Role of CD5⁺B-1 cells in EAE pathogenesis

Abstract

Hybridoma cell lines producing natural autoantibodies (NAA), generated from A.SW mice with progressive experimental autoimmune encephalomyelitis (P-EAE), have been shown to cause demyelination and renal pathology when injected into naïve mice. To investigate the relative contribution of these antibodies to disease pathogenesis, B-1 cells, the major producers of NAA, were depleted by hypotonic shock. Depletion of B-1 cells during the effector phase of EAE significantly decreased the severity of demyelination and overall pathology in the brain. There was also a decreased incidence of P-EAE and a decrease in clinical score. Depletion during the induction phase of the disease resulted in an increase in the incidence of P-EAE and in the clinical score. Overall, B-1 cells were found to modulate EAE pathogenesis.

B Cell Subsets Contribute to Renal Injury and Renal Protection after Ischemia/Reperfusion

“…Depletion of the B-1 population was confirmed by flow cytometry analysis of B220, CD5, and CD19 (Figure 2). This protocol has previously been reported to reduce peritoneal B-1 cells, thereby preventing tissue injury by pathogenic natural IgM antibody (15). Lysis of the peritoneal B-1 cells did not alter overall levels of circulating IgM (Figure 2C), but it did reduce levels of mesangial IgM after sham treatment and after renal I/R compared to control mice (Figures 2D–H).…”

“…Peritoneal B-cells were depleted as previously described (15). Mice received intraperitoneal injections of 0.5 mL of distilled water 12 days and 6 days prior to undergoing renal I/R.…”

IgM Contributes to Glomerular Injury in FSGS

“…Strategies that deplete peritoneal B-1a cells or that block binding of specific natural antibody clones within injured tissues have proven successful for attenuating injury in a number of different models. 23,26 We hypothesized that natural antibody IgM binds to glomerular epitopes that are exposed after adriamycin-induced injury of glomerular cells, and that bound IgM activates the complement system. To test this hypothesis, we utilized three strategies to deplete B cells in mice with adriamycin nephropathy.…”

Susceptibility to experimental autoimmune encephalomyelitis is associated with altered B-cell subsets distribution and decreased serum BAFF levels

“…Increased levels were observed only during the late phase of remission. Previous work demonstrated that depletion of B1a B cells in mice in the induction phase of EAE development resulted in harmful effects on the incidence and clinical evolution of the pathology [42]. Thus, an association between EAE clinical evolution and B1a B cells' homeostatic maintenance could be postulated.…”