Table 2.
The Role of B cells in SLE and Atherosclerosis
| Statement | Experimental evidence | Clinical evidence |
|---|---|---|
|
| ||
| B cells are atheroprotective |
EVIDENCE SUPPORTING:
|
|
| Increased atherosclerosis in B cell-deficient mice (57,58) | ||
| Breg make IL-10, an atheroprotective cytokine (98,99) | ||
| Treg are reduced in B cell-deficient mice (67) | ||
|
| ||
|
EVIDENCE OPPOSING:
| ||
| Depletion of mature B cells decreased atherosclerosis (59,60) | ||
| BAFF-R−/−, ApoE−/− mice have reduced atherosclerosis (96,97) | ||
|
| ||
| B cells contribute to SLE pathogenesis |
EVIDENCE SUPPORTING:
|
|
| B cells in SLE are hyperactivated and produce autoantibodies (8) | B cells in SLE are hyperactivated and produce autoantibodies (8) | |
| B cell dysregulation in SLE leads to T cell activation, DC recruitment, induction of Th1 and Th17 cells and inhibition of Treg (64) | Breg have reduced regulatory capacity (70) | |
|
| ||
|
EVIDENCE OPPOSING:
| ||
| Breg suppress T cell-mediated inflammation (65–68) | ||
| Breg reduce EAE (69), SLE (65,70), CIA (71) | ||
B cells are a major player in SLE pathogenesis, but the Breg subset can be important for suppression of autoimmunity and may explain differing results concerning the role of B cells in atherosclerosis.