Do CD4+ T Cell Functional Responses to Epstein–Barr Virus Provide Protective Immunity Against CNS Lymphoma in AIDS 英文参考文献.docVIP

Perspectives Do CD4 T Cell Functional Responses + to Epstein–Barr Virus Provide Protective Immunity Against CNS Lymphoma in AIDS? Mark A. Jacobson S ince highly active antiretroviral treatment (HAART) regimens became widely available in North America and Europe in 1996, the incidence of AIDS-de?ning individuals. This means that potential correlates of protective immunity can be identi?ed by comparing infection appears to have a critical pathogenic role. Like CMV retinitis, AIDS-associated PCNS lymphomas usually occur in patients with very advanced AIDS. The role of EBV in the pathogenesis of this disease is supported by studies that show the presence of EBV-encoded small RNA in tissue specimens from virtually all cases [5] and the high sensitivity and speci?city of EBV DNA in cerebrospinal ?uid for biopsy- or autopsy-con?rmed primary CNS lymphoma [6]. immunoassay results in patients who have clear evidence of absent CMV- protective immunity (i.e., patients with AIDS with active CMV retinitis) to those in patients who have clear evidence of restored CMV-protective immunity (i.e., patients with AIDS and CMV retinitis who, after HAART, are able to discontinue anti-CMV therapy without further retinitis reactivation or progression). For example, we recently identi?ed a pattern of immune function that was completely absent in the peripheral blood mononuclear cells (PBMC) of 100% of 24 patients with active CMV retinitis but was partially or completely present in the PBMC of 85% of 34 patients with CMV retinitis patients who had been clinically immuno-restored by HAART [4]. The pattern that we found was the presence of CMV antigen- opportunistic infections and malignancies has declined dramatically. This decline has been attributed to restoration of protective immunity by HAART since HAART improves many of the de?cits in T and B cell function that are caused by uncontrolled HIV infection. Some of these de?cits include diminished antigen-speci?c T cell proliferation and