| Literature DB >> 26943952 |
Makoto Kubo1, Ryuichi Nagashima2, Etsuro Ohta3, Tatsunori Maekawa4, Yumiko Isobe2, Mitsue Kurihara2, Koji Eshima5, Kazuya Iwabuchi5, Toshikuni Sasaoka6, Sadahiro Azuma7, Heather L Melrose8, Matthew J Farrer9, Fumiya Obata3.
Abstract
LRRK2 is the causal molecule of autosomal dominant familial Parkinson's disease. B2 cells express a much higher LRRK2 mRNA level than B1 cells. To reveal the function of LRRK2 in B cells, we analyzed B cell functions in LRRK2-knockout (LRRK2(-/-)) mice. LRRK2(-/-) mice had significantly higher counts of peritoneal B1 cells than wild-type mice. After BCR stimulation, phosphor-Erk1/2 of splenic B2 cells was enhanced to a higher degree in LRRK2(-/-) mice. LRRK2(-/-) mice had a significantly higher serum IgA level, and TNP-Ficoll immunization increased the titer of serum anti-TNP IgM antibody. LRRK2 may play important roles in B cells.Entities:
Keywords: B cell receptor signaling; B1 cell; B2 cell; IgA; Leucine-rich repeat kinase 2; TI antigen
Mesh:
Substances:
Year: 2016 PMID: 26943952 DOI: 10.1016/j.jneuroim.2016.01.005
Source DB: PubMed Journal: J Neuroimmunol ISSN: 0165-5728 Impact factor: 3.478