Table 1: Transgenic overexpression of regulatory genes in the islets and their effects on islet transplantation.

PromoterGene of interestAnimal strainDiabetic incidenceEffect on isletsEffects on islet transplantationReference

Human insulinIL-4NODDecreasedProtect islets from autoimmune destructionNo significant protective effect[21]
Rat insulinTGF-βNODDecreasedSmall clusters of micro-isletN, and no protective effect when use pancreata in an allogeneic transplantation model[22, 23]
GlucagonTGF-βNODDecreasedMorphologically normal, no other phenotypes mentionedN[24]
Rat insulinTNF-αNODDecreasedMassive insulitisN[25]
Human insulinSOCS1B6B6 is not a diabetes-prone mouse strainNot mentionedExpression of SOCS-1 in islets delays allografts rejection (B6 to Balb/c) but cannot circumvent destruction of the islets by the recurrence of the tissue-specific autoimmune process of spontaneous diabetes (B6 to diabetic NOD)[26]
Human insulinPD-L1NODDecreasedProtect from autoimmune destructionNo significant protective effect[27]
Glial fibrillary acidic proteinPD-L1NODIncreasedEnhance the severity of insulitisN[28]
Rat insulinPD-L1B6Induces T-cell-mediated spontaneous diabetes in B6 mouseInduce insulitisAccelerate allograft rejection[29]
Human insulinSingle chain anti-CTLA-4 FvNODDecreasedProtect islets from autoimmune destructionProlong islet grafts survival in diabetic NOD mice[30]
Rat insulinCTLA-4-IgB6B6 is not a diabetes-prone mouse strainMorphologically normalN, and transplantation of CTLA4-Ig transgenic pancreata combine with transient systemic CD4 T cell depletion in recipients enhance allograft acceptance[31]
Human insulinThioredoxinNODDecreasedDo not attenuate the development of insulitisN[32]
Human insulinHeme oxygenase 1NODDecreasedProtect islets from autoimmune destruction
Resistant to inflammatory cytokine-induced apoptosis
Prolong islet grafts survival in diabetic NOD mice[33]
Human insulinDcR3NODDecreasedProtect islets from autoimmune destructionIncrease the successful rate of implantation and prolong islet grafts survival in diabetic NOD mice[34]
Human insulinD6NODDecreasedProtect islets from autoimmune destructionN[35]

NOD: Nonobese diabetic mouse, a spontaneous autoimmune diabetes mouse strain; SOCS-1: suppressor of cytokine signaling-1; PD-L1: programmed death 1 ligand 1; CTLA-4: cytotoxic T lymphocyte antigen 4; DcR3: decoy receptor 3; D6: an inflammatory CC chemokine decoy receptor; N: not tested.