51st Conference of the European-Society-of-Human-Genetics (ESHG) in conjunction with the European Meeting on Psychosocial Aspects of Genetics (EMPAG), Milan, Italy, 16 - 19 June 2018, vol.27, pp.907-908
Introduction: Allorecognition of antigen-presenting cells activated by peptide/human leukocyte antigen (HLA) complex and thus changing its course through lymph nodes where T cells reside. In solid organ transplantation, cultured tissue cells were presumed as passenger-leukocyte free which ensures prolonged graft survival. The aim of this study was to evaluate the potential changes of HLA class II mRNA and protein expression levels during parathyroid cell culture.
Materials and Methods: Parathyroid hyperplasia tissues were obtained from patients diagnosed with secondary hyperparathyroidism (n=11).After histopathological confirmation, glands were digested using collagenase type II and cultured. Afterwar., cells were collected at day 0(after isolation) and 3,6,9 respectively. HLA class-II (-DR,-DP,-DQα1,-DQα2) antibodies were selected according to the binding region and dissociation constant (KD) value which is the equilibrium between antibody and target, then verified by BLAST. Primers were designed for HLA-DR and -DQ but not for DP. Correlation between protein and gene-level results were investigated.
Results: HLA-DR mRNA expression levels remained unchanged, only HLA-DQ mRNA expression level decreased during culture (p = 0.03). Protein expression levels of HLA-DP and -DQα2 were higher than -DR and -DQα1 levels during culture (p<0.0001).
Conclusions: This study demonstrates that cultured parathyroid tissues are still potential targets for allorecognition even during culture. In addition, -DQα2 and -DR protein expression was found higher in parathyroid tissues. Concordance between DQ and DR indicates a possible linkage in rejection/poor graft survival of parathyroid tissue transplantation via allorecognition.
The presented work was financially supported by Bezmialem Vakif University Scientific Research Funding Unit (3.2016/7).