Article

Elevated serum soluble CD30 precedes the development of AIDS-associated non-Hodgkin's B cell lymphoma

Department of Obstetrics and Gynecology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095-1740, USA.
Tumor Biology (Impact Factor: 3.61). 02/2006; 27(4):187-94. DOI: 10.1159/000093022
Source: PubMed

ABSTRACT CD30, first described as the Ki antigen on malignant B cells in Hodgkin's lymphoma, is also expressed on normal activated B and T cells. It can be cleaved from the cell surface and detected in normal serum as soluble CD30 (sCD30), where it can be an indicator of levels of immune activation. In a cross-sectional study utilizing archived sera at a time point close to but preceding a diagnosis of acquired immunodeficiency syndrome (AIDS)-associated non-Hodgkin's B cell lymphoma, AIDS lymphoma subjects (n = 49) showed elevated mean levels of sCD30 compared to controls with AIDS but no malignancy (n = 44, p < 0.01), HIV-infected but relatively healthy (n = 47, p < 0.001), or HIV-seronegative controls (n = 44, p < 0.001). Serum sCD30 was significantly correlated to serum levels of the B cell cytokines interleukin-6 (IL-6), IL-10, and sCD23, but only among lymphoma subjects (p < or = 0.05). Correlations between sCD30 and other markers of immune system activation were seen among all HIV-infected subjects (sCD27, sCD44, CXCL13, p < 0.05). These observations suggest that sCD30, especially in combination with other immune system molecules, could be an important biomarker for an immune system environment conducive to B cell hyperactivation and the development of AIDS-associated B cell lymphoma.

1 Follower
 · 
118 Views
  • Source
    • "HIV also causes an inflammatory milieu which further drives the activation and proliferation of B lymphocytes . Specifically levels of soluble CD30 have been noted to be elevated prior to diagnosis of NHL in HIV patients [26]. Other cytokines have also been implicated in this process, notably IL-6, IL-10, and TNF-α [27, 28] (Figure 1). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Immune surveillance is a dynamic process that involves an intact immune system to identify and protect the host against tumor development. The increased understanding of the genetics, infections and hematological malignancies in congenital immune deficiency states supports the concept that impaired T cells and Natural-killer/T cells leads to B-cell lymphoma. Furthermore, severe combined immunodeficient mice are prone to spontaneous tumor development and therefore serve as experimental models. Here we discuss the acquired conditions and mechanisms involved in dysregulation of the immune system that lead to lymphoma. Preemptive strategies to improve immune regulation and response and restore a competent immune system may lead to a decrease in lymphoid malignancies.
    01/2013; 3(2):91-101.
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Environmental and immunologic cofactors for the risk of classic Kaposi sarcoma in Sicily
  • [Show abstract] [Hide abstract]
    ABSTRACT: We discuss recently published studies that elucidate the pathogenesis of AIDS-associated lymphoma. Several recent reports have provided valuable new information on the role of gamma-herpesviruses in the pathogenesis of AIDS-associated lymphoma. In addition to this, significant new information has become available on how B cell activation-associated DNA-modifying events, involving activation-induced cytidine deaminase and DNA polymerase-eta, contribute to the molecular lesions that result in AIDS-associated lymphoma. In particular, new evidence that oncogenic viruses can directly induce activation-induced cytidine deaminase expression and oncogene mutation in human B cells is of central relevance to better understanding the pathogenesis of AIDS-associated lymphoma. New information provides insights into the contributions of immune dysfunction and oncogenic virus infection to pathogenesis of AIDS-associated lymphoma, and may lead to new potential targets for therapeutic intervention in these cancers.
    Current Opinion in Oncology 10/2006; 18(5):444-8. DOI:10.1097/01.cco.0000239882.23839.e5 · 3.76 Impact Factor
Show more