Table 1.

Summary of GC alterations resulting in premature termination of GCs and the proposed mechanism of action.

Alterations	Observation/proposed mechanism of action	Reference
Activating mutation of CARD11 in GC B cells	Rapid terminal differentiation of B cells	(26)
Inhibition of c-Myc	Prevent DZ re-entry	(27)
c-Rel deletion in GC B cells	Failure in metabolic program directing cell growth	(28)
Bam 32 deficiency in GC B cells	Reduced Tfh recruitment and increased GC B apoptosis	(29)
FDC ablation/absence of FDC	Increased GC B cell apoptosis	(30, 31)
BAFF deficiency	Defect in FDC development and immune complex trapping	(32)
BAFF-R deficiency	Defect in B cell proliferation	(32)
Cr2 deficient mice	Reduced long-term antigen retention	(16)
Absence of T cells	Apoptosis and loss of proliferating cells	(33)
Absence of IL-21 or IL-21 receptor	Reduced GC B cell proliferation	(34)
Absence of Tfh αv integrins	Defect in Tfh accumulation at late stages	(35)
Absence of PD-1	Increased GC B cell apoptosis and reduced cytokine production from Tfh	(36)
anti-CD40L administration	Increased GC B cell apoptosis	(37)
Constitutive CD40 signaling	Early terminal differentiation	(38)

DZ, dark zone; Tfh, T follicular helper cells; GC, Germinal Centres; FDC, Follicular Dendritic Cells; BAFF, B cell activating factor.