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DRAK2 alters IL-2 sensitivity and Treg development

ABSTRACT: Drak2¬-deficient (Drak2-/-) mice are resistant to multiple models of autoimmunity, yet effectively eliminate pathogens and tumors. Thus, DRAK2 is an ideal target to treat autoimmune diseases. However, the mechanisms by which DRAK2 contributes to autoimmunity, particularly type 1 diabetes (T1D), remain unresolved. Our data indicate that DRAK2 contributes to autoimmunity in multiple ways by regulating thymic Treg development and by impacting the sensitivity of conventional T cells to Treg-mediated suppression.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): T Cell

DISEASE(S): Type 2 Diabetes Mellitus

SUBMITTER: Ashutosh Mishra

LAB HEAD: Maureen A. McGargill

PROVIDER: PXD037922 | Pride | 2023-02-09

REPOSITORIES: Pride

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			Action	DRS
	Drak_treg_Cell_report_resubmission221101_AM_PRIDE_Release_Form.docx	Other
	Fig_7A_AQUA_Y694p_human_STAT5A_01.mzXML	Mzxml
	Fig_7A_AQUA_Y694p_human_STAT5A_01.raw	Raw
	Fig_7A_AQUA_Y694p_human_STAT5A_02.mzXML	Mzxml
	Fig_7A_AQUA_Y694p_human_STAT5A_02.raw	Raw

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