Tissue/organ rejection may occur when tissue/organ transplants are performed between individuals of different species or between individuals of the same species and different lineages, it is essentially an immune response induced by allogenic antigens on the cell surface.
Such an allogenic antigen that represents an individual specificity is called A
Transplantation antigens or Histocompatibility antigens, in which the antigens causing strong and rapid rejection are called major histocompatibility antigen, MHA，the antigen that causes the weaker or slower rejection is calledminor histocompatibility antigen, MiHA
In clinical tissue/organ transplantation, MHA matching is usually a prerequisite for successful transplantation.
MHA is also known in humans as human leukocyte antigen, HLA.
There are two main types of HLA:
Class I, including HLA-A, HLA-B and HLA-C, is widely distributed in various tissues and cells
Class II, which includes HLA-DP, HLA-DQ, and HLA-DR, is found in B cells, macrophages, and activated T cells.
In clinical kidney transplantation, only HLA-A, HLA-B and HLA-DR are usually tested for a total of six loci, because previous studies have shown that these three molecules are most closely related to graft rejection.
Recently, foreign research teams have explored the effect of HLA-DQ mismatch on renal allograft rejection.
The study used data from dialysis and transplant centers in Australia and New Zealand between 2004 and 2012, the adjusted Cox regression model was used to explore the relationship between HLA-DQ locus mismatch and acute rejection in living or dead kidney transplant recipients.
Nearly 800 kidney transplant patients received nearly 3 years of mean follow-up time, and 40.7% of patients did not receive or received 1 HLA-DQ locus mismatched donor kidney, suggesting that this is not the case, 59.3% of patients received 2 HLA-DQ locus mismatched donors. Patients who received one or two HLA-DQ mismatched donor kidney transplants were more likely to develop rejection (late rejection was more likely to occur 6 months after transplantation) and antibody-mediated rejection than patients who did not receive an HLA-DQ mismatched donor kidney transplant.
After adjusting for age, race, donor kidney type, BMI, age, number of HLA-A, B, and DR mismatches, panel reactive antibodies, kidney transplant waiting time, ischemia time, induction therapy, and primary immunosuppressive response, the results were similar between donors and recipients, follow-up results showed that renal transplant recipients with 1 or 2 HLA-DQ mismatched donor kidneys were significantly more likely to have an increased risk of heart failure than renal transplant recipients without HLA-DQ mismatch, the adjusted hazard ratios for acute or late rejection were 1.54 and 2.85, respectively. HLA-DR loci can effectively regulate HLA-DQ mismatch and antibody-mediated rejection.
Therefore, the association was more significant in donors with one or two HLA-DQ mismatches, with an adjusted hazard value of 2.50.
The results confirmed that the increase in acute rejection in this study was due to HLA-DQ mismatch, not HLA-A, B, DR mismatch or primary immunosuppression.
Therefore, in our clinical work, in addition to HLA-A, B, Dr Loci Matching, we should also pay attention to HLA-DQ loci matching when evaluating the immune-related risk of renal transplant patients before surgery.
Text | Jina Wang, editor | Yichen Jia, photo | C.M. et al.
