What is transplant rejection ?

Transplant rejection occurs when a recipient’s immune system recognizes a transplanted organ or tissue as foreign, initiating an immune response to attack it. This complex process is influenced by multiple factors, including genetic incompatibility, immune cell activity, and cytokine release. Over time, rejection can lead to organ dysfunction, compromising the transplant’s success and the patient’s health.

AnyGenes offers specialized qPCR arrays designed to study key biomarkers and immune pathways involved in transplant rejection. Our arrays allow researchers to identify gene expression profiles critical for understanding immune responses, cytokine release, and T-cell activation, enhancing insights into both acute and chronic rejection mechanisms. By leveraging AnyGenes qPCR array products, researchers can gain precise, reliable data to support the development of new immunosuppressive therapies and strategies to improve transplant outcomes.

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Receptors sense endogenous DAMPs activation intracellular signals.

Types of transplant rejection

Rejection is generally classified into three main types:

Hyperacute Rejection: Occurs within minutes to hours post-transplant due to pre-existing antibodies against donor antigens. This type is rare today due to improved matching techniques.
Acute Rejection: Can occur within days to months after transplantation and involves T-cell mediated responses against the transplanted tissue. Acute rejection is common and often manageable with immunosuppressive therapy.
Chronic Rejection: Develops over months or years, characterized by ongoing immune responses leading to gradual loss of function in the transplanted organ. Chronic rejection is a leading cause of transplant failure and is more complex to manage than acute rejection.

Mechanisms of graft rejection

Antigen Recognition: the immune system identifies foreign antigens on the transplanted tissue, primarily through MHC (major histocompatibility complex) molecules, which triggers an immune response.
Activation of Immune Cells: T and B lymphocytes play central roles in rejection of organ transplant. T cells initiate the immune attack, while B cells produce antibodies that target the donor tissue.
Cytokine and Chemokine Release: cytokines and chemokines facilitate communication between immune cells, amplifying the rejection process by attracting more immune cells to the transplant site.
Chronic Rejection: occurs gradually and can result in fibrosis and blood vessel changes within the transplanted organ, leading to long-term failure.

Key players in transplantation rejection

Antigen-Presenting Cells (APCs): APCs such as dendritic cells initiate the immune response by presenting donor antigens to T cells, activating the rejection cascade.
T Lymphocytes (T Cells): Activated T cells play a critical role in organ or tissue rejection by recognizing donor tissue as foreign and initiating an immune response against it.
Cytokines and Chemokines: These signaling molecules facilitate communication among immune cells, amplifying inflammation and guiding immune cells to the transplant site.
B Lymphocytes (B Cells) and Antibodies: B cells produce donor-specific antibodies, which can contribute to both acute and chronic rejection processes.
Natural Killer (NK) Cells: NK cells can target donor cells lacking « self » markers, contributing to rejection, especially in cases of mismatched transplants.
Complement System: This component of the immune system can cause direct damage to the transplanted tissue through the formation of the membrane attack complex, leading to cell lysis and inflammation.
Antibodies: Antibody-mediated rejection occurs when recipient antibodies target donor antigens, particularly mismatched Human Leukocyte Antigens (HLA). This response can lead to chronic rejection, characterized by endothelial dysfunction and inflammation.

Therapeutic applications

The clinical implications of organs or tissues rejection are significant, as they can lead to the failure of the transplanted organ and necessitate additional medical interventions. Early detection and management of rejection are critical to improving transplant outcomes.

Diagnosis of graft rejection typically involves monitoring clinical signs and conducting biopsies of the transplanted organ to assess for histological changes indicative of rejection.

Management strategies include the use of immunosuppressive drugs to dampen the immune response. Regular monitoring of the patient’s immune status and function of the transplanted organ is essential for timely intervention.

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Transplant rejection biomarker list

You can check the biomarker list included in this pathway, see below:

Species : Homo sapiens (human)

Human signaling pathways

Signaling Pathways	Product ref	Informations
Transplant Rejection	TR1H1	Download biomarker list

Species : Mus musculus (mouse)

Mouse signaling pathways

Signaling Pathways	Product ref	Informations
Transplant Rejection	TR1M1	Download biomarker list

Species : Rattus norvegicus (rat)

Rat signaling pathways

Signaling Pathways	Product ref	Informations
Transplant Rejection	*******	Biomarker list in progress.

Species : Sus Scrofa (Pig)

Pig Transplant Rejection

Signaling Pathways	Product ref	Informations
Transplant Rejection	*******	Biomarker list in progress.

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Bibliography

1. Short S, et al. An Immune Atlas of T Cells in Transplant Rejection: Pathways and Therapeutic Opportunities. Transplantation. (2023)1;107(11):2341-2352.

2. Win TS, et al. Immunoregulatory and lipid presentation pathways are upregulated in human face transplant rejection. J Clin Invest. (2021)15;131(8):e135166.

3. Tamargo CL, et al. Pathophysiology of Rejection in Kidney Transplantation. J Clin Med. (2023)19;12(12):4130.

4. Alasfar S, et al. Current Therapies in Kidney Transplant Rejection. J Clin Med. (2023)27;12(15):4927.

5. Becker JU, et al. Evolution of the Definition of Rejection in Kidney Transplantation and Its Use as an Endpoint in Clinical Trials. Transpl Int. (2022)20:35:10141.

6. Li Q, et al. Activation of immune signals during organ transplantation. Signal Transduct Target Ther. (2023)11;8(1):110.

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