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© Research
Publication : Blood Advances

Replacing mouse BAFF with human BAFF does not improve B-cell maturation in hematopoietic humanized mice

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Blood Advances - 19 Dec 2017

Lang J, Zhang B, Kelly M, Peterson JN, Barbee J, Freed BM, Di Santo JP, Matsuda JL, Torres RM, Pelanda R

Link to Pubmed [PMID] – 29296925

Blood Adv 2017 Dec;1(27):2729-2741

Hematopoietic humanized mice (hu-mice) have been developed to study the human immune system in an experimental in vivo model, and experiments to improve its performance are ongoing. Previous studies have suggested that the impaired maturation of human B cells observed in hu-mice might be in part due to inefficient interaction of the human B-cell-activating factor (hBAFF) receptor with mouse B-cell-activating factor (mBAFF), as this cytokine is an important homeostatic and differentiation factor for B lymphocytes both in mice and humans. To investigate this hypothesis, we created a genetically engineered mouse strain in which a complementary DNA (cDNA) encoding full-length hBAFF replaces the mBAFF-encoding gene. Expression of hBAFF in the endogenous mouse locus did not lead to higher numbers of mature and effector human B cells in hu-mice. Instead, B cells from hBAFF knock-in (hBAFFKI) hu-mice were in proportion more immature than those of hu-mice expressing mBAFF. Memory B cells, plasmablasts, and plasma cells were also significantly reduced, a phenotype that associated with diminished levels of immunoglobulin G and T-cell-independent antibody responses. Although the reasons for these findings are still unclear, our data suggest that the inefficient B-cell maturation in hu-mice is not due to suboptimal bioactivity of mBAFF on human B cells.

https://www.ncbi.nlm.nih.gov/pubmed/29296925