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Non-HLA Antibody Detection Assay

All products and services are For Research Use Only and CANNOT be used in the treatment or diagnosis of disease.

Antibodies that are specific to organ donor human leukocyte antigen (HLA) have been involved in the majority of cases of antibody-mediated rejection in solid organ transplant recipients. However, recent data show that non-HLA autoantibodies may occur before transplant in the form of natural autoantibodies. Creative Biolabs provides a set of non-HLA antibody detection assays to assess an individual's sensitization status and identify the antigens specifically targeted by those antibodies. Our selection of non-HLA antibody detection assays varies in format and coverage from Major-histocompatibility-complex class I related chain A (MICA) single antigen antibody screen and Angiotensin II type 1 receptor (AT1R) ELISA to endothelial cell crossmatch.

Non-HLA Antibody

The development of post-transplant antibodies against non-HLA autoantigens is associated with rejection and decreased long-term graft survival. Recent studies have shown that antibodies directed against autoantigens contribute to the process of antibody-mediated acute and chronic rejection. Non-HLA antibodies are classified into two main categories: alloantibodies directed against polymorphic antigens that differ between the recipient and donor, and antibodies that recognize self-antigens - autoantibodies.

Non-HLA Antibody Detection Assays

MICA Single Antigen Antibody Screening

  • MICA is a kind of surface glycoprotein with functions related to innate immunity. Same as HLA antigens, MICA antigens can elicit antibody formation when exposed to allogeneic MICA during transplantation. Creative Biolabs provides MICA single antigen antibody screening to detect antibodies against a panel of the most common MICA antigens coupled to Luminex beads.

AT1R Assay

  • AT1R antibody is the most widely studied non-HLA antibody until recently. It is expressed on the surface of endothelial cells and combines with angiotensin II to regulate water-salt balance and blood pressure. Creative Biolabs offers a new approach, AT1R assay, to perform transplant research testing at a non-HLA level.

Endothelial Cell Crossmatch

  • Endothelial cell is the first point of contact between the allograft and the recipient's immune system and therefore a source of non-HLA antigens that can stimulate a humoral immune response. Creative Biolabs provides endothelial cell crossmatch to detect non-HLA antibodies that have been implicated in antibody-mediated rejections.

Comparison of Different Assays

Non-HLA antibodies reactive with donor endothelial cell antigens have been implicated in rejection and graft loss. MICA single antigen antibody screening detects IgG antibodies against the most common MICA alleles. AT1R antibodies are assessed by ELISA based platform. Endothelial cell crossmatch detects IgG antibodies to surrogate endothelial cell lines. Specific differences between these three assays are shown in the following table:

Assay Phase Specificity Result
MICA Single Antigen Antibody Screen Solid Phase lgG, MICA Positive HLA specificities
AT1R ELISA Solid Phase lgG, AT1R >10 U/mL is associated with endothelial cell dysfunction
Endothelial Cell Crossmatch Cell Phase lgG Median channel shift (MCS)

As a world leader in HLA testing, Creative Biolabs offers a collection of integrated solutions to help you identify non-HLA antibodies that may cause graft rejection. Our non-HLA antibodies detection assays vary in format, sensitivity, and specificity. Moreover, all products are designed for ease of use, lab efficiency, and optimized automation. If you are interested in our non-HLA antibody detection assays and products, please feel free to contact us directly.

References

  1. Tait, B.D.; et al. Consensus guidelines on the testing and clinical management issues associated with HLA and non-HLA antibodies in transplantation. Transplantation. 2013, 95(1): 19-47.
  2. Zhang, Q.; et al. The importance of non-HLA antibodies in transplantation. Nat Rev Nephrol. 2016, 12(8): 484-495.
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