Regulatory aspects of clonally expanded B-1 (CD5+B) cells

Raveché, Elizabeth; J, Phillips; Mahboudi, F; Dang, Anju; Fernandes, Helen; Ramachandra, Sumant; Lin, Tao-Zhen; Peng, Bihai

doi:10.1007/bf02591428

Cited by 10 publications

(2 citation statements)

References 157 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Concerning the phenotype of B cell tumors, IgM levels in normal B-1 cells were high in mice, humans and bovine [12,27]. IgM levels were also high in B cell tumors of mice and proliferative B cell chronic lymphocyte leukemia in humans.…”

Section: Discussionmentioning

confidence: 82%

Relation between Phenotype of Tumor Cells and Clinicopathology in Bovine Leukosis

Yin

Makara

Pan

et al. 2003

The Journal of Veterinary Medical Science

View full text Add to dashboard Cite

ABSTRACT. Thirty-three cases of enzootic bovine leukosis (EBL) and 14 cases of sporadic bovine leukosis (SBL) were examined by immunohistochemistry using 6 monoclonal antibodies against leukocyte differentiation molecules of bovine leukocytes. There were 17 cases of B-1a cell type, 10 cases of B-1b cell type and 6 cases of B-2 cell type in EBL, and 5 cases originating from B cells (B-2 cell type) and 9 cases originating from immature T cells in SBL. The average age for the EBL cases of B-1a cell type was 8.6 years, B-1b cell type was 6.5 years, and of B-2 cell type was 4.5 years. In cases of SBL, immature T cell type patients were younger than B-2 ce ll type ones. The lymphoma originating from B cells differed from that originating from T cells in morphology. In T cell tumors, the nucleus of tumor cells was round, the edge of the cytoplasm obvious, and tumor cells were sporadically present and proliferated. When compared with T cells, the region among B cells was obscure. But, there was no relation between phenotype and the histologic classification of tumor cells. In EBL, beyond the lymph node, tumors of B-1a and B-1b types had developed in the heart and abomasum, and those of the B-2 type tended to occur in liver. In SBL, B-2 type and T type cells formed tumors in the liver, kidney, thymus, and one case of T-cell type tumor formed on the skin. We would like to propose a new classification of bovine leukosis as EBL, calf type B-cell lymphoma, juvenile T-cell lymphoma and skin type T-cell lymphoma.

show abstract

Section: Discussionmentioning

confidence: 82%

Relation between Phenotype of Tumor Cells and Clinicopathology in Bovine Leukosis

Yin

Makara

Pan

et al. 2003

The Journal of Veterinary Medical Science

View full text Add to dashboard Cite

show abstract

“…Our laboratory has an ongoing interest in the proliferative disease processes of NZB mice, particularly in the genetic basis of this process (Raveche et al , 1979, 1981, 1988, 1992, 2007; Raveche & Tjio, 1991). The NZB strain is a naturally occurring model of late‐onset CLL (Phillips et al , 1992).…”

Section: The Nzb Model Of Cllmentioning

confidence: 99%

Murine models of chronic lymphocytic leukaemia: role of microRNA‐16 in the New Zealand Black mouse model

Scaglione¹,

Salerno²,

Balan³

et al. 2007

Br J Haematol

View full text Add to dashboard Cite

SummaryMouse models are valuable tools in the study of human chronic lymphocytic leukaemia (CLL). The New Zealand Black (NZB) strain is a naturally occurring model of late-onset CLL characterized by B-cell hyperproliferation and autoimmunity early in life, followed by progression to CLL. Other genetically engineered models of CLL that have been developed include (NZB · NZW) F1 mice engineered to express IL5, mice expressing human TCL1A, and mice overexpressing both BCL2 and a tumour necrosis factor receptor-associated factor. The applicability to human CLL varies with each model, suggesting that CLL is a multifactorial disease. Our work with the de novo NZB model has revealed many similarities to the human situation, particularly familial CLL. In NZB, the malignant clones express CD5, zap-70, and have chromosomal instability and germline Ig sequence. We also identified a point mutation in the 3¢-flanking sequence of Mirn16-1, which resulted in decreased levels of the microRNA, miR-16 in lymphoid tissue. Exogenous restoration of miR-16 to an NZB malignant B-1 cell line resulted in cell cycle alterations, suggesting that the altered expression of Mirn15a/16-1 is an important molecular lesion in CLL. Future studies utilizing the NZB mouse could ascertain the role of environmental triggers, such as low dose radiation and organic chemicals in the augmentation of a pre-existing propensity to develop CLL.Keywords: mouse models of chronic lymphocytic leukaemia, New Zealand Black, microRNA.The development of chronic lymphocytic leukaemia (CLL) in humans is believed to be polygenetic, exhibiting the highest incidence of familial leukaemia, yet emerging from many factors (Ishibe et al, 2001;Caporaso et al, 2004;Sellick et al, 2006). Molecular cytogenetic abnormalities associated with CLL have been reported (Stilgenbauer & Dohner, 2004), and include chromosome duplications (Juliusson et al, 1990;Molica et al, 1995;Dohner et al, 2000) and deletions, particularly 13q14 deletions (Juliusson et al, 1990;Dohner et al, 2000). Mouse models with known genetic backgrounds allow for the development of CLL murine models, which serve as valuable tools, not only in understanding disease mechanisms, but also in evaluating dietary/environmental triggers and efficacy of novel therapies. Mouse models of CLLThis article presents a comparison of several mouse models of CLL (Table I). With the exception of the New Zealand Black (NZB) model, all the models are induced by the expression of exogenous genes. The NZB mouse model of CLL, in contrast, is a de novo model that has been studied extensively as a model to investigate both autoimmune diseases, such as systemic lupus erythematosus (SLE), as well as B-cell lymphoproliferative disorders (Raveche et al, 1981;Manohar et al, 1982;Stall et al, 1988;Theofilopoulos, 1996). Autoreactivity has also been associated with CLL (Lugassy et al, 1992;Barcellini et al, 2006), and the NZB model displays mild autoimmunity that is associated with B-cell hyperactivity, resulting in autoimmune haemolytic anaemia ...

show abstract