Antibodies against glutathione S‐transferase T1 in non–solid organ transplanted patients

Abstract

It is concluded that anti-GSTT1 can appear in a context different from the previously published alloreactivity after liver and kidney transplantation, as a consequence of transfusions and pregnancies. So far, no adverse clinical outcomes in our patients have been observed.

Autoantibodies to glutathione S-transferase theta 1 in patients with primary sclerosing cholangitis and other autoimmune diseases

“…This finding confirms the results in previous reports. The frequency of GSTT1-antibodies we have observed is, however, more than 100 times higher than the frequency that has been reported earlier [24]. The role of GSTT1-antibodies in autoimmune disorders is yet to be determined.…”

“…GSTT1-antibodies might mediate the reaction against the graft that results in typical histologic features of autoimmune hepatitis [23]. Antibodies against GSTT1 have also been found in persons with null genotypes that have had either a blood transfusion or have given birth to a GSTT1-positive child [24].…”

Glutathione S-transferase T1-null seems to be associated with graft failure in hematopoietic SCT

“…Anti-GSTT1 antibodies have been documented in GSTT1-null individuals with a history of blood transfusions or a previous pregnancy, 11 because of GSTT1-positive transfusions or pregnancy of a GSTT1-positive fetus, which could induce production of anti-GSTT1 antibodies in a GSTT1-negative individual.…”

Influence of glutathione S-transferase T1 donor/recipient mismatch and anti-GSTT1 antibodies in hepatic graft-versus-host-disease

“…Glutathione S-transferase T1 (GSTT1) is a member of a family of drug metabolizing enzymes, highly expressed in liver, kidney and erythrocytes. Immune recognition of the GSTT1 alloantigen has already been described in different settings such as: (I) after liver transplant between a null recipient and a positive donor with production of donor specific antibodies, in which this particular mismatch constitutes a risk factor to develop de novo immune hepatitis [13]; (II) after kidney transplant between a null recipient and a positive donor with production of donor specific antibodies, sometimes associated with chronic antibody-mediated rejection [14]; (III) in a GSTT1-null individual after receiving blood transfusions [15]; (IV) in GSTT1-null women after pregnancy [15] and in null-GSTT1 children with congenital hemoglobinopathies after HSCT resulting in graft rejection [16]. It is worth mentioning that the null allele is present in 20% of caucasian population [17].…”