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1 tion in the human brain and the influence of central nervous system inflammation.
2 rosis and potentially other types of chronic central nervous system inflammation.
3 e the proinflammatory chemokines crucial for central nervous system inflammation.
4 8+ Tc1 cells could play a pathogenic role in central nervous system inflammation.
5 or laparotomy and after induction of sterile central nervous system inflammation.
6 lesion size and did not reduce the degree of central nervous system inflammation.
7 elements influence the extent and course of central nervous system inflammation.
8 ales within the brain and spinal cord during central nervous system inflammation.
9 in hemorrhagic stroke, seizure activity, and central nervous system inflammation.
10 neurocognitive function and these markers of central nervous system inflammation.
11 y HIV infection through mechanisms involving central nervous system inflammation.
12 than did effector CD4(+) T cells with marked central nervous system inflammation and axonal damage.
13 and submeningeal infiltrates at the onset of central nervous system inflammation and clinical disease
14 ototypic autoimmune disease characterized by central nervous system inflammation and demyelination.
15 , must be distinguished from other causes of central nervous system inflammation and from noninflamma
16 y, multiple brain petechial hemorrhages, and central nervous system inflammation, and all had postict
17 se onset, lowered clinical scores, decreased central nervous system inflammation, and reduced demyeli
18 actor, on the development and remission from central nervous system inflammation, and their therapeut
20 immunohistochemical staining at the onset of central nervous system inflammation does not parallel th
22 ory lymphocytes underlies the suppression of central nervous system inflammation in patients with mul
24 -10) in the treatment of autoimmune-mediated central nervous system inflammation is controversial.
27 ivities, and their role in the generation of central nervous system inflammation is well documented.
28 les in tumor immunosurveillance, asthma, and central nervous system inflammation, it may contribute t
30 ken together, infectious agents that trigger central nervous system inflammation may serve as a comor
31 gy for diseases characterized by systemic or central nervous system inflammation, such as septic shoc
33 y S100A8/A9, are closely associated with the central nervous system inflammation that characterizes T
34 e system plays a central role in the chronic central nervous system inflammation that drives neurolog
35 opolysaccharide (LPS)-induced model of acute central nervous system inflammation to compare the bindi
36 ptica patients does not require pre-existing central nervous system inflammation to produce lesions.
37 was demonstrated by their ability to prevent central nervous system inflammation, when targeted to th
38 from children during initial presentation of central nervous system inflammation, who may or may not
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