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Heart transplant is the best treatment option for end-stage heart failure. The major goals in solid-organ transplant are organ survivability and functionality. The effects of anti-HLA antibodies and cytokines are important for immune response. Cytokine gene polymorphisms are also effective during cytokine release. Here, we report a heart transplant recipient who was diagnosed with antibody-mediated rejection posttransplant and had an antibody response resistant to desensitization therapy. After transplant, panel reactive antibody screening and identification class I and II tests and Luminex single antigen class I and II tests were performed. Desensitization treatment included intravenous immunoglobulin, plasmapheresis, rituximab, and bortezomib. Because of these reasons, cytokine gene polymorphism tests (consistent with low, intermediate, and high expression levels for tumor necrosis factor α, transforming growth factor β1, interleukin 6 and 10, and interferon γ) were conducted. We found polymorphic regions compatible with the high-release, proinflammatory action of tumor necrosis factor α and interleukin 6, which induced inflammation and B-cell activation, and polymorphic regions compatible with the intermediate release of the potent immunosuppressive effects of transforming growth factor β1 and interleukin 10, suggesting that the patient may not be able to effectively suppress the activation of the immune system. The influence of cytokine gene polymorphism on the formation of a resistant antibody response in a patient, despite desensitization, contributed to the proinflammatory response in which these cytokines were involved. |
