arasing from Qin Zhang et al. Nature Immunology https://doi.org/10.1038/ni.3233 (2015).

Genetic variants in the LRRK2 gene, which encodes a large serine-threonine kinase, are linked to Parkinson’s disease and the inflammatory bowel disease, Crohn’s disease¹. Crohn’s disease involves transmural inflammation of the gastrointestinal tract, particularly the ileum. In ileal Crohn’s disease, several lines of evidence support a pathogenic role for abnormal Paneth cells, which is characterized by defective lysozyme-containing granules². Zhang et al.³ suggested a key role for LRRK2 in lysozyme sorting and secretion in Paneth cells. However, we found no evidence that LRRK2 is expressed in murine or human Paneth cells or that it was required for lysozyme expression in the gut. Thus, while LRRK2 polymorphisms in Crohn’s disease may cause defects in Paneth cell function, these defects are most likely not driven by LRRK2 in a cell-autonomous manner.

arasing 来自Qin Zhang et al. Nature Immunology https://doi.org/10.1038/ni.3233 （2015）.

LRRK2 基因编码大丝氨酸-苏氨酸激酶，其遗传变异与帕金森病和炎症性肠病（克罗^恩病）有关1。克罗恩病涉及胃肠道的透壁炎症，尤其是回肠。在回肠克罗恩病中，几行证据支持异常潘氏细胞的致病作用，其特征是含溶菌酶的颗粒有缺陷²。Zhang 等人³ 认为 LRRK2 在 Paneth 细胞的溶菌酶分选和分泌中起关键作用。然而，我们没有发现 LRRK2 在小鼠或人潘氏细胞中表达的证据，也没有证据表明它是肠道中溶菌酶表达所必需的。因此，虽然克罗恩病中的 LRRK2 多态性可能导致潘氏细胞功能缺陷，但这些缺陷很可能不是由 LRRK2 以细胞自主方式驱动的。