B-cell biomarkers in transplantation - from genes to therapy

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B-cell biomarkers in transplantation - from genes to therapy. / Banham, Gemma; Clatworthy, M R.

In: Tissue Antigens, Vol. 85, No. 2, 02.2015, p. 82-92.

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Banham, Gemma ; Clatworthy, M R. / B-cell biomarkers in transplantation - from genes to therapy. In: Tissue Antigens. 2015 ; Vol. 85, No. 2. pp. 82-92.

Bibtex

@article{e345b38b65c54c59af7af59e99e21157,
title = "B-cell biomarkers in transplantation - from genes to therapy",
abstract = "An increased understanding of the mechanisms by which the immune system mounts a response to transplanted organs has allowed the development of immunosuppressive regimens that limit acute T-cell-mediated rejection (TCMR). However, the treatment of acute and chronic antibody-mediated rejection (ABMR) in kidney transplants remains sub-optimal. The occurrence and severity of antibody-mediated graft pathology are variable, and genetic polymorphisms that affect the magnitude and nature of the B-cell response, as well as effector functions of antibody, are likely to contribute to such phenotypic variation. Here we review current efforts to understand and quantify the contribution of B cells to renal transplant pathology by studying variation in DNA, mRNA and proteins. Large genetic studies with information on B-cell-specific genetic variants are scarce. At a transcriptomic level, there is evidence that B cells are essential contributors to transplant tolerance and may protect against TCMR and ABMR. In contrast, at the protein level, the detection of donor-specific human leukocyte antigen (HLA) antibodies and an assessment of their capacity to bind complement allow patients of high immunological risk to be identified. Other biomarkers, such as serum B-cell-activating factor (BAFF) or interleukin (IL)-10-producing B cells, may allow this risk stratification to be refined. An increased understanding of the significance of these biomarkers should allow a more accurate assessment of how an individual patient's B cells will impact allograft responses and thereby allow clinicians to adjust therapeutic strategies appropriately. ",
keywords = "Animals, B-Lymphocytes/immunology, Biomarkers/metabolism, Genes, Humans, Kidney Transplantation, Lymphocyte Activation/immunology, Transcriptome/genetics, B cells, transcriptomics, genetic variation, tolerance",
author = "Gemma Banham and Clatworthy, {M R}",
note = "{\textcopyright} 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.",
year = "2015",
month = feb,
doi = "10.1111/tan.12520",
language = "English",
volume = "85",
pages = "82--92",
journal = "Tissue Antigens",
issn = "0001-2815",
publisher = "Wiley",
number = "2",

}

RIS

TY - JOUR

T1 - B-cell biomarkers in transplantation - from genes to therapy

AU - Banham, Gemma

AU - Clatworthy, M R

N1 - © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

PY - 2015/2

Y1 - 2015/2

N2 - An increased understanding of the mechanisms by which the immune system mounts a response to transplanted organs has allowed the development of immunosuppressive regimens that limit acute T-cell-mediated rejection (TCMR). However, the treatment of acute and chronic antibody-mediated rejection (ABMR) in kidney transplants remains sub-optimal. The occurrence and severity of antibody-mediated graft pathology are variable, and genetic polymorphisms that affect the magnitude and nature of the B-cell response, as well as effector functions of antibody, are likely to contribute to such phenotypic variation. Here we review current efforts to understand and quantify the contribution of B cells to renal transplant pathology by studying variation in DNA, mRNA and proteins. Large genetic studies with information on B-cell-specific genetic variants are scarce. At a transcriptomic level, there is evidence that B cells are essential contributors to transplant tolerance and may protect against TCMR and ABMR. In contrast, at the protein level, the detection of donor-specific human leukocyte antigen (HLA) antibodies and an assessment of their capacity to bind complement allow patients of high immunological risk to be identified. Other biomarkers, such as serum B-cell-activating factor (BAFF) or interleukin (IL)-10-producing B cells, may allow this risk stratification to be refined. An increased understanding of the significance of these biomarkers should allow a more accurate assessment of how an individual patient's B cells will impact allograft responses and thereby allow clinicians to adjust therapeutic strategies appropriately.

AB - An increased understanding of the mechanisms by which the immune system mounts a response to transplanted organs has allowed the development of immunosuppressive regimens that limit acute T-cell-mediated rejection (TCMR). However, the treatment of acute and chronic antibody-mediated rejection (ABMR) in kidney transplants remains sub-optimal. The occurrence and severity of antibody-mediated graft pathology are variable, and genetic polymorphisms that affect the magnitude and nature of the B-cell response, as well as effector functions of antibody, are likely to contribute to such phenotypic variation. Here we review current efforts to understand and quantify the contribution of B cells to renal transplant pathology by studying variation in DNA, mRNA and proteins. Large genetic studies with information on B-cell-specific genetic variants are scarce. At a transcriptomic level, there is evidence that B cells are essential contributors to transplant tolerance and may protect against TCMR and ABMR. In contrast, at the protein level, the detection of donor-specific human leukocyte antigen (HLA) antibodies and an assessment of their capacity to bind complement allow patients of high immunological risk to be identified. Other biomarkers, such as serum B-cell-activating factor (BAFF) or interleukin (IL)-10-producing B cells, may allow this risk stratification to be refined. An increased understanding of the significance of these biomarkers should allow a more accurate assessment of how an individual patient's B cells will impact allograft responses and thereby allow clinicians to adjust therapeutic strategies appropriately.

KW - Animals

KW - B-Lymphocytes/immunology

KW - Biomarkers/metabolism

KW - Genes

KW - Humans

KW - Kidney Transplantation

KW - Lymphocyte Activation/immunology

KW - Transcriptome/genetics

KW - B cells

KW - transcriptomics

KW - genetic variation

KW - tolerance

U2 - 10.1111/tan.12520

DO - 10.1111/tan.12520

M3 - Review article

C2 - 25626600

VL - 85

SP - 82

EP - 92

JO - Tissue Antigens

JF - Tissue Antigens

SN - 0001-2815

IS - 2

ER -