Hyporesponsiveness following booster immunization with bacterial polysaccharides is caused by apoptosis of memory B cells.

Background: Repeated immunizations with polysaccharide (PS) vaccines cause hyporesponsiveness through undefined mechanisms. We assessed the effects of a PS booster on immune responses, frequency, and survival of PS-specific B-cell subpopulations in spleen and bone marrow.

Methods: Neonatal mice were primed with meningococcus serotype C (MenC) conjugate MenC-CRM(197)+CpG1826, boosted with MenC-CRM(197), MenC-PS, or saline; subsequently, bromodeoxyuridine (BrdU) was injected daily intraperitoneally.

Meningococcal serogroup C polysaccharide specific memory B cells, directly enumerated by labeled polysaccharide, are not affected by age at vaccination.

The influence of age on the generation and persistence of specific memory B cells after vaccination with Neisseria meningitidis type C polysaccharide (MenC-PS) conjugate is unknown. MenC-PS-specific B cells could be directly enumerated by fluorochrome-labeled MenC-PS and flow cytometry in blood up to at least 4 years after vaccination, ranging from 0.01% to 0.

Differential expression of chemokine receptors on peripheral blood B cells from patients with rheumatoid arthritis and systemic lupus erythematosus.

Chemokines and their receptors are essential in the recruitment and positioning of lymphocytes. To address the question of B cell migration into the inflamed synovial tissue of patients with rheumatoid arthritis (RA), peripheral blood naive B cells, memory B cells and plasma cells were analyzed for cell surface expression of the chemokine receptors CXCR3, CXCR4, CXCR5, CCR5, CCR6, CCR7 and CCR9. For comparison, B cells in the peripheral blood of patients with the autoimmune disease systemic lupus erythematosus (SLE) or with the degenerative disease osteoarthritis (OA) were analyzed.