The terminal differentiation of a B cell is becoming a plasma cell which is essentially a cell devoted to secreting antibodies. From the germinal center or the memory B cell population, antigen specific B cells will proliferate (in the presence of the antigen) and become plasmablasts and then plasma cells. plasma cell differentiation in vitro Feb 15, 2007 CpG DNA activation and plasmacell differentiation of CD27 While most studies use the CD38 IgD phenotype to define the plasmacell state with in vitro differentiation systems, our data suggest that this phenotypic classification may be suboptimal.
Plasma cell differentiation and survival. Author links open overlay panel David Tarlinton 1 Andreas Radbruch 2 Falk Hiepe 2 Thomas Drner 2. Show more. [54, but to date there is no magic cocktail to maintain plasma cells in vitro, nor is there a magic bullet to eliminate them in vivo. plasma cell differentiation in vitro
A Unique in vitro Model The differentiation of B cells to plasma cells (PCs) is essential for humoral immunity and protect the host against infections. In human, PC are rare cells with differentiation stages taking place in anatomic places that hamper full biological characterization. XBP1 transcripts were rapidly upregulated in vitro by stimuli that induce plasmacell differentiation, and were found at high levels in plasma cells from rheumatoid synovium. When introduced into Figure 1: In vitro plasma cell differentiation model. The PC differentiation model recapitulates the various steps of human PC generation. In a first step, memory B cells are first activated for four days by CD40 ligand, and cytokine combination and differentiate into preplasmablasts. plasma cell differentiation in vitro In current in vitro models of B cell differentiation, 17 Soluble CD40L was removed since it partially blocks plasma cell differentiation. 20 We also found that presence of ODN blocked PC differentiation (results not shown). CAP treatment offers a onestep way to enhance both C17. 2 NSC and primary rat NSC differentiation in vitro with a short treatment time and little cell damage. Moreover, the results showed a 75 directed differentiation into neurons, which made plasma treatment a promising method for future tissue transplantations in the clinic. In vitro experiments indicate that plasma cell formation is inefficient in response to BCR ligation alone, suggesting that the BCR may not drive GC Bcell differentiation, but rather may facilitate the process. More importantly, APRIL and LPS strongly synergized to drive the plasma cell differentiation program, observations suggest that TACI cooperates with TLR4 to drive B cell differentiation and immunoglobulin production in vitro and in vivo. Clinical Implications.