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Abstract
BackgroundAltered immune mechanisms play a critical role in the pathogenesis of non-Hodgkin’s lymphoma (NHL). HIV-1 (HIV) infection is associated with a state of excessive T-cell activation, which can lead to increased T-cell turnover and lymph node fibrosis.ObjectivesThis study aimed to determine the serum levels of circulating B-cell activation markers, and the expression of T-cell activation and regulatory markers in HIV-positive NHL patients.MethodThe serum levels of circulating soluble(s) sCD20, sCD23, sCD27, sCD30 and sCD44 molecules, all of which are biomarkers of B-cell activation, were determined by enzyme-linked immunosorbent assays (ELISA), while biomarkers of T-cell activation (CD8+CD38+) and regulation (FoxP3) were determined by flow cytometry in 141 subjects who were divided into five groups: Combination antiretroviral therapy (ART)-naïve HIV-positive patients; ART-treated HIV-positive patients; HIV-negative NHL patients; HIV-positive NHL patients on ART; and healthy controls.ResultsHIV-positive NHL patients had significantly higher serum levels of sCD20, sCD23, sCD30 and sCD44 than HIV-negative NHL patients, while all five biomarkers were significantly elevated in HIV-positive NHL patients when compared with ART-treated HIV-positive patients. HIV-positive NHL patients had higher CD8+CD38+ and lower FoxP3 expression than HIV-negative NHL and ART-treated HIV-positive patients.ConclusionB-cell activation is increased in HIV-positive NHL patients and is associated with reduced regulatory T-cell populations and increased CD8+ T-cell activation.
Highlights
Non-Hodgkin’s lymphoma (NHL) refers to a heterogeneous group of haematopoietic malignancies originating in the lymphocytes.[1,2,3] Non-Hodgkin’s lymphoma is the second most common malignancy affecting HIV-1 (HIV)-infected individuals.[4]
B-cell activation is characterised by lymphocyte proliferation, class switch recombination and somatic hypermutation, all of which are prone to DNA mutations that may lead to lymphomagenesis.[5]
Patients diagnosed with HIV infection (ART-treated and naïve) and a CD4+ T-cell count of ≤ 350 cells/μL, patients with HIVassociated NHL, HIV-negative NHL patients and a healthy control group were included in this study
Summary
Non-Hodgkin’s lymphoma (NHL) refers to a heterogeneous group of haematopoietic malignancies originating in the lymphocytes.[1,2,3] Non-Hodgkin’s lymphoma is the second most common malignancy affecting HIV-1 (HIV)-infected individuals.[4] Altered immune mechanisms play a critical role in the pathogenesis of NHL, as evidenced by increased rates of NHL among HIVpositive patients, transplant recipients and autoimmune disease patients.[5,6] HIV infection has been associated with a state of excessive T-cell activation, which has been shown to be a strong prognostic indicator for disease progression at different stages of HIV infection.[7]. HIV-1 (HIV) infection is associated with a state of excessive T-cell activation, which can lead to increased T-cell turnover and lymph node fibrosis
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