Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2012:2012:230173.
doi: 10.1155/2012/230173. Epub 2012 Apr 17.

Posttransplant lymphoproliferative disorders

Hazem A H Ibrahim  1 , Kikkeri N Naresh
Affiliations

Posttransplant lymphoproliferative disorders

Hazem A H Ibrahim et al. Adv Hematol. 2012.

Abstract

Posttransplant lymphoproliferative disorders (PTLDs) are a group of diseases that range from benign polyclonal to malignant monoclonal lymphoid proliferations. They arise secondary to treatment with immunosuppressive drugs given to prevent transplant rejection. Three main pathologic subsets/stages of evolution are recognised: early, polymorphic, and monomorphic lesions. The pathogenesis of PTLDs seems to be multifactorial. Among possible infective aetiologies, the role of EBV has been studied in depth, and the virus is thought to play a central role in driving the proliferation of EBV-infected B cells that leads to subsequent development of the lymphoproliferative disorder. It is apparent, however, that EBV is not solely responsible for the "neoplastic" state. Accumulated genetic alterations of oncogenes and tumour suppressor genes (deletions, mutations, rearrangements, and amplifications) and epigenetic changes (aberrant hypermethylation) that involve tumour suppressor genes are integral to the pathogenesis. Antigenic stimulation also plays an evident role in the pathogenesis of PTLDs. Plasmacytoid dendritic cells (PDCs) that are critical to fight viral infections have been thought to play a pathogenetically relevant role in PTLDs. Furthermore, regulatory T cells (Treg cells), which are modulators of immune reactions once incited, seem to have an important role in PTLDs where antigenic stimulation is key for the pathogenesis.

PubMed Disclaimer

Figures

Figure 1
Figure 1
A typical case of polymorphic PTLD. (a) Infiltrate is a mix of plasma cells, small lymphoid cells and larger cells with nucleoli. The cells are positive for CD20 (b), CD30 (c), MUM1 (d), EBER (e), and EBV-LMP-1. Magnification: (b,d): ×100; (a,e,f): ×200.
Figure 2
Figure 2
A proposed model of pathogenesis of EBV infection in the development of PTLDs in sold organ transplant recipients. CTL: cytotoxic T lymphocytes, IL-10: interleukin-10, INF-α: Interferon-α, NK cells: natural killer cells, PDC: plasmacytoid dendritic cells, TLR-9: toll-like receptor-9.
See this image and copyright information in PMC

References

    1. Kwong YL, Lam CCK, Chan TM. Post-transplantation lymphoproliferative disease of natural killer cell lineage: a clinicopathological and molecular analysis. British Journal of Haematology. 2000;110(1):197–202. - PubMed
    1. Kumar S, Kumar D, Kingma DW, Jaffe ES. Epstein-Barr virus-associated T-cell lymphoma in a renal transplant patient. American Journal of Surgical Pathology. 1993;17(10):1046–1053. - PubMed
    1. Swerdlow SH, Webber SA, Chadburn A, et al. Post-transplant lymphoproliferative disorders. In: Swerdlow SH, Campo E, Harris NL, et al., editors. WHO Classification of Tumours of Haematopoietic and Lymphoid Tissues. Lyon, France: IARC; 2008. pp. 343–349.
    1. Yin CC, Medeiros LJ, Abruzzo LV, Jones D, Farhood AI, Thomazy VA. EBV-associated B- and T-cell posttransplant lymphoproliferative disorders following primary EBV infection in a kidney transplant recipient. American Journal of Clinical Pathology. 2005;123(2):222–228. - PubMed
    1. Chadburn A, Suciu-Foca N, Cesarman E, Reed E, Michler RE, Knowles DR. Post-transplantation lymphoproliferative disorders arising in solid organ transplant recipients are usually of recipient origin. American Journal of Pathology. 1995;147(6):1862–1870. - PMC - PubMed