CDB25:0003344 CLEC4G — PILRA

Experimentally validated in Human; Orthology-inferred in Rat, Macaque, Pig, Dog, Cow, Chimp, Horse, Marmoset

Title

Journal:; Year Published:

Abstract

PILRα negatively regulates mouse inflammatory arthritis.

Journal of immunology, 2014; PubMed, Homo sapiens CLEC4G — Homo sapiens PILRA
ABSTRACT: Paired Ig-like type 2 receptor (PILR)α inhibitory receptor and its counterpart PILRβ activating receptor are coexpressed on myeloid cells. In this article, we report that PILRα, but not PILRβ, is elevated in human rheumatoid arthritis synovial tissue and correlates with inflammatory cell infiltration. Pilrα(-/-) mice produce more pathogenic cytokines during inflammation and are prone to enhanced autoimmune arthritis. Correspondingly, engaging PILRα with anti-PILRα mAb ameliorates inflammation in mouse arthritis models and suppresses the production of proinflammatory cytokines. Our studies suggest that PILRα mediates an important inhibitory pathway that can dampen inflammatory responses.
Basic Information on CLEC4G
Ligand Name: C-type lectin domain family 4 member G
Other Symbols: UNQ431, LSECTIN
Ligand Location: cell membrane based on perplexity, uniprot
HGNC Gene Symbol Report: CLEC4G
GeneCards: CLEC4G
Interactions with other Receptors for CLEC4G
Basic Information on PILRA
Receptor Name: paired immunoglobin like type 2 receptor alpha
Other Symbols: FDF03
Receptor Location: cell membrane based on perplexity, uniprot
HGNC Gene Symbol Report: PILRA
GeneCards: PILRA
Interactions with other Ligands for PILRA