scholarly journals B-ly-7, a monoclonal antibody reactive with hairy cell leukemia, also defines an activation antigen on normal CD8+ T cells [see comments]

Blood ◽  
1990 ◽  
Vol 76 (5) ◽  
pp. 959-964
Author(s):  
SP Mulligan ◽  
P Travade ◽  
E Matutes ◽  
C Dearden ◽  
L Visser ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
T Cells ◽  
T Cell ◽  
B Cell ◽  
Cd8 T Cells ◽  
Peripheral Blood ◽  
Hairy Cell Leukemia ◽  
Hairy Cell ◽  
Cell Leukemia ◽  
Activation Antigen

We undertook a study to determine the specificity of the monoclonal antibody, B-ly-7, for hairy cell leukemia (HCL) by examining the expression in 150 samples from B-cell lymphoproliferative diseases as well as screening for reactivity in a number of other hematologic malignancies. Within the B-cell lineage we found that the expression of B-ly-7 was highly specific for HCL and reacted with all 28 cases examined, as well as with 3 of 9 cases of a variant form of HCL. Cells of other closely related B-cell disorders, prolymphocytic leukemia, and splenic lymphoma with villous lymphocytes were negative. Investigation of the peripheral blood and bone marrow of patients with HCL before and after treatment with alpha-interferon or deoxycoformycin suggests that B-ly-7 may be useful in the assessment of minimal disease after therapy. In addition to HCL, we found that B-ly-7 was positive with cells of three mature, CD4+ T-cell malignancies. In view of the reactivity with malignancies of activated B and T cells, we searched for the expression of B-ly-7 on activated, normal B and T cells and found that B-ly-7 reacted specifically with activated normal peripheral blood CD8+ T cells. B-ly-7 has a number of applications, including the precise classification of mature B-cell neoplasia and the diagnosis HCL and its assessment after treatment. In addition, B-ly-7 recognizes a small subset of T-cell disorders. Its expression on these malignancies and on in vitro activated peripheral blood CD8+ T cells suggests that B- ly-7 detects a lymphocyte activation antigen.

scholarly journals B-ly-7, a monoclonal antibody reactive with hairy cell leukemia, also defines an activation antigen on normal CD8+ T cells [see comments]

Blood ◽  
1990 ◽  
Vol 76 (5) ◽  
pp. 959-964 ◽  
Author(s):  
SP Mulligan ◽  
P Travade ◽  
E Matutes ◽  
C Dearden ◽  
L Visser ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
T Cells ◽  
T Cell ◽  
B Cell ◽  
Cd8 T Cells ◽  
Peripheral Blood ◽  
Hairy Cell Leukemia ◽  
Hairy Cell ◽  
Cell Leukemia ◽  
Activation Antigen

Abstract We undertook a study to determine the specificity of the monoclonal antibody, B-ly-7, for hairy cell leukemia (HCL) by examining the expression in 150 samples from B-cell lymphoproliferative diseases as well as screening for reactivity in a number of other hematologic malignancies. Within the B-cell lineage we found that the expression of B-ly-7 was highly specific for HCL and reacted with all 28 cases examined, as well as with 3 of 9 cases of a variant form of HCL. Cells of other closely related B-cell disorders, prolymphocytic leukemia, and splenic lymphoma with villous lymphocytes were negative. Investigation of the peripheral blood and bone marrow of patients with HCL before and after treatment with alpha-interferon or deoxycoformycin suggests that B-ly-7 may be useful in the assessment of minimal disease after therapy. In addition to HCL, we found that B-ly-7 was positive with cells of three mature, CD4+ T-cell malignancies. In view of the reactivity with malignancies of activated B and T cells, we searched for the expression of B-ly-7 on activated, normal B and T cells and found that B-ly-7 reacted specifically with activated normal peripheral blood CD8+ T cells. B-ly-7 has a number of applications, including the precise classification of mature B-cell neoplasia and the diagnosis HCL and its assessment after treatment. In addition, B-ly-7 recognizes a small subset of T-cell disorders. Its expression on these malignancies and on in vitro activated peripheral blood CD8+ T cells suggests that B- ly-7 detects a lymphocyte activation antigen.

scholarly journals Hairy cell leukemia: a tumor of pre-plasma cells

Blood ◽  
1985 ◽  
Vol 65 (3) ◽  
pp. 620-629 ◽  
Author(s):  
KC Anderson ◽  
AW Boyd ◽  
DC Fisher ◽  
D Leslie ◽  
SF Schlossman ◽  
...  
Keyword(s):  
T Cell ◽  
B Cell ◽  
Plasma Cell ◽  
Hairy Cell Leukemia ◽  
Plasma Cells ◽  
Tartrate Resistant Acid Phosphatase ◽  
Hairy Cell ◽  
Cell Leukemia ◽  
Cell Surface Antigens ◽  
Hairy Cells

Monoclonal antibodies defining B-, T-, and myeloid-restricted cell surface antigens were used to characterize the lineage and state of differentiation of tumor cells isolated from 22 patients with hairy cell leukemia (HCL). These tumors were shown to be of B lineage because they strongly expressed the B cell-restricted antigens B1 and B4 and lacked T cell- and monocyte-restricted antigens. Moreover, the strong expression of the plasma cell-associated PCA-1 antigen on the majority of hairy cells suggested that these tumors correspond to later stages of B cell ontogeny. Dual fluorescence experiments further confirmed that HCL splenocytes that coexpressed B1 and PCA-1 demonstrated both the morphology and tartrate-resistant acid phosphatase positivity of hairy cells. The observation that some hairy cells either spontaneously produce immunoglobulin (Ig) or could be induced to proliferate and secrete Ig provides complementary support for the view that HCL is a pre-plasma cell tumor. However, staining of hairy cells with anti-IL2R1 monoclonal antibody, which is directed to the T cell growth factor receptor and/or with the anti-Mo1 reagent, directed to C3bi complement receptor, distinguish these cells from currently identified B cells.

scholarly journals Rearrangement of both immunoglobulin and T-cell receptor genes in a prolymphocytic variant of hairy cell leukemia patient resistant to interferon-alpha [published erratum appears in Blood 1989 Feb;73(2):624]

Blood ◽  
1988 ◽  
Vol 72 (5) ◽  
pp. 1708-1716
Author(s):  
SL Giardina ◽  
HA Young ◽  
CR Faltynek ◽  
ES Jaffe ◽  
JW Clark ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Peripheral Blood ◽  
Hairy Cell Leukemia ◽  
Cell Receptor ◽  
Hairy Cell ◽  
Cell Leukemia ◽  
Ifn Gamma ◽  
Ifn Alpha ◽  
Alpha Receptors

We describe a patient with the so-called “prolymphocytic variant” form of hairy cell leukemia (HCL) resistant to treatment with interferon- alpha (IFN-alpha). Analysis of immunoglobulin (Ig) and T-cell receptor- beta (TCR beta) gene rearrangements from serial peripheral blood mononuclear cell specimens (MNCs) confirmed not only the B-cell nature of the disease, but also the subsequent emergence of a morphologically indistinguishable population of cells with a clonal TCR beta rearrangement in addition to the original Ig gene rearrangement. With the exception of a transient increase in peripheral blood T cells during treatment with deoxycoformycin (DCF), the MNCs remained essentially constant throughout therapy with no evidence of a co- existing T-cell clone to account for the TCR beta rearrangement. Although MNCs from this patient bound significantly less IFN-alpha than did MNCs from other HCL patients, the binding was of high affinity with a kd similar to that of control cells. The number of IFN-gamma receptors on our patient's MNCs was four times higher than the number of IFN-alpha receptors and was similar to the number of IFN-alpha receptors on MNCs from HCL patients responsive to IFN-alpha. While various treatments including IFN-alpha, DCF, chlorambucil, splenectomy, leukopheresis, and IFN-gamma were not able to change the clinical progression of the disease, they may have provided an opportunity for the divergent TCR beta rearranged clone to expand and displace the initially dominant clone.

Hairy Cell Leukemia-Specific Recognition by Multiple Autologous HLA-DQ or DP-Restricted T-Cell Clones

Blood ◽  
1999 ◽  
Vol 93 (1) ◽  
pp. 251-259
Author(s):  
Lisette van de Corput ◽  
Hanneke C. Kluin-Nelemans ◽  
Michel G.D. Kester ◽  
Roel Willemze ◽  
J.H. Frederik Falkenburg
Keyword(s):  
T Cells ◽  
T Cell ◽  
Hairy Cell Leukemia ◽  
Lymphoblastic Leukemia ◽  
Hairy Cell ◽  
Cell Leukemia ◽  
T Cell Clones ◽  
Cell Clones ◽  
Hla Dq ◽  
T Cell Clone

We studied in patients with hairy cell leukemia (HCL) whether autoreactive T cells could be isolated with specific reactivity to the HCL cells. HCL cells were activated via triggering of CD40 on the cell membrane and used as stimulator cells to generate autologous T-cell clones. Two types of CD4+BV2+ T-cell clones with different CDR3 rearrangements and one type of CD4+BV8S3+ T-cell clone were generated from the spleen or blood. These clones specifically recognized the autologous HCL cells, without reactivity to autologous peripheral blood mononuclear cells (PBMC), phytohemagglutinin blasts, or Epstein-Barr virus–transformed B cells in a primed lymphocyte test. Blocking and panel studies using HCL cells from 11 other patients showed that recognition of the HCL cells by the BV2+ T cells was restricted by HLA-DQA1*03/DQB1*0301, and the BV8S3+ T cells were restricted by DPB1*04. The T-cell clones did not recognize DPB1*04+ or DQ3+ PBMC from healthy donors or DP/DQ matched malignant cells from patients with other hematologic malignancies, except for one patient with acute lymphoblastic leukemia. These HCL-specific T-cell clones may be used for the detection of an HCL-specific tumor antigen.

scholarly journals Hairy Cell Leukemia (Morphologic and Immunophenotypic Profile)

2021 ◽  
Vol 27 (3) ◽  
pp. 346
Author(s):  
Anindita Novia Damayanti ◽  
Arifoel Hajat
Keyword(s):  
Differential Diagnosis ◽  
B Cell ◽  
Peripheral Blood ◽  
Hairy Cell Leukemia ◽  
Lymphocytic Leukemia ◽  
Hairy Cell ◽  
Cell Leukemia ◽  
Cell Markers ◽  
Hla Dr ◽  
Positive Results

Hairy Cell Leukemia (HCL) is a lymphoproliferative B cell abnormality dominated by mature lymphocytes with cytoplasmic projections and often misunderstood as Chronic Lymphocytic Leukemia (CLL). Misdiagnosis can be caused by errors in the preparation of peripheral Blood Smear Evaluation (BSE). Immunophenotyping is an option to differentiate HCL from CLL. A 56-year-old female presented with complaints of weakness. Physical examination showed conjunctival anemia 3 3 and hepatosplenomegaly. Hematological test results were as follows: Hb 7.4 g/dL; WBC 131.24x10 /uL; and Plt 61x10 /uL. BSE And Bone Marrow Aspiration (BMA) showed predominantly mature lymphocytes with cytoplasmic projections and suspected CLL with HCL as the differential diagnosis. Immunophenotyping with peripheral blood samples showed CD19+, CD20+, CD79a+, HLA-DR+, CD5-, and CD7- suggesting an increasing mature lymphocytes population (74.16%) that expressed B lymphoid lineage. White Precursor Cell (WPC) channel test showed an abnormal lymphocytes population. The differential diagnosis of patients with dominant mature lymphocytes BSE with cytoplasmic projections was CLL and HCL. Immunophenotyping of CLL showed positive results on B cell markers (CD19, CD20, CD79a, and HLA-DR) with aberrant CD5. However, in such an HCL case like this, there were strongly positive results on B cell markers but the absence of aberrant CD5. This study was supported by the presence of abnormal lymphocytes population in the WPC test. The diagnosis of HCL in this patient was based on interpretation of BSE and immunophenotyping, supported by the WPC test.

scholarly journals Persistent clonal excess and skewed T-cell repertoire in T cells from patients with hairy cell leukemia

Blood ◽  
1996 ◽  
Vol 87 (9) ◽  
pp. 3795-3802 ◽  
Author(s):  
JC Kluin-Nelemans ◽  
MG Kester ◽  
JJ Melenhorst ◽  
JE Landegent ◽  
L van de Corput ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Hairy Cell Leukemia ◽  
T Cell Subsets ◽  
Cell Populations ◽  
T Cell Repertoire ◽  
Hairy Cell ◽  
Cell Leukemia ◽  
Cell Repertoire ◽  
Blood Samples

Hairy cell leukemia (HCL) is characterized by a severe T-cell-mediated immune deficiency. At the same time, spontaneous T-cell activation is noted when splenic T cells are studied in vivo and in vitro. Therefore, we searched for oligoclonal T-cell populations in the blood and spleens of 25 patients with HCL using a T-cell receptor gamma-polymerase chain reaction (TCR gamma-PCR). Subsequently, in 6 patients, the CDR3 length and conformation from 22 different TCRBV subfamilies were analyzed after PCR amplification of cDNA using TCRBV subfamily-specific primers. T cells from 15 of 25 HCL patients showed clonal excess by the TCR gamma-PCR. In fluorescence-activated cell sorted T-cell subsets, more clonal bands were observed than in the unseparated T cells, with most of these in CD8+ subsets, but also in CD4+, CD3+ gamma/delta+, and a double-negative CD3+ alpha/beta+ subset. In other B-cell malignancies, 6 of 16 samples showed oligoclonal T cells, whereas only 2 of 18 normal spleen and blood samples showed abnormal bands. Analysis of the TCRBV subfamilies disclosed in all 6 HCL patients a markedly abnormal pattern, with many clonal bands in 5 to 15 subfamilies, and absent or abnormal weak patterns in another 1 to 8 subfamilies. In comparison, 6 normal samples (2 spleens and 4 blood samples) showed in only 1 blood donor 1 clonal band. Two patients with active HCL but without infections or treatment were tested several times during the course of the disease and showed a complete identical skewed T-cell repertoire with the same oligoclonal T-cell populations. In conclusion, T cells in the blood and spleen of HCL patients show impressive abnormalities with many oligoclonal T-cell populations and a very restricted and skewed TCRBV repertoire.

Hairy Cell Leukemia-Specific Recognition by Multiple Autologous HLA-DQ or DP-Restricted T-Cell Clones

Blood ◽  
1999 ◽  
Vol 93 (1) ◽  
pp. 251-259 ◽  
Author(s):  
Lisette van de Corput ◽  
Hanneke C. Kluin-Nelemans ◽  
Michel G.D. Kester ◽  
Roel Willemze ◽  
J.H. Frederik Falkenburg
Keyword(s):  
T Cells ◽  
T Cell ◽  
Hairy Cell Leukemia ◽  
Lymphoblastic Leukemia ◽  
Hairy Cell ◽  
Cell Leukemia ◽  
T Cell Clones ◽  
Cell Clones ◽  
Hla Dq ◽  
T Cell Clone

Abstract We studied in patients with hairy cell leukemia (HCL) whether autoreactive T cells could be isolated with specific reactivity to the HCL cells. HCL cells were activated via triggering of CD40 on the cell membrane and used as stimulator cells to generate autologous T-cell clones. Two types of CD4+BV2+ T-cell clones with different CDR3 rearrangements and one type of CD4+BV8S3+ T-cell clone were generated from the spleen or blood. These clones specifically recognized the autologous HCL cells, without reactivity to autologous peripheral blood mononuclear cells (PBMC), phytohemagglutinin blasts, or Epstein-Barr virus–transformed B cells in a primed lymphocyte test. Blocking and panel studies using HCL cells from 11 other patients showed that recognition of the HCL cells by the BV2+ T cells was restricted by HLA-DQA1*03/DQB1*0301, and the BV8S3+ T cells were restricted by DPB1*04. The T-cell clones did not recognize DPB1*04+ or DQ3+ PBMC from healthy donors or DP/DQ matched malignant cells from patients with other hematologic malignancies, except for one patient with acute lymphoblastic leukemia. These HCL-specific T-cell clones may be used for the detection of an HCL-specific tumor antigen.

Cyclophosphamide Plus Allogeneic CD4+ T Cell Infusion Induces Anti-Lymphoma Immunity Despite Lack of Graft-Versus-Host Disease (GVHD) or Sustained Engraftment.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3063-3063
Author(s):  
Sanju Jalla ◽  
Jie Wang ◽  
Leo Luznik ◽  
Ephraim J. Fuchs
Keyword(s):  
T Cells ◽  
T Cell ◽  
B Cell ◽  
Tumor Immunity ◽  
Cd8 T Cells ◽  
Cd4 T Cells ◽  
Cd4 T Cell ◽  
Cell Leukemia ◽  
B Cell Leukemia ◽  
T Cell Help

Abstract Recent evidence suggests that tumor-bearing animals contain CD8+ T cells that can respond productively to a tumor vaccine, but that these T cells do not respond because of insufficient help from tumor-specific CD4+ T cells, which have either been inactivated or turned into anti-tumor suppressor T cells. We therefore devised a strategy to augment anti-tumor immunity by administering cyclophosphamide (Cy), to eliminate suppressor CD4+ T cells, followed by combining autologous tumor cell vaccination and infusion of partially MHC-mismatched, or haploidentical, CD4+ T cells as a source of T cell help for endogenous CD8+ T cells. Interestingly, the combination of Cy followed by haploidentical T cell infusion, with or without vaccine, induced potent systemic anti-tumor immunity resulting in cure of 40-50% of BALB/c mice harboring the A20 B cell leukemia/lymphoma. Depletion of CD8+ T cells from the infusate abrogated GVHD but did not compromise anti-tumor immunity. Allogeneic donor spleen cells that contained CD8+ T cells engrafted durably and caused lethal GVHD. In contrast, the combination of Cy plus CD8+ T cell-depleted spleen cell infusion induced only transient engraftment, peaking on day 7 and declining to undetectable levels by day 14. In the absence of Cy conditioning, allogeneic donor spleen cell infusions did not induce detectable chimerism beyond day 3. In summary, Cy plus allogeneic CD4+ T cell infusion induces potent anti-tumor immunity in a mouse model of B cell leukemia/lymphoma. Potential mechanisms of the therapeutic effect include direct tumor cytotoxicity by CD4+ T cells or allogeneic CD4+ T cell help for endogenous, tumor-specific CD8+ T cells.

scholarly journals Integrated human T-cell leukemia virus II genome in CD8 + T cells from a patient with "atypical" hairy cell leukemia: evidence for distinct T and B cell lymphoproliferative disorders

Blood ◽  
1988 ◽  
Vol 71 (2) ◽  
pp. 363-369
Author(s):  
JD Rosenblatt ◽  
JV Giorgi ◽  
DW Golde ◽  
JB Ezra ◽  
A Wu ◽  
...  
Keyword(s):  
T Cell ◽  
Peripheral Blood ◽  
Hairy Cell Leukemia ◽  
Mononuclear Cells ◽  
Lymphoproliferative Disorders ◽  
Lymphoid Cells ◽  
T Cell Leukemia ◽  
Hairy Cell ◽  
Cell Leukemia ◽  
Human T Cell

We previously reported isolation of human T-cell leukemia virus II (HTLV-II) from a second patient (N.R.A.) with atypical hairy cell leukemia. Follow-up analysis of the characteristics of the patient's HTLV-II infection over a 2-year period has revealed that the patient had two coexistant lymphoproliferative disorders. Oligoclonally integrated HTLV-II was detected in DNA extracted from the patient's peripheral blood mononuclear cells on separate occasions greater than 1 year apart, similar to integration of HTLV-I seen in adult T cell leukemia/lymphoma. Although integrated provirus was readily detected, no HTLV-II viral RNA expression was seen in fresh peripheral blood lymphoid cells. Although the patient's peripheral blood consistently contained a majority of atypical lymphoid cells with a T cell antigenic phenotype, he ultimately developed extensive pleural, hepatic and soft tissue infiltration with malignant Tac+, tartrate-resistant, acid phosphatase-positive (TRAP+) B cells of clonal origin. To further characterize the role of HTLV-II, the patient's peripheral blood mononuclear cells were fractionated into four enriched subpopulations at autopsy. Oligoclonally integrated HTLV-II was detected in DNA from a T cell-enriched fraction and a CD8+ T cell-enriched fraction, but not in a CD4+ T cell-enriched fraction, a non-T cell fraction, or in B cells obtained from the malignant pleural effusion. We conclude that the patient harbored two distinct lymphoproliferative disorders, a TRAP+, Tac+ B cell malignancy consistent with hairy cell leukemia that did not contain HTLV-II and a Tac-, CD8+ lymphoproliferative syndrome with oligoclonally integrated HTLV-II.

Rearrangement of both immunoglobulin and T-cell receptor genes in a prolymphocytic variant of hairy cell leukemia patient resistant to interferon-alpha [published erratum appears in Blood 1989 Feb;73(2):624]

Blood ◽  
1988 ◽  
Vol 72 (5) ◽  
pp. 1708-1716 ◽  
Author(s):  
SL Giardina ◽  
HA Young ◽  
CR Faltynek ◽  
ES Jaffe ◽  
JW Clark ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Peripheral Blood ◽  
Hairy Cell Leukemia ◽  
Cell Receptor ◽  
Hairy Cell ◽  
Cell Leukemia ◽  
Ifn Gamma ◽  
Ifn Alpha ◽  
Alpha Receptors

Abstract We describe a patient with the so-called “prolymphocytic variant” form of hairy cell leukemia (HCL) resistant to treatment with interferon- alpha (IFN-alpha). Analysis of immunoglobulin (Ig) and T-cell receptor- beta (TCR beta) gene rearrangements from serial peripheral blood mononuclear cell specimens (MNCs) confirmed not only the B-cell nature of the disease, but also the subsequent emergence of a morphologically indistinguishable population of cells with a clonal TCR beta rearrangement in addition to the original Ig gene rearrangement. With the exception of a transient increase in peripheral blood T cells during treatment with deoxycoformycin (DCF), the MNCs remained essentially constant throughout therapy with no evidence of a co- existing T-cell clone to account for the TCR beta rearrangement. Although MNCs from this patient bound significantly less IFN-alpha than did MNCs from other HCL patients, the binding was of high affinity with a kd similar to that of control cells. The number of IFN-gamma receptors on our patient's MNCs was four times higher than the number of IFN-alpha receptors and was similar to the number of IFN-alpha receptors on MNCs from HCL patients responsive to IFN-alpha. While various treatments including IFN-alpha, DCF, chlorambucil, splenectomy, leukopheresis, and IFN-gamma were not able to change the clinical progression of the disease, they may have provided an opportunity for the divergent TCR beta rearranged clone to expand and displace the initially dominant clone.

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