Large Granular Lymphocytosis in a Patient Infected with HTLV-II

Martin, Maureen P.; Biggar, Robert J.; Hamlin-Green, Gina; Staal, Stephen; Mann, Dean L.

doi:10.1089/aid.1993.9.715

Cited by 36 publications

(17 citation statements)

References 24 publications

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“…8 Although other groups grated in the normal CD3 + CD8 + cells but not in the expanded neoplastic large granular cell population of NK phenotype report evidence for HTLV-I or -II infection in LGL leukemia (Table 2), there is only one case with convincing demon-(CD3 − CD16 + ). 29 In summary, our findings do not support a role for HTLV-I stration of clonal integration of either retrovirus in the neoplastic cells. 28 In this patient, a case of LGL leukemia was associaor -II in T-PLL or LGL leukemia.…”

Section: Reverse Transcriptase (Rt) Assaycontrasting

confidence: 81%

“…29,[31][32][33][34] For example, in the largest study of HTLV-II in Again, in keeping with our results, two groups found no serological or molecular evidence of HTLV infection in LGL…”

Section: Reverse Transcriptase (Rt) Assaysupporting

confidence: 81%

“…28 disease. 29 LGL lymphocytosis may be reactive to a number of viral genome in the current study makes failure of amplifi-…”

Section: Reverse Transcriptase (Rt) Assaymentioning

confidence: 69%

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The human T-cell lymphotropic viruses types I/II are not involved in T prolymphocytic leukemia and large granular lymphocytic leukemia

et al. 1997

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The possible involvement of the human T lymphotropic viruseswith T-PLL is also complicated by the inconsistent classi- LGL leukemia is also rare and, unlike T-PLL or ATLL, the involvement is a frequent feature of T prolymphocytic leukemia (T-PLL) and antibodies against HTLV-I and -II have been malignant cell usually has a CD4 − CD8 + or, rarely, a natural and -II in T-PLL and LGL leukemia, we investigated 64 such reverse transcriptase assay patients for the presence of HTLV-I/II by serology and molecular techniques using PCR primers against HTLV-II and all parts of the HTLV-I genome. The sensitivity of the technique was Introduction increased by using nested PCR. Reverse transcriptase (RT) activity was also measured in supernatants from peripheral The human T cell lymphotropic virus type I (HTLV-I) was first blood mononuclear cells (PBMCs) in short-term culture (STC). isolated from a patient with a mature CD4 + T cell lymphoproliferative disorder subsequently diagnosed as adult T cell leukemia/lymphoma (ATLL). 1 A related retrovirus, HTLV-II, Patients and methods was later isolated from cell lines from two patients thought to have a T cell variant of hairy cell leukemia. 2,3 This led to a hunt for the retrovirus in other mature T cell lymphoproliferPatients ative disorders. A few groups have reported the presence of HTLV-I sequences in seronegative cases of cutaneous T cell T-PLL is a lymphoproliferative disorder of mature (TdT+) T lymphoma (CTCL), although the proportion of positive cases cells characterized by splenomegaly, lymphadenopathy, fredocumented varies widely and findings remain controquent skin involvement and circulating abnormal prolymphoversial. 4,5 T prolymphocytic leukemia (T-PLL) shares some cytes (often greater than 200 × 10 9 /l) whose phenotype is usuclinical and histopathological features with ATLL, namely skin ally CD4 + CD8 − . The diagnostic features of LGL leukemia are infiltration, aggressive course and a CD4 + phenotype of maliga sustained lymphocytosis Ͼ4 × 10 9 /l with Ͼ80% of lymphonant lymphocytes in two-thirds of cases. 6 However, T-PLL is cytes showing prominent azurophilic granules, neutropenia or a rare disorder representing only around 3% of mature B and other cytopenia not related to heavy bone marrow infiltration, T cell leukemias 7 and few cases have been studied for eviand predominance of a discrete T cell or natural killer subset dence of HTLV-I or -II infection using a range of sensitive techby membrane marker analysis, commonly CD3 + CD4 − CD8 + niques. The question of whether HTLV-I or -II is associated or CD3 − CD4 − CD8 − CD16 + CD56 + , respectively. Sixty-four patients were studied, 36 with T-PLL and 28 with LGL leukemia, three of the latter having NK phenotype. Serology for HTLV-I/II by ELISA and particle agglutination, performed at the PHLS Reference Laboratory, Colindale, London,

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Section: Reverse Transcriptase (Rt) Assaycontrasting

confidence: 81%

“…29,[31][32][33][34] For example, in the largest study of HTLV-II in Again, in keeping with our results, two groups found no serological or molecular evidence of HTLV infection in LGL…”

Section: Reverse Transcriptase (Rt) Assaysupporting

confidence: 81%

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The human T-cell lymphotropic viruses types I/II are not involved in T prolymphocytic leukemia and large granular lymphocytic leukemia

et al. 1997

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“…38 The fact that transgenic mice for the HTLV-I tax gene develop NK cell LGL leukemia 39,40 and that sera from patients with both T-cell and NK cell LGL leukemia frequently react with HTLV-I/II p21 envelope proteins 41 had lead to the hypothesis of a direct relationship between CNKCL and infection by retroviruses. As in this series, cases of HTLV 42,43 or HIV-infected individuals 44 associated with CNKCL have been previously described. However, efforts to document association of CNKCL and infection with these 45,46 or other retroviruses 47 have been also unsuccessful.…”

Section: Discussionmentioning

confidence: 69%

Clinicobiological, Immunophenotypic, and Molecular Characteristics of Monoclonal CD56−/+dim Chronic Natural Killer Cell Large Granular Lymphocytosis

Lima

Almeida

Montero

et al. 2004

The American Journal of Pathology

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Indolent natural killer (NK) cell lymphoproliferative disorders include a heterogeneous group of patients in whom persistent expansions of mature, typically CD56 ؉ , NK cells in the absence of any clonal marker are present in the peripheral blood. In the present study we report on the clinical, hematological, immunophenotypic, serological, and molecular features of a series of 26 patients with chronic large granular NK cell lymphocytosis, whose NK cells were either CD56 ؊ or expressed very low levels of CD56 (CD56 ؊/؉dim NK cells), in the context of an aberrant activation-related mature phenotype and proved to be monoclonal using the human androgen receptor gene polymerase chain reaction-based assay. As normal CD56 ؉ NK cells, CD56 ؊/؉dim NK cells were granzyme B ؉ , CD3 ؊ , TCR␣␤/ ␥␦ ؊ , CD5 ؊ , CD28 ؊ , CD11a ؉bright , CD45RA ؉bright , CD122 ؉ , and CD25 ؊ and they showed variable and heterogeneous expression of both CD8 and CD57. Nevertheless, they displayed several unusual immunophenotypic features. Accordingly, besides being CD56 ؊/؉dim , they were CD11b ؊/؉dim (heterogeneous), CD7 ؊/؉dim (heterogeneous), CD2 ؉ (homogeneous), CD11c ؉bright (homogeneous), and CD38 ؊/؉dim (heterogeneous). Moreover, CD56 ؊/؉dim NK cells heterogeneously expressed HLA-DR. In that concerning the expression of killer receptors, CD56 ؊/؉dim NK cells showed bright and homogeneous CD94 expression, and dim and heterogeneous reactivity for CD161, whereas CD158a and NKB1 expression was variable. From the functional point of view, CD56 ؊/؉dim showed a typical Th1 pattern of cytokine production (interferon-␥ ؉ , tumor necrosis factor-␣ ؉ ). From the clinical point of view, these patients usually had an indolent clinical course, progression into a massive lymphocytosis with lung infiltration leading to death being observed in only one case. Despite this, they frequently had associated cytopenias as well as neoplastic diseases and/or viral infections. In summary, we describe a unique and homogeneous group of monoclonal chronic large granular NK cell lymphocytosis with an aberrant activation-related CD56 ؊/؉dim /CD11b ؊/؉dim phenotype and an indolent clinical course, whose main clinical features are related to concomitant diseases. (Am J

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“…Unlike HTLV-1, the related virus HTLV-2 has not been linked to human malignancies (33,55). HTLV-2, however, encodes a Tax protein (Tax2) which is highly homologous to HTLV-1 Tax (Tax1).…”

Section: Resultsmentioning

confidence: 99%

Genetic Evidence of a Role for ATM in Functional Interaction between Human T-Cell Leukemia Virus Type 1 Tax and p53

Van

Yim

Jin

et al. 2001

J Virol

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Recent evidence from several investigators suggest that the human T-cell leukemia virus type 1 Tax oncoprotein represses the transcriptional activity of the tumor suppressor protein, p53. An examination of published findings reveals serious controversy as to the mechanism(s) utilized by Tax to inhibit p53 activity and whether the same mechanism is used by Tax in adherent and suspension cells. Here, we have investigated Tax-p53 interaction simultaneously in adherent epithelial (HeLa and Saos) and suspension T-lymphocyte (Jurkat) cells. Our results indicate that Tax activity through the CREB/CREB-binding protein (CBP), but not NF-B, pathway is needed to repress the transcriptional activity of p53 in all tested cell lines. However, we did find that while CBP binding by Tax is necessary, it is not sufficient for inhibiting p53 function. Based on knockout cell studies, we correlated a strong genetic requirement for the ATM, but not protein kinasedependent DNA, protein in conferring a Tax-p53-repressive phenotype.

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Large Granular Lymphocytosis in a Patient Infected with HTLV-II

Cited by 36 publications

References 24 publications

The human T-cell lymphotropic viruses types I/II are not involved in T prolymphocytic leukemia and large granular lymphocytic leukemia

The human T-cell lymphotropic viruses types I/II are not involved in T prolymphocytic leukemia and large granular lymphocytic leukemia

Clinicobiological, Immunophenotypic, and Molecular Characteristics of Monoclonal CD56−/+dim Chronic Natural Killer Cell Large Granular Lymphocytosis

Genetic Evidence of a Role for ATM in Functional Interaction between Human T-Cell Leukemia Virus Type 1 Tax and p53

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