کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5665690 | 1591296 | 2017 | 6 صفحه PDF | دانلود رایگان |
- The mutational landscape in B-NHL can be mechanistically assessed in murine models.
- Murine models can mimic the etiology and evolution of human B-NHL in vivo.
- Authentic murine models for B-NHL are a crucial tool in pre-clinical studies.
The germinal center (GC) reaction is an adaptive immune response to select B cells bearing high-affinity B cell receptors (BCRs) to undergo further differentiation into antibody-producing cells or memory B cells. To drive affinity maturation, (GC) B cells undergo rounds of hypermutation and rapid proliferation, which can enhance susceptibility to malignant transformation. Lymphomas frequently originate from GC B cells, but the etiology for most lymphoma subtypes is unknown. Work in the past decade has more fully documented the mutational landscape in lymphomas, but the impact of these genomic lesions is often difficult to ascertain. In addition, while mutations affecting BCR signaling are well studied, the impact of extrinsic microenvironmental factors has not been widely addressed. Murine models are useful tools to study lymphomagenesis and disease progression, as well as potential treatment in a pre-clinical setting. Herein we discuss advances in murine models of lymphoma and how they inform on key characteristics of human lymphomas.
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Journal: Current Opinion in Immunology - Volume 45, April 2017, Pages 31-36