Table 3.

Role of PARP1 depletion in EAE mouse models

PARP1 genetic mice	MS models, genetic background	EAE severity (KO vs WT mice)	Pathological alterations (KO vs WT mice)	Ref.
PARP1‐KO (129S background)	MOG35‐55‐EAE in 129S mice (n = 30 PARP1‐WT and 30 PARP1‐KO), disease monitored throughout day 35	Increased incidence, early onset, and increased severity on days 11–17	Increased CNS infiltration of CD4+ T cells at day 10. Increased number in CNS macroglia and macrophages at day 10. No changes in the number of peripheral T lymphocytes, dendritic cells, or macrophages	[ 22b ]
PARP1‐KO (129S background)	MOG35‐55‐EAE in 129S mice (n = 5 PARP1‐WT, 9 PARP1‐KO), disease monitored throughout day 17	Statistics not determined Peak clinical score (mean ± s.e.m.): PARP1‐WT:2.2 ± 0.2 PARP1‐KO:1.61 ± 0.7	No changes in the mRNA levels of CCL2, iNOS, TNFα in CD11b+ cells isolated from the spinal cord of EAE	[ 14 ]
PARP1‐KO (129S background)	MOG35‐55‐EAE in 129S background mice	The authors described consistent results as those reported by Selvaraj et al., 2009[ 22b ] but did not show the data	Not determined	[ 103 ]
PARP2‐KO (C57BL/6)	MOG35‐55‐EAE in C57BL6/J mice (n = 9 PARP2‐WT and 6 PARP2‐KO) disease monitored throughout day 35	Delayed onset and reduced severity of EAE	Reduced number of spinal CD4+ T cells and Th1 and Th17 T cell subpopulations (by immunohistochemistry) Reduced demyelination at peak EAE disease (by immunohistochemistry) Reduced number of spinal CD11b+ macrophages and microglia (by immunohistochemistry)	[ 103 ]