Transgene-mediated hyper-expression of IL-5 inhibits autoimmune disease but increases the risk of B cell chronic lymphocytic leukemia in a model of murine lupus

2004 ◽  
Vol 34 (10) ◽  
pp. 2740-2749 ◽  
Author(s):  
Xiangshu Wen ◽  
Danqing Zhang ◽  
Yuji Kikuchi ◽  
Yi Jiang ◽  
Kazuhiro Nakamura ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Autoimmune Disease ◽  
B Cell ◽  
Lymphocytic Leukemia ◽  
Murine Lupus ◽  
Cell Chronic Lymphocytic Leukemia

Susceptibility Alleles for Aberrant B-1 Cell Proliferation Involved in Spontaneously Occurring B-Cell Chronic Lymphocytic Leukemia in a Model of New Zealand White Mice

Blood ◽  
1998 ◽  
Vol 92 (10) ◽  
pp. 3772-3779
Author(s):  
Yoshitomo Hamano ◽  
Sachiko Hirose ◽  
Akinori Ida ◽  
Masaaki Abe ◽  
Danqing Zhang ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Autoimmune Disease ◽  
B Cell ◽  
Genetic Alterations ◽  
Lymphocytic Leukemia ◽  
Chromosome 17 ◽  
Mouse Strains ◽  
Autoantibody Production ◽  
Age Related ◽  
Cell Chronic Lymphocytic Leukemia

B-cell chronic lymphocytic leukemia (B-CLL) and autoimmune disease are a related event, and genetic factors are linked to both diseases. As B-CLL is mainly of B-1 cell type that participates in autoantibody production, genetically-determined regulatory abnormalities in proliferation and/or differentiation of B-1 cells may determine their fate. We earlier found that, in H-2–congenic (NZB × NZW) F1 mice, while H-2d/z heterozygosity predisposes to autoimmune disease, H-2z/z homozygosity predisposes to B-CLL. Studies also suggested the involvement of non–H-2-linked NZW allele(s) in leukemogenesis. Using H-2–congenic NZW and B10 mouse strains, their F1 and backcross progeny, we have now identified three major NZW susceptibility loci for abnormal proliferation of B-1 cells, which form the basis of leukemogenesis; one H-2–linked locus on chromosome 17 and the other two non–H-2-linked loci, each on chromosome 13 and chromosome 17. Each susceptibility allele functioned independently, in an incomplete dominant fashion, the sum of effects determining the extent of aberrant B-1 cell frequencies. The development of leukemia was associated with age-related increase in B-1 cell frequencies in the blood. Thus, these alleles probably predispose B-1 cells to accumulate genetic alterations, giving rise to B-CLL. Potentially important candidate genes and correlation of the findings with autoimmune disease are discussed.

Susceptibility Alleles for Aberrant B-1 Cell Proliferation Involved in Spontaneously Occurring B-Cell Chronic Lymphocytic Leukemia in a Model of New Zealand White Mice

Blood ◽  
1998 ◽  
Vol 92 (10) ◽  
pp. 3772-3779 ◽  
Author(s):  
Yoshitomo Hamano ◽  
Sachiko Hirose ◽  
Akinori Ida ◽  
Masaaki Abe ◽  
Danqing Zhang ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Autoimmune Disease ◽  
B Cell ◽  
Genetic Alterations ◽  
Lymphocytic Leukemia ◽  
Chromosome 17 ◽  
Mouse Strains ◽  
Autoantibody Production ◽  
Age Related ◽  
Cell Chronic Lymphocytic Leukemia

Abstract B-cell chronic lymphocytic leukemia (B-CLL) and autoimmune disease are a related event, and genetic factors are linked to both diseases. As B-CLL is mainly of B-1 cell type that participates in autoantibody production, genetically-determined regulatory abnormalities in proliferation and/or differentiation of B-1 cells may determine their fate. We earlier found that, in H-2–congenic (NZB × NZW) F1 mice, while H-2d/z heterozygosity predisposes to autoimmune disease, H-2z/z homozygosity predisposes to B-CLL. Studies also suggested the involvement of non–H-2-linked NZW allele(s) in leukemogenesis. Using H-2–congenic NZW and B10 mouse strains, their F1 and backcross progeny, we have now identified three major NZW susceptibility loci for abnormal proliferation of B-1 cells, which form the basis of leukemogenesis; one H-2–linked locus on chromosome 17 and the other two non–H-2-linked loci, each on chromosome 13 and chromosome 17. Each susceptibility allele functioned independently, in an incomplete dominant fashion, the sum of effects determining the extent of aberrant B-1 cell frequencies. The development of leukemia was associated with age-related increase in B-1 cell frequencies in the blood. Thus, these alleles probably predispose B-1 cells to accumulate genetic alterations, giving rise to B-CLL. Potentially important candidate genes and correlation of the findings with autoimmune disease are discussed.

Abnormal Intracellular Level of Bax in CD3 + Cells from Untreated B-Cell Chronic Lymphocytic Leukemia Patients

2006 ◽  
Vol 12 (4) ◽  
pp. 187-192
Author(s):  
F. Scamardella ◽  
M. Maconi ◽  
L. Albertazzi ◽  
B. Gamberi ◽  
L. Gugliotta ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Lymphocytic Leukemia ◽  
Intracellular Level ◽  
Cell Chronic Lymphocytic Leukemia

Cutaneous leukocytoclastic vasculitis in B-cell chronic lymphocytic leukemia patients

2019 ◽  
Vol 154 (5) ◽  
Author(s):  
Alessandro Pileri ◽  
Carlotta Baraldi ◽  
Alessandro Broccoli ◽  
Roberto Maglie ◽  
Annalisa Patrizi ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Leukocytoclastic Vasculitis ◽  
Lymphocytic Leukemia ◽  
Cell Chronic Lymphocytic Leukemia

scholarly journals Relation of Gene Expression Phenotype to Immunoglobulin Mutation Genotype in B Cell Chronic Lymphocytic Leukemia

2001 ◽  
Vol 194 (11) ◽  
pp. 1639-1648 ◽  
Author(s):  
Andreas Rosenwald ◽  
Ash A. Alizadeh ◽  
George Widhopf ◽  
Richard Simon ◽  
R. Eric Davis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Germ Line ◽  
Gene Expression Signature ◽  
Lymphocytic Leukemia ◽  
Common Mechanism ◽  
Human Leukemia ◽  
Mutational Status ◽  
Cell Chronic Lymphocytic Leukemia

The most common human leukemia is B cell chronic lymphocytic leukemia (CLL), a malignancy of mature B cells with a characteristic clinical presentation but a variable clinical course. The rearranged immunoglobulin (Ig) genes of CLL cells may be either germ-line in sequence or somatically mutated. Lack of Ig mutations defined a distinctly worse prognostic group of CLL patients raising the possibility that CLL comprises two distinct diseases. Using genomic-scale gene expression profiling, we show that CLL is characterized by a common gene expression “signature,” irrespective of Ig mutational status, suggesting that CLL cases share a common mechanism of transformation and/or cell of origin. Nonetheless, the expression of hundreds of other genes correlated with the Ig mutational status, including many genes that are modulated in expression during mitogenic B cell receptor signaling. These genes were used to build a CLL subtype predictor that may help in the clinical classification of patients with this disease.

scholarly journals A 58‐year‐old man with B‐cell chronic lymphocytic leukemia and multiple strokes

2021 ◽  
Author(s):  
Francesca Magrinelli ◽  
Sara Mariotto ◽  
Gianpaolo Nadali ◽  
Giuseppe Todeschini ◽  
Massimiliano Lanzafame ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Cell ◽  
Lymphocytic Leukemia ◽  
Cell Chronic Lymphocytic Leukemia
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