LPIN2 mutation causes Majeed syndrome, characterized by chronic recurrent multifocal osteomyelitis (CRMO) ( 6, 7). For example, Familial Mediterranean fever (FMF) is an autosomal recessive self-inflammatory disorder caused by a mutation in the gene encoding MEFV ( 4). Interestingly, many AIDs result from single gene mutations. The field of AIDs has become a cornerstone of modern medicine, yet remains a growing area of research. And monocytes, macrophages and neutrophils are the main cell types of the innate immune system ( 4).ĪIDs are characterized by excessive apoptosis, hyperactive inflammatory cytokine production, and an overreaction to chemotactic stimuli ( 5), resulting in chronic, systemic inflammation. AIDs arise from chronic activation of B and T cells of the innate immune system ( 2, 3), which begin to attack the body’s own tissues, causing loss of function in the composite organs and resulting in diseases.
The concept of “autoinflammatory diseases (AIDs)” was first proposed in 1999 ( 1). PSTPIP2 also provides a new therapeutic target for the treatment of AIDs. This article reviews the research progress and mechanisms of PSTPIP2 in AIDs. However, the mechanisms underlying the function of PSTPIP2 have not been fully elucidated. Current research indicates that the protein tyrosine phosphatase PTP-PEST, Src homology domain-containing inositol 5’-phosphatase 1 (SHIP1), and C‐terminal Src kinase (CSK) can bind to PSTPIP2 and inhibit the development of AIDs. In recent years, it has been observed to play important roles in innate immune diseases and autoinflammatory diseases (AIDs). PSTPIP2 is known to participate in macrophage activation, neutrophil migration, cytokine production, and osteoclast differentiation. It exhibits lipid-binding, membrane deformation, and F-actin binding activity, suggesting broader roles at the membrane–cytoskeleton interface. Proline-serine-threonine-phosphatase-interacting protein 2 (PSTPIP2) belongs to the Fes/CIP4 homology-Bin/Amphiphysin/Rvs (F-BAR) domain family. Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, China.Jie-Jie Xu †, Hai-Di Li †, Xiao-Sa Du, Juan-Juan Li, Xiao-Ming Meng, Cheng Huang and Jun Li *
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