Table 1.
Summary of common pathways in the innate immune system during the development of MS and AD.
| Common mechanisms | MS | AD |
|---|---|---|
| CNS neutrophil infiltration is related to disease progression | (26) (human) (27) (human) (28) (mouse) (29) (mouse) |
(10) (mouse) |
| High NLR correlates with disease progression | (33) (human) (34) (human) |
(32) (human) (35) (human) |
| Circulating neutrophils display a primed-activated phenotype | (36) (human) (38) (human) (40) (human) |
(37) (human) (39) (human) (41) (human) (42) (human) (43) (mouse) |
| CD11b expression on circulating neutrophils correlates with disease progression | (36) (human) | (37) (human) |
| CXCL8 is elevated in the plasma and CSF and is related to disease activity | (44) (human) (45) (human) |
(46) (human) (47) (human) (48) (human) |
| Elevated CXCL1 expression in the CNS is related to clinical impairment | (36) (human) (44) (human) (49) (mouse) |
(50) (human) (51) (mouse) |
| Elevated IL-1 expression in the CNS | (52) (human) (53) (mouse) |
(54) (human) (55) (mouse) |
| Increased levels of MPO in the blood and CNS correlates with neuropathology | (56) (human) (57) (human) (58) (mouse) (59) (mouse) |
(46) (human) (60) (human) (10) (human and mouse) |
| Circulating neutrophils show a more intense oxidative burst | (40) (human) | (41) (human) (42) (human) |
| Systemic phenotype alteration in circulating monocytes (increased frequency of non-classical monocytes at the expense of classical ones) | (61) (human) (62) (human) |
(63) (human) |
| Circulating monocytes display a pro-inflammatory state | (64) (human) | (63) (human) (65) (human and mouse) |
| CCR2 is involved in monocyte CNS invasion | (66) (mouse) | (67) (mouse) (68) (mouse) |
| Monocytes display impaired phagocytosis and an enhanced pro-inflammatory phenotype | (69) (human) | (70) (human) |