Basic information of Ptpn22 :

Official Symbol of Gene	Ptpn22
Species	Mus musculus
Entrez Gene ID	19260
Official Full Name	protein tyrosine phosphatase, non-receptor type 22 (lymphoid)
Also known as	PEP; Ptpn8; 70zpep
Gene Type	protein coding
dbXrefs	Ensembl:ENSMUSG00000027843 AllianceGenome:MGI:107170
Map Location	3; 3 F2.2
Variation Type	DNA methylation
refSNP ID	DNA methylation

Sample information of multiple sclerosis:

Detected Sample	Peripheral blood
Sample Detail	N/A
Detected Method	PCR
Disease	MS
Disease subtype	N/A
Population	Rag1KO female mice
Sample Size	n = 5–6 mice group

Literature information of multiple sclerosis :

Pubmed ID	32047502
Year	2020
Title	PTPN22 Acts in a Cell Intrinsic Manner to Restrict the Proliferation and Differentiation of T Cells Following Antibody Lymphodepletion

Results of multiple sclerosis :

Risk Type	Disease risk
Main Result	Foxp3+ Tregs were also considerably expanded in PTPN22-deficient and PTPN22 R619W mice, as was the frequency of both CD25+ and CD25 CD4 T cells that produce IL-10. Using bone marrow chimeric mice, we showed that PTPN22 influenced.Overall the expansion of Tregs is likely to keep the expanded T effector populations in check and sparing Treg during therapeutic mAb depletion may be a useful strategy to prevent occurrence of secondary autoimmunity
Result	Based on our findings we conclude that antibody mediated T cell lymphopenia does not trigger overt auto-aggression in PTPN22 KO mice although PTPN22 deficient T cells showed a pronounced effector phenotype. High abundance of Tregs and IL-10 producing cells in PTPN22 KO mice have been previously associated with increased tolerance in a model of pancreatic islet transplantation and might suppress excessive T cell proliferation and keep activated T cell clones in check
Mechanism/Pathway	We induced lymphopenia by treating wild-type or PTPN22 knock-out mice with T cell depleting antibodies and monitored reconstitution of the T cell pool. We found that PTPN22 deficient T cells acquired a more activated effector phenotype, with significantly more IFNγ producing cells. This resulted from expansion driven by self-peptide MHC, as it was evident when the contribution of IL-7 to lymphopenic expansion was blocked with IL-7R Ab