Key result
Caveolin-1 deficiency in mice is linked to persistent splenomegaly and decreased splenic B cells.
Why the study?
Does Cav1-deficiency or heterozygosity impact the development and composition of lymphoid organs in mice?
Does Cav1-deficiency or heterozygosity impact the development and composition of lymphoid organs in mice?
Caveolin-1 deficiency leads to splenomegaly and age-related B-cell and secondary-follicle atrophy in mice, suggesting a role in maintaining the mature splenic microenvironment.
Suggests Cav1 maintains splenic B-cell niches with aging; hypothesis-generating in mice and leaves open human relevance.
Caveolin-1 (CAV1) is known for its role as both a tumor suppressor and an oncogene, harboring a highly context-dependent role within a myriad of malignancies and cell types. In an immunological context, dysregulation of CAV1 expression has been shown to alter immunological signaling functions and suggests a pivotal role for CAV1 in the facilitation of proper immune responses. Nonetheless, it is still unknown how Cav1 -deficiency and heterozygosity would impact the development and composition of lymphoid organs in mice. Herein, we investigated the impacts of Cav1 -dysregulation on the lymphoid organs in young (12 weeks) and aged (36 weeks) Cav1 + / + , Cav1 + / − , and Cav1 − / − mice. We observed that only Cav1 -deficiency is associated with persistent splenomegaly at all timepoints. Furthermore, no differences in overall body weight were detected (and without sexual dimorphisms). Both aged Cav1 + / − and Cav1 −/− mice present with decreased CD19 + CD22 + B cells and secondary-follicle atrophy, specifically in the spleen, compared with wild-type controls and irrespective of splenomegaly status. Consequently, the demonstrated effects on B cell homeostasis and secondary follicle characteristics prompted our investigation into follicle-derived human B-cell lymphomas. Our investigation points toward CAV1 as a dysregulated protein in follicle-derived B-cell malignancies without harboring a differential expression between more aggressive and indolent hematological malignancies.
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Herek et al. (2018) studied Lymphoid development and splenic microenvironment. Cav1 deficiency and heterozygosity vs. Wild-type (Cav1+/+) mice was evaluated on Splenomegaly and splenic B-cell homeostasis (CD19+CD22+ B cells). Caveolin-1 deficiency is associated with persistent splenomegaly, and both aged Cav1+/- and Cav1-/- mice present with decreased CD19+CD22+ B cells and secondary-follicle atrophy in the spleen.
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