Trappc1 intrinsically prevents ferroptosis of naive T cells to avoid spontaneous autoinflammatory disease in mice.

T lymphocytes are pivotal in adaptive immunity. The role of the trafficking protein particle complex (TRAPPC) in regulating T-cell development and homeostasis is unknown. Using CD4 -Trappc1 (Trappc1 cKO) mice, we found that Trappc1 deficiency in T cells significantly decreased cell number of naive T cells in the periphery, whereas thymic T-cell development in Trappc1 cKO mice was identical as WT mice.

Absence of TSC1 Accelerates CD8 T cell-mediated Acute Cardiac Allograft Rejection.

Tuberous sclerosis complex (TSC) is an autosomal dominant disease caused by inactivating mutations in or .Patients with TSC often require organ transplantation after organ failure. TSC1 serves as an important control node in immune cell development and responses; however, its effect on T cells in transplant immunity has not yet been explored.

Skin and heart allograft rejection solely by long-lived alloreactive T cells in skin of severe combined immunodeficient mice.

Whether induced tissue-resident memory T (T) cells in nonlymphoid organs alone can mediate allograft rejection is unknown. By grafting alloskin or heart into severe combined immunodeficient or Rag2KO mice in which a piece of induced CD4 and/or CD8 T cell-containing MHC-matched or syngeneic skin was transplanted in advance, we addressed this issue. The induced CD4 T cells in the skin alone acutely rejected alloskin or heart grafts.

Skills to Perform Vessel Eversion in Mouse Cervical Cardiac Transplantation with Cuff Technique.

Introduction: The mouse heterotopic cardiac transplant model has been extensively used to explore transplant immunity. Although the cuff technique facilitates the operation, the procedure remains difficult, and vessel eversion is the most difficult step. Cuff movement and everted vessel wall slippage are the main adverse factors in vessel eversion.

The biological function and the regulatory roles of wild-type p53-induced phosphatase 1 in immune system.

Wild-type p53-induced phosphatase 1 (WIP1) belongs to the protein phosphatase 2C (PP2C) family and is a mammalian serine/threonine specific protein phosphatase to dephosphorylate numerous signaling molecules. Mammalian WIP1 regulates a wide array of targeting molecules and plays key regulatory roles in many cell processes such as DNA damage and repair, cell proliferation, differentiation, apoptosis, and senescence. WIP1 promotes the formation and development of tumors as an oncogene and a negative regulator of p53.