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Decreased CCR 2 and CD 62 L expressions on peripheral blood classical monocytes in amyotrophic lateral sclerosis
Author(s) -
Cui Yi Wen,
Kawano Yuji,
Yamasaki Ryo,
Shi Nan,
Masaki Katsuhisa,
Isobe Noriko,
Yonekawa Tomomi,
Matsushita Takuya,
Tateishi Takahisa,
Hayashi Shintaro,
Kira Junichi
Publication year - 2014
Publication title -
clinical and experimental neuroimmunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.297
H-Index - 15
ISSN - 1759-1961
DOI - 10.1111/cen3.12088
Subject(s) - monocyte , pathogenesis , amyotrophic lateral sclerosis , ccr2 , flow cytometry , immunology , immune system , medicine , biology , chemokine , disease , chemokine receptor
Objective Recent evidence has suggested the importance of an aberrantly activated monocyte system in amyotrophic lateral sclerosis ( ALS ) pathogenesis. However, the roles of each monocyte subset, namely CD 14+ CD 16− classical monocytes, CD 14dim CD 16+ non‐classical monocytes and CD 14+ CD 16+ intermediate monocytes, in ALS remain unknown. We aimed to clarify the alterations in the monocyte subset proportions and the surface marker expressions on each monocyte subset in ALS . Methods Blood samples were collected from 19 ALS patients and 28 healthy controls ( HC ). The surface expressions of CCR 2, CX 3 CR 1, CD 64 and CD 62 L were measured in the three monocyte subsets (classical, non‐classical and intermediate) by flow cytometry. Results The percentages of CCR 2 and CD 62 L on CD 14+ CD 16− classical monocytes were significantly lower in ALS patients than in HC ( P = 0.0012 and P = 0.0296, respectively). No differences were found in CX 3 CR 1 and CD 64 on each monocyte subset. The percentage of intermediate monocytes showed a significant negative correlation with the revised ALS functional rating scale score ( r = −0.631, P = 0.0038). Conclusions Reductions in chemotaxis‐ and adhesion‐related molecules on classical inflammatory monocytes are present in ALS , further suggesting the involvement of an aberrant innate immune system in ALS pathogenesis.