Leptin signaling protects NK cells from apoptosis during development in mouse bone marrow.

Increasing evidence indicates a role of leptin in immune response, but it remains largely unclear whether leptin signaling is involved in regulating NK cell development in the bone marrow (BM). In this study, we have characterized NK cell differentiation and maturation in the BM of leptin-receptor deficient db/db mice at a prediabetic stage. Although the BM cellularity was similar to the control value, the total number of NK cells was severely reduced in mutant mice.

Natural killer cell degeneration exacerbates experimental arthritis in mice via enhanced interleukin-17 production.

Objective: An altered phenotype and dysfunction of natural killer (NK) cells have been observed in patients with rheumatoid arthritis. The aim of this study was to determine whether dysregulated NK cells contribute to the pathogenesis of experimental arthritis.

Methods: For initiation of collagen-induced arthritis (CIA), DBA/1J mice were immunized with type II collagen in Freund's adjuvant.

Hoxb3 deficiency impairs B lymphopoiesis in mouse bone marrow.

Objective: Hox genes are involved in hematopoietic lineage commitment and differentiation. In this study, we investigated the roles of Hoxb3 in hematopoiesis by examining the phenotypes of a Hoxb3 knockout mutant mouse line.

Results: Despite previous reports describing the apparently normal phenotype of these mutant mice, we found that by 6 months of age, Hoxb3(-/-) mice began to exhibit significantly impaired B lymphopoiesis in the bone marrow (BM).

Impaired V(D)J recombination and increased apoptosis among B cell precursors in the bone marrow of c-Abl-deficient mice.

Previous studies on c-Abl-deficient mice have shown high post-natal mortality and lymphopenia. However, the mechanisms by which c-Abl may influence B lymphopoiesis remain obscure. In this study, we analyzed B cell sub-populations at various differentiation stages in the bone marrow (BM) of c-Abl-deficient mice.

Novel function of TNF cytokines in regulating bone marrow B cell survival.

Two newly identified tumor necrosis factor (TNF) family cytokines, B cell activation factor from the TNF family (BAFF) and a proliferation-inducing ligand (APRIL), have recently been shown to enhance the maturation and survival of peripheral B cells. However, whether BAFF and APRIL are expressed in the bone marrow (BM) microenvironment and if these two cytokines modulate early B cell development remain unclear. In the present study, we have detected the abundant expression of BAFF and APRIL transcripts in BM non-lymphoid cells.

Expression and function of TNF family member B cell-activating factor in the development of autoimmune arthritis.

B cell-activating factor (BAFF), a member of tumor necrosis factor family cytokines, has been shown to enhance the maturation and survival of peripheral B cells. While BAFF is implicated in regulating B cell function and autoimmunity, its role in the development of autoimmune arthritis has not been fully clarified. Using a collagen-induced arthritis (CIA) mouse model, we detected dysregulated expression of BAFF and its receptors in the peripheral lymphoid organs during arthritis induction.

Requirement of PPARalpha in maintaining phospholipid and triacylglycerol homeostasis during energy deprivation.

The peroxisome proliferator-activated receptor alpha (PPARalpha) has been implicated as a key control of fatty acid catabolism during the cellular fasting. However, little is known regarding changes of individual fatty acids in hepatic triacylglycerol (TG) and phospholipid (PL) as a result of starvation. In the present work, the effects of 72 h fasting on hepatic TG and PL fatty acid profiles in PPARalpha-null (KO) mice and their wild-type (WT) counterparts were investigated.