Cell-mediated immunity against epstein-barr virus infected B lymphocytes

Klein, Eva; Masucci, Maria G.

doi:10.1007/bf00201957

Cited by 9 publications

(4 citation statements)

References 48 publications

(36 reference statements)

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“…EBV is a DNA virus that primarily infects B-lymphocytes, and can transform and immortalize the host cell (Epstein and Achong, 1979). This virus has been associated with several conditions including infectious mononucleosis, benign lymphoproliferative disorders, nasopharyngeal carcinoma, Burkitt's lymphoma, and NHL of both B-and T-cell types (Epstein and Achong, 1973;Henle et al, 1976;Klein and Masucci, 1982;Evans, 1988;Cartwright et al, 1988;Jones et al, 1988).…”

Section: Discussionmentioning

confidence: 99%

Epstein‐barr virus antibody patterns preceding the diagnosis of non‐hodgkin's lymphoma

Müeller

Mohar

Evans

et al. 1991

Intl Journal of Cancer

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Immunosuppressed patients who develop non-Hodgkin's lymphoma (NHL) have abnormal antibody responses against the Epstein-Barr virus (EBV) prior to the diagnosis of malignancy. To see if this is also true of "spontaneous" cases in the general population, we undertook a collaborative serologic case-control study. From 4 serum banks containing specimens from over 240,000 persons, 104 subjects were identified for whom a blood specimen had been stored an average of 63 months before diagnosis of NHL, and 259 controls matched for age, sex, ethnic group and date of serum collection. The relative risks (RR) for subsequent development of NHL associated with elevated levels of IgG and IgM antibodies against viral capsid antigen were 2.5 (95% confidence interval = 1.1-5.7) and 3.2 (1.3-7.5), respectively; these associations increased with age at diagnosis. For the nuclear antigen, the distribution of titers for cases was more restricted than that of controls, with fewer cases having either elevated or low titers, RR = 0.5 (0.2-1.4) and 0.5 (0.2-1.2), respectively. Cases had significantly lower antibody titers against the cytomegalovirus, RR = 0.4 (0.2-0.9). These findings suggest that, at least for some patients, NHL is preceded by an enhanced level of endogenous immunosuppression with resultant EBV activation. This observation supports the role of EBV either directly in the development of NHL or as a primary marker of immune dysfunction.

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Section: Discussionmentioning

confidence: 99%

Epstein‐barr virus antibody patterns preceding the diagnosis of non‐hodgkin's lymphoma

Müeller

Mohar

Evans

et al. 1991

Intl Journal of Cancer

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“…In the normal host, EBV-induced lymphoproliferation is primarily controlled by EBV-specific cytotoxic T cells. [27][28][29] In the absence of T-cell surveillance, clonal subpopulations can develop, leading to monoclonal lymphomas. 2' 24 Regression of EBVtransformed B cells in vitro has been shown to depend on the presence of viral-specific cytotoxic T cells 27,30 EBV has been implicated in virtually all cases of posttransplant lymphoma.…”

Section: Discussionmentioning

confidence: 99%

“…EBV is a herpes group virus that infects and immortalizes B lymphocytes in vitro 25 and in vivo, 26 resulting in their polyclonal activation and proliferation. In the normal host, EBV‐induced lymphoproliferation is primarily controlled by EBV‐specific cytotoxic T cells 27‐29 . In the absence of T‐cell surveillance, clonal subpopulations can develop, leading to monoclonal lymphomas 2 , 24 .…”

Section: Discussionmentioning

confidence: 99%

Tonsil lymphoma presenting as tonsillitis after bone marrow transplantation

Yellin¹,

Weiss²,

Kraus³

et al. 1995

Otolaryngol.--head neck surg.

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Bone marrow transplantation for the treatment of leukemia is increasingly successful in rendering patients disease free. However, it has become evident that the associated severe immunosuppression predisposes this population to an increased risk for other neoplastic disorders. We report on six patients in whom non-Hodgkin's lymphoma of the tonsillar region developed within 5 months after T-cell-depleted bone marrow transplantation for the treatment of leukemia at Memorial Sloan-Kettering Cancer Center from October 1990 to October 1992. These patients initially had what appeared to be infectious exudative pharyngitis/tonsillitis; however, they did not improve with medical therapy. Because of the persistence of pharyngitis/tonsillitis in association with cervical lymphadenopathy and odynophagia, the patients underwent definitive biopsy in the form of tonsillectomy, cervical lymph node biopsy, or both. Histopathologic review revealed non-Hodgkin's lymphoma. An association with Epstein-Barr virus has been noted in five of these patients. This article is aimed at alerting the clinician to consider the diagnosis of lymphoma in a patient with persistent pharyngitis/tonsillitis despite adequate medical therapy after bone marrow transplantation.

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“…When EBV infects Old World primates, it immortalizes a proportion of their B cells. However, the immune system in Old World primates evolved to mount an extensive T cell response against EBV antigens, which in humans results in the transient infectious mononucleosis disease (Klein and Masucci, 1982;Callan, 2003). The proliferating T cells kill the majority of B cells infected by the virus and immortalized.…”

Section: Enveloped Viruses Appearing After New World Monkeys/old Worlmentioning

confidence: 99%

Why Do We Produce Anti-Gal

Galili

2018

The Natural Anti-Gal Antibody as Foe Turned Friend in Medicine

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Cell-mediated immunity against epstein-barr virus infected B lymphocytes

Cited by 9 publications

References 48 publications

Epstein‐barr virus antibody patterns preceding the diagnosis of non‐hodgkin's lymphoma

Epstein‐barr virus antibody patterns preceding the diagnosis of non‐hodgkin's lymphoma

Tonsil lymphoma presenting as tonsillitis after bone marrow transplantation

Why Do We Produce Anti-Gal

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