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Norway

PMID:29902238  

LatY136F knock-in mouse model for human IgG4-related disease.

Kazunori Yamada | Masahiko Zuka | Kiyoaki Ito | Keishi Mizuguchi | Yasushi Kakuchi | Tamehito Onoe | Yasunori Suzuki | Masakazu Yamagishi | Shozo Izui | Marie Malissen | Bernard Malissen | Mitsuhiro Kawano
PloS one | 2018

The adaptor protein Linker for activation of T cell (LAT) is a key signaling hub used by the T cell antigen receptor. Mutant mice expressing loss-of-function mutations affecting LAT and including a mutation in which tyrosine 136 is replaced by a phenylalanine (LatY136F) develop lymphoproliferative disorder involving T helper type 2 effector cells capable of triggering a massive polyclonal B cell activation that leads to hypergammaglobulinemia G1 and E and to non-resolving inflammation and autoimmunity. The purpose of this study was to evaluate whether the phenotypes of LatY136F knock-in mice resemble the immunohistopathological features of immunoglobulin G4-related disease (IgG4-RD).

Pubmed ID: 29902238

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Japanese Ministry of Health Labor and Welfare (tool)

RRID:SCR_011326

Cabinet level ministry of the Japanese government. It is commonly known as Kōrō-shō in Japan. The ministry provides services on health, labour and welfare.

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C57BL/6J (tool)

RRID:IMSR_JAX:000664

Mus musculus with name C57BL/6J from IMSR.

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