Transplant Rejection and Antibodies
Organ transplantation provides an avenue for patients with end-stage organ failure to regain health and improve their quality of life. However, transplant rejection, characterized by the recipient's immune system attack on the donor organ remains a constant threat. Antibodies produced by the recipient's immune system are key players in this process. Classically, IgG antibodies have been studied extensively as potential contributors to post-transplant complications. Nonetheless, a focus on IgG responses may neglect a potentially relevant humoral response. Recent findings suggest that non-IgG antibodies, particularly IgM and IgA, could equally play crucial roles in mediating graft rejection.
Non-IgG Antibodies in Transplant Rejection
Research has provided evidence that the presence of IgM and IgA donor-specific antibodies (DSA) in the recipient's serum is linked with a greater risk of graft failure. However, the understanding of how these non-IgG antibodies contribute to transplant rejection is still in its infancy. IgM antibodies, the largest in size amongst all antibodies, are usually the first responders to infections. There is accumulating evidence that IgM DSA pre-transplantation might infer a higher risk of graft loss. These findings suggest that IgM DSA may modulate allograft immunogenicity resulting in heightened organ rejection. Meanwhile, IgA antibodies play a significant role in mucosal immunity and have a very low prevalence in transplantation. The existence of IgA DSA has been connected with worse graft survival rates, particularly in kidney transplants. These antibodies might induce direct graft injury or act through complement-mediated pathways, causing graft dysfunction and eventual rejection.
Involvement of IgM antibodies in allograft rejection. (Matsuda, 2020)
Clinical Implications of Non-IgG in Transplant Rejection
The presence of non-IgG antibodies, especially pre-transplantation, should prompt more careful patient monitoring due to an elevated risk of organ rejection. Screening for these antibodies may provide complementary information to classical IgG-based results and will facilitate enhanced risk stratification. Also, the presence of non-IgG antibodies could indicate the need for tailored immunosuppressive strategies to prevent the premature loss of graft function. Furthermore, further investigation of non-IgG antibodies could also lead to a more comprehensive understanding of the rejection process. Unravelling the mechanisms involved in non-IgG mediated transplant rejection may enable us to intervene in this process, thereby improving overall transplant outcomes.
The role of non-IgG antibodies in transplant rejection is increasingly being recognized. Although much remains to be discovered about their function in graft rejection, preliminary findings suggest that they may have detrimental effects on graft survival. Acknowledging this could revolutionize transplantation protocols, providing strategies for risk prevention and management, thereby enhancing graft survival and patient outcome. As researchers decode the mysteries of transplant immunology further, the hope remains that all transplant recipients will receive a chance at long-term health improvement.
As a biological service provider focusing on non-IgG antibody research, Creative Biolabs has built a comprehensive technology platform to provide non-IgG therapeutic antibody development services to clients around the world, covering all aspects of antibody discovery, antibody engineering, and customized production. In addition, products such as non-IgG antibody and non-IgG elisa test kit are also available. If you have related needs, please feel free to contact us.
- Matsuda Y; et al. Characteristics of Immunoglobulin M Type Antibodies of Different Origins from the Immunologic and Clinical Viewpoints and Their Application in Controlling Antibody-Mediated Allograft Rejection. Pathogens. 2020, 10(1): 4.
!! For Research Use Only. Our products and services are NOT intended for diagnostic or therapeutic applications.