significantly higher mortality. Histopathologic analysis of spleen and lymph nodes of B6lpr/lpr/Tir8−/− mice documented clear-cut DLBCL areas arising within a context of atypical lymphoproliferative disorder; these results were corroborated by both molecular analysis and transplantation experiments.
DISCUSSION AND CONCLUSIONS: These observations unveil a role of TIR8 in the occurrence and development of DLBCL, suggesting its potential role in targeted therapy. Moreover, the B6lpr/lpr/Tir8−/− mouse could be a model to establish and evaluate studies of novel therapeutic protocols in DLBCL.
BIBLIOGRAPHY:
Garlanda et al. 2004, PNAS
Lech et al. 2007, J Exp Med
Bertilaccio et al. 2011, Bloo
A novel Rag2-/- c-/--xenograft model of human CLL
No full textEasily reproducible animal models that allow for study of the biology of chronic lymphocytic leukemia (CLL) and to test new therapeutic agents have been very difficult to establish. We have developed a novel transplantable xenograft murine model of CLL by engrafting the CLL cell line MEC1 into Rag2(-/-)gamma(c)(-/-) mice. These mice lack B, T, and natural killer (NK) cells, and, in contrast to nude mice that retain NK cells, appear to be optimal recipient for MEC1 cells, which were successfully transplanted through either subcutaneous or intravenous routes. The result is a novel in vivo model that has systemic involvement, develops very rapidly, allows the measurement of tumor burden, and has 100% engraftment efficiency. This model closely resembles aggressive human CLL and could be very useful for evaluating both the biologic basis of CLL growth and dissemination as well as the efficacy of new therapeutic agents
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