Table 2.
Summary of characteristic differences seen in the GCs induced by chronic viral infections, GCs of Peyer’s patches and GC-derived B cell lymphomas when compared to the transient GC responses induced by model protein antigens.
| Condition | Characteristics | References |
|---|---|---|
| Chronic viral infections | Persistent GCs and efficient affinity maturation | (167) |
| Alterations in Tfh and Tfr proportions | (168, 169) | |
| Peyer’s patches | Sustained maintenance phase | (39) |
| Chronic antigen stimulation | (170, 171) | |
| Rapid clonal turnover | (172) | |
| Il-4 and Il-12 expressing Tfr cells | (173) | |
| High IL-21 expression in Tfh cells | (174) | |
| IgA as predominant antibody isotype | (175) | |
| FDCs producing high levels of CXCL13, BAFF and TGF-β1 | (76) | |
| B cell lymphomas | Disruption of GC B cell apoptosis. Example: BCL-2 translocation | (176) |
| Increased B cell divisions. Example: overexpression of c-Myc | (177) | |
| Block in the terminal differentiation. Example: Activated B cell like – Diffuse Large B cell lymphomas | (67, 178) | |
| Preferential re-entry of cells into GCs due to BCL-2 translocation | (179) | |
| Altered intrinsic apoptotic pathways. Example: EBV infection | (180) |
Tfh, T follicular helper cell; Tfr, T follicular regulatory cell; FDC, Follicular dendritic cell; EBV, Epstein-Barr Virus; BAFF, B cell activating factor; TGF, Transforming growth factor.