Monoclonal antibodies reactive in routinely processed tissue sections of malignant lymphoma, with emphasis on T-cell lymphomas

The immunoreactivity of eight monoclonal antibodies was evaluated on 45 routinely processed lymphomas (22 T-cell lymphomas, 11 B-cell lymphomas, and 12 cases of Hodgkin's disease). Two antibodies reactive with leukocyte common (T200) antigens (PD7/26 and 2B11) stained most of the B- and T-cell lymphomas but did not stain the Reed-Sternberg cells and variants in Hodgkin's disease. Two antibodies known to stain B cells (LN-1 and LN-2) reacted with some of the B-cell lymphomas, but LN-2 also reacted with the neoplastic cells in six of 22 T-cell lymphomas and with the Reed-Sternberg variants in eight of 12 cases of Hodgkin's disease. The granulocyte antibody anti-Leu M1 reacted with most cases of Hodgkin's disease but also reacted with two of 11 B-cell non-Hodgkin's lymphomas. An antibody to epithelial membrane antigen (anti-EMA) stained some cases of T-cell lymphoma, B-cell lymphoma, and Hodgkin's disease. Leu 7 was expressed in one T-cell lymphoma and in one case of Hodgkin's disease. A novel antibody reactive with T cells (L60) stained all cases of T-cell lymphoma but also stained some cases of B-cell lymphoma and one case of Hodgkin's disease. We conclude that none of these antibodies, when used alone on routinely fixed paraffin-embedded material, is completely sensitive and specific for T-cell lymphoma, B-cell lymphoma, or Hodgkin's disease. However, a panel of antibodies is useful in distinguishing Hodgkin's disease from non-Hodgkin's lymphoma and in suggesting the B- or T-cell phenotype of non-Hodgkin's lymphomas.     

Expression of vimentin and epithelial membrane antigen in human malignant lymphomas

Immunoreactivity with monoclonal antibodies against the intermediate filament protein, vimentin, and epithelial membrane antigen (EMA) was examined in 330 cases of lymphoma (317 non-Hodgkin's and 13 Hodgkin's lymphomas), 12 reactive lymph nodes and mononuclear cells of the peripheral blood using either indirect immunoperoxidase staining or the avidin-biotin immunoperoxidase complex technique. The cell origin of each tumor was established using a panel of monoclonal antibodies against lymphocyte differentiation antigens. There were 41 T-cell, 247 B-cell and 29 undetermined lymphomas, and 13 cases of Hodgkin's disease in the series. Vimentin was expressed in 24 T-cell lymphomas (58.5%) and 60 B-cell lymphomas (24.2%). This difference in frequency was statistically significant. Vimentin expression in follicular lymphomas was less frequent than in diffuse B-cell lymphomas. In diffuse lymphomas, small and medium cell types were more reactive with anti-vimentin than large cell types. Reed-Sternberg cells (R-S cells) in Hodgkin's disease were positive for vimentin in 11 cases (84.6%). The frequency of EMA reactivity in lymphomas was low, particularly in T-cell lymphomas. No positive cases were found among follicular lymphomas. In diffuse non-Hodgkin's lymphomas, EMA was expressed only in mixed and large cell types, but never in smaller ones. In conclusion, monoclonal antibodies against vimentin and EMA appear to be of limited usefulness for the diagnosis of non-Hodgkin's lymphomas, but anti-vimentin antibody may be used as an adjunct to the diagnosis of R-S cells in Hodgkin's disease.     

Expression of lymphoid-associated antigens on Hodgkin''s and Reed-Sternberg cells of Hodgkin''s disease. An immunocytochemical study on lymph node cytospins using monoclonal antibodies

The aim of this study was to elucidate the origin of Hodgkin's and Reed-Sternberg cells. Lymph node cytospins and frozen sections from 20 cases of Hodgkin's disease of different histological subtypes were immunostained by the immuno-alkaline phosphatase technique using a panel of monoclonal antibodies. As expected, the Hodgkin's and Reed-Sternberg cells of all cases were positive for the CD30 (Ki-1), CD15 (hapten X) and CD25 (Tac) antigens. In eight cases, a variable percentage of typical Hodgkin's and Reed-Sternberg cells showed a clear-cut cytoplasmic and/or surface positivity for the T-cell-associated antigens CD3, CD5, CD6 and CD4 (seven cases) or CD8 (one case), but consistently lacked B-cell and macrophage-associated markers. The best visualization of T-cell antigens was obtained in cytocentrifuge preparations and in areas of lymph node frozen sections that had been infiltrated by clusters of Hodgkin's and Reed-Sternberg cells. In two cases of Hodgkin's disease (nodular sclerosis, mixed cellularity) the neoplastic cells weakly expressed the B-cell antigens CD19 and CD22, but not T-cell or macrophage-associated markers. In 10 cases, Hodgkin's and Reed-Sternberg cells were negative for all the lymphoid- and macrophage-associated antigens. These results suggest a lymphoid (either T or B) rather than histiocytic origin for the Hodgkin's and Reed-Sternberg cells in a number of Hodgkin's disease cases.     

Expression of Vimentin and Epithelial Membrane Antigen in Human Malignant Lymphomas

Immunoreactivity with monoclonal antibodies against the intermediate filament protein, vimentin, and epithelial membrane antigen (EMA) was examined in 330 cases of lymphoma (317 non-Hodgkin's and 13 Hodgkin's lymphomas), 12 reactive lymph nodes and mononuclear cells of the peripheral blood using either indirect immunoperox-idase staining or the avidin-biotin immunoperoxidase complex technique. The cell origin of each tumor was established using a panel of monoclonal antibodies against lymphocyte differentiation antigens. There were 41 T cell, 247 B cell and 29 undetermined lymphomas, and 13 cases of Hodgkin's disease in the series. Vimentin was expressed in 24 T-cell lymphomas (58.5%) and 60 B cell lymphomas (24.2%). This difference in frequency was statistically significant. Vimentin expression in follicular lymphomas was less frequent than in diffuse B-cell lymphomas. In diffuse lymphomas, small and medium cell types were more reactive with anti-vimentin than large cell types. Reed-Sternberg cells (R-S cells) in Hodgkin's disease were positive for vimentin in 11 cases (84.6%). The frequency of EMA reactivity in lymphomas was low, particularly in T cell lymphomas. No positive cases were found among follicular lymphomas. In diffuse non Hodgkin's lymphomas, EMA was expressed only in mixed and large cell types, but never in smaller ones. In conclusion, monoclonal antibodies against vimentin and EMA appear to be of limited usefulness for the diagnosis of non Hodgkin's lymphomas, but anti vimentin antibody may be used as an adjunct to the diagnosis of R-S cells in Hodgkin's disease.     

T-cell variant of classical Hodgkin's lymphoma with nodal and cutaneous manifestations demonstrated by single-cell polymerase chain reaction

The atypical cells of CD30(+) cutaneous lymphoproliferative disorders (CD30CLD) are commonly of T-cell origin and frequently have a similar morphology as Hodgkin or Reed-Sternberg cells of Hodgkin's lymphoma (HL). HL is one of the tumors associated with CD30CLD. Although most studies support a B-cell derivation of the tumor cells in HL, recently a few cases of classical HL with T-cell genotype have been reported. We report a patient who presented with CD30CLD whose lymph nodes showed classical HL of mixed cellularity subtype at presentation. By single-cell PCR, the same clonal gene rearrangements of the T cell receptor-beta gene locus could be assigned to the CD30(+) and CD15(+) cells of both skin and lymph node. In a lymph node biopsy specimen taken in relapse after several courses of chemotherapy, the CD30(+) tumor cells were abundant. The T cell-derived tumor cells displayed aberrant expression of the Pax-5 gene in all specimens. A common clonal origin of both CD30CLD and HL of the lymph node in the patient presented here suggests that HL with T-cell genotype exists in association with CD30CLD as well as in sporadic cases and may share clonal origin with the skin tumor.     

Genotypic analysis of large cell lymphomas which express the Ki-1 antigen

The monoclonal antibody Ki-1 reacts with Reed-Sternberg cells in Hodgkin's disease and with the tumour cells in a minority of large cell non-Hodgkin's lymphomas. This study describes the results of immunophenotypic and DNA analysis in 30 cases of non-Hodgkin's lymphoma, all of which expressed the Ki-1 antigen. The genotypic analysis has been undertaken using both immunoglobulin and T-cell receptor gene probes. Sixteen cases were shown by this method to be of monoclonal T-cell origin, six of B-cell origin, while in eight cases there was no evidence of either T- or B-cell lineage. This confirms previous immunohistological data indicating that non-Hodgkin's lymphomas which express the Ki-1 antigen may be of either T-cell or B-cell origin.     

CD40 ligand is constitutively expressed in a subset of T cell lymphomas and on the microenvironmental reactive T cells of follicular lymphomas and Hodgkin's disease.

Although CD40 has been extensively studied in B- and T-cell non-Hodgkin's lymphomas (NHLs)/leukemias, and more recently in Hodgkin's disease (HD), little is known about the expression of its ligand (CD40L) in lymphoproliferative disorders other than T-cell NHLs/leukemias. A series of 121 lymphoma/leukemia samples, including 35 cases of HD, 34 T-cell and 39 B-cells NHLs, 2 cases of adult T-cell leukemia/lymphoma, and 11 cases of T-cell acute lymphoblastic leukemia, were evaluated for CD40L expression by immunostaining of frozen tissue sections and flow cytometry with the anti-CD40L monoclonal antibody M90. CD40L was constitutively expressed by neoplastic cells in 15 of 36 (42%) T-cell NHLs/adult T-cell leukemia/lymphomas, almost invariably those displaying the CD4+/CD8- phenotype, whereas no CD40L-expressing tumor cells could be found in B-cell NHL and HD. Among T-cell acute lymphoblastic leukemias, CD40L was detected only on 2 cases displaying a stem-cell-like phenotype. In follicular B-cell lymphomas a large number of CD40L-expressing CD3+/CD4+ T lymphocytes were found admixed with tumor cells within the neoplastic follicles and in their surrounding areas. In the nonfollicular B-cell lymphomas, CD40L-positive CD3+/CD4+ T lymphocytes were few or absent. In all HD subtypes other than the nodular lymphocytic predominance, CD40L-expressing CD3+/CD4+ T lymphocytes were numerous in the HD-involved areas and were mainly located in close proximity to the Reed-Sternberg cells. Our data indicate that in human lymphomas CD40L is preferentially expressed by a restricted subset of T-cell lymphomas, mostly with CD4 immunophenotype. Finally, we have provided morphological evidence that CD40L may play an important role in the cell contact-dependent interaction of tumor B-cells (CD40+) within the neoplastic follicles or Reed-Sternberg cells (CD40+) in HD-involved areas and the microenvironmental CD3+/CD4+/CD40L+ T lymphocytes.     

Aberrant expression of T-cell-associated antigens on B-cell non-Hodgkin lymphomas

We describe 9 well-characterized cases of B-cell non-Hodgkin lymphoma (NHL) that showed aberrant expression of T-cell-associated antigens by 2-color flow cytometry. Cases were as follows: chronic lymphocytic leukemia/small lymphocytic lymphoma, 4; follicle center cell lymphoma, 2; mantle cell lymphoma, 1; and diffuse large B-cell lymphoma, 2. CD2 was the most commonly expressed antigen (5 cases). CD8 and CD7 were identified in 2 cases each, including 1 case that expressed both CD7 and CD4. The disease course and response to treatment were compatible with the type and stage of lymphoma. No unusually aggressive behavior was noted in any case. A control group of 59 cases of benign lymph nodes analyzed during the same period showed no aberrant expression of T-cell-associated antigens; thus, such expression is not a feature of benign lymphoid proliferations. Study of these B-cell lymphomas may prove invaluable to study aberrant activation of silent or repressed T-cell differentiation genes. CD2-expressing B-cell NHLs may represent clonal expansion of CD2+ B lymphocytes that normally constitute a small fraction of peripheral B lymphocytes and should not be confused with composite B- and T-cell lymphomas. Unless aggressive behavior is noted consistently, no aggressive treatment is justified.     

Paraffin section immunohistochemistry. II. Hodgkin''s disease and large cell anaplastic (Ki1) lymphoma

A panel of antibodies that recognize antigens that survive fixation and conventional processing have been applied to 43 cases of Hodgkin's disease and five cases of large cell anaplastic lymphoma. Reed-Sternberg cells in all five cases of nodular lymphocyte predominance Hodgkin's disease were positive with leucocyte common (CD45) and B-cell antibodies, and negative with LeuM1 (CD15) and BerH2 (CD30) antibodies. In other types of Hodgkin's disease, Reed-Sternberg cells were positive with BerH2 in all cases, positive with LeuM1 in 63% of cases (with enzymic predigestion), positive with at least one B-cell antibody in 29% of cases and positive for CD45 in 8% of cases. In 19% of all cases, Reed-Sternberg cells were positive for epithelial membrane antigen and in 93% they were positive with TAL1B5 (anti-class II MHC). No case showed immunoreactivity with anti-T-cell antibodies. The patterns of immunoreactivity of large cell anaplastic lymphoma were similar, except that none was positive with B-cell antibodies and three were positive with T-cell antibodies. All five were positive with BerH2 (CD30) and TAL1B5. Comparison of the results with those seen in other cases of non-Hodgkin's lymphoma indicates that, with the currently available reagents, this immunohistological profile cannot be used as the sole diagnostic discriminant of these conditions; this must still be based upon careful morphological assessment.     

Leu-M1 antigen expression in T-cell neoplasia.

The Leu-M1 antigen has been recently proposed as a valuable immunodiagnostic marker of the Reed-Sternberg cells of Hodgkin's disease and to be particularly helpful is distinguishing Hodgkin's disease from other lymphoproliferative disorders such as peripheral T-cell lymphomas. In this study, the authors examined paraffin-embedded tissue sections obtained from 38 patients with previously well-characterized T-cell neoplasms for the presence of the Leu-M1 antigen. The cases comprised a spectrum of T-cell malignancies and were divided into four broad clinicopathologic groups: lymphoblastic lymphoma/ leukemias (6), mature T-cell leukemias (3), peripheral T-cell lymphomas (11), and cutaneous T-cell lymphomas (18), which included both mycosis fungoides and nonmycosis fungoides types. The neoplastic T cells in 19 patients (50%) expressed the Leu-M1 antigen. The proportion of Leu-M1-positive cells and the immunostaining pattern varied greatly among these cases but correlated with mature, postthymic stages of T-cell differentiation and activation. Of particular significance was the observation that the more pleomorphic neoplastic T cells, including Reed-Sternberg-like cells, exhibited an intense cytoplasmic and membranous staining pattern which was often indistinguishable from the immunostaining pattern observed in Hodgkin's disease. The authors conclude that Leu-M1 is not a specific immunodiagnostic marker of Hodgkin's disease and has limited value in distinguishing Hodgkin's disease from T-cell neoplasms which stimulate Hodgkin's disease morphologically.     

Epstein-Barr virus DNA in Reed-Sternberg cells of Hodgkin''s disease is frequently associated with CR2 (EBV receptor) expression

We studied 44 cases of Hodgkin's disease for the presence of Epstein-Barr virus (EBV) DNA, its localization and the expression of the EBV receptor on the tumour cells. EBV DNA was found in 52% (16/31) of the Hodgkin's lymphomas using the polymerase chain reaction. With a very sensitive non-radioactive DNA in situ hybridization technique in combination with immunohistochemistry for CD 30 or CD 15 antigens, EBV DNA was localized to Reed-Sternberg cells and its mononuclear variants. The relationship between the presence of EBV DNA and the expression of the EBV-receptor CR2 (CD 21) on Reed-Sternberg cells was studied using the same techniques and two different monoclonal anti-CD 21 antibodies. CR2 could be detected on a substantial number of the Reed-Sternberg cells in EBV DNA positive Hodgkin's lymphomas (9/12; 75%), whereas in EBV negative cases positivity with anti-CD 21 was rare (1/13; 8%). The results indicate that CR2 expression on Reed-Sternberg cells and the presence of EBV DNA sequences are frequently associated in Hodgkin's lymphomas.     

T-cell/histiocyte-rich large B-cell lymphoma is a disseminated aggressive neoplasm: differential diagnosis from Hodgkin's lymphoma

AIMS: An accurate diagnosis of T-cell/histiocyte-rich large B-cell lymphoma needs to take into consideration those forms of Hodgkin's lymphoma also characterized by a predominance of small lymphocytes and histiocytes, i.e. nodular lymphocyte predominance Hodgkin's lymphoma and lymphocyte-rich classical Hodgkin's lymphoma. We have studied the clinical, phenotypic and genetic features of a series of 12 cases of T-cell/histiocyte-rich large B-cell lymphoma along with 18 cases of Hodgkin's lymphoma for comparative purposes. METHODS AND RESULTS: Of the Hodgkin's lymphoma cases, there were 11 lymphocyte predominance type and seven classic type. T-cell/histiocyte-rich large B-cell lymphomas presented usually in advanced stages (III or IV in 11/12 cases), frequently with 'B' symptoms (6/9 cases), and followed a more aggressive course than Hodgkin's lymphoma (4/8 patients died due to the tumour in T-cell/histiocyte-rich large B-cell lymphoma versus 0/15 in Hodgkin's lymphoma). T-cell/histiocyte-rich large B-cell lymphoma cases showed diffuse effacement of the nodal architecture by a proliferation of scattered large atypical B-cells obscured by a background of small T-lymphocytes (more CD8+, TIA1+ than CD57+). Five cases showed also a prominent histiocytic component. The large B-cells expressed CD45 and often EMA (6/10 cases). On the other hand, CD 30, CD15 and latent infection by Epstein-Barr virus (EBV) were generally lacking. bc l6 and CD10 were, respectively, detected in 6/6 and 1/5 cases. Conventional polymerase chain reaction (PCR) showed monoclonal immunoglobulin heavy chain (IgH) gene rearrangements in all T-cell/histiocyte-rich large B-cell lymphomas studied (5/5), but did not detect any case with t(14;18) involving the major breakpoint region (0/4). CONCLUSIONS: The differential diagnosis of T-cell/histiocyte-rich large B-cell lymphoma from Hodgkin's lymphoma is facilitated by the integration of different immunophenotypic, molecular and clinical findings. T-cell/histiocyte-rich large B-cell lymphoma is a monoclonal neoplasm of bc l6+ B-cells with a phenotypic profile similar to lymphocyte predominance Hodgkin's lymphoma, suggesting a germinal centre origin and a possible relation to this disease. Therefore, in order to distinguish it from lymphocyte predominance Hodgkin's lymphoma, characterization of the reactive background, IgH gene rearrangement studies by conventional PCR and clinical features are more useful. In contrast, T-cell/histiocyte-rich large B-cell lymphoma can be distinguished from classical Hodgkin's lymphoma thanks to the presence of monoclonal IgH rearrangement and the CD 30-CD15-CD45+EMA+ immunophenotypic profile of the neoplastic cells in T-cell/histiocyte-rich large B-cell lymphoma.     

Relation of follicular dendritic reticulum cells to Reed-Sternberg cells of Hodgkin's disease with emphasis on the expression of CD21 antigen.

Based on observations of 66 cases, in which tissues were specially processed to optimize the simultaneous preservation of cell membrane antigens and morphology, we provide evidence in favor of a relationship between follicular dendritic reticulum cells (FDRC) and Reed-Sternberg (RS) cells of Hodgkin's disease (HD) other than the lymphocyte predominance subtype. RS cells were intimately related to the FDRC network (75% of cases), and the expression of CD21 antigen was frequent (41% of cases). Exclusive expression of CD21 antigen was found in 11 cases of HD, while the expression of other B-cell-associated markers (CD19, CD20, CD22) was both variable and inconsistent. The expression of T-cell antigens (CD3, CD4, CD8) was rare. Null phenotype of RS cells was observed in 27 of 66 cases (41%). Epstein-Barr virus (EBV) nucleic acids were found in 34 of 66 (51.5%) cases. Double labeling techniques showed the presence of EBV-positive RS cells within the FDRC network. A non-B-cell origin of RS cells was supported by the differential expression of EBV latent antigens in HD (latent membrane protein+, EB nuclear antigen 2-), which is unusual in EBV-driven lymphoblastoid cell lines and EBV-positive B-cell lymphomas. FDRC and RS cells are known to share morphological traits (binucleated cells), and both cell types possess Fc receptor for IgG. The hypothesis is further backed by the findings of CD15 antigen expression by occasional RS-like dysplastic FDRC in Castleman's disease (five cases), which is characterized by hyperplasia of FDRC. Whether FDRC might be the only cells involved in the conversion to RS cells by the loss or gain of antigens remains to be determined.     

Clusterin expression in malignant lymphomas: a survey of 266 cases.

Clusterin expression has been reported to be characteristic of systemic anaplastic large cell lymphoma and usually negative in cutaneous anaplastic large cell lymphoma as well as other lymphoma types. We surveyed clusterin expression using immunohistochemical methods in 266 cases of non-Hodgkin's lymphoma and Hodgkin's disease to further assess the diagnostic utility of this marker. Clusterin immunostaining was observed in 40 of 49 (82%) systemic anaplastic large cell lymphomas and 12 of 29 (41%) cutaneous anaplastic large cell lymphomas. Clusterin also was expressed in 5 of 43 (12%) diffuse large B-cell lymphomas (4 of 5 CD30+), 1 of 14 (7%) peripheral T-cell lymphomas, 1 of 32 (3%) cases of nodular sclerosis Hodgkin's disease, and 1 case of mycosis fungoides in large cell transformation. Clusterin was negative in all other neoplasms assessed including follicular lymphoma of all grades (n = 24), mantle cell lymphoma (n = 13), marginal zone B-cell lymphoma (n = 12), precursor T-cell or B-cell lymphoblastic leukemia/lymphoma (n = 10), mixed cellularity Hodgkin's disease (n = 8), chronic lymphocytic leukemia/small lymphocytic lymphoma (n = 7), Burkitt lymphoma (n = 7), mycosis fungoides (n = 4), nodular lymphocyte predominant Hodgkin's disease (n = 3), lymphoplasmacytic lymphoma/Waldenstrom macroglobulinemia (n = 2), and plasmacytoma (n = 2). We conclude that clusterin is a marker of anaplastic large cell lymphoma and that addition of clusterin to antibody panels designed to distinguish systemic anaplastic large cell lymphoma from classical Hodgkin's disease is useful. However, clusterin is also positive in a substantial subset of cutaneous anaplastic large cell lymphomas, a smaller subset of diffuse large B-cell lymphomas, and rarely in cases of peripheral T-cell lymphoma and nodular sclerosis Hodgkin's disease.     

Classical Hodgkin's lymphoma: biology and grey zones

Advances in the biology of Hodgkin's lymphoma have lead to the distinction between two entities, "classical" Hodgkin's lymphoma and nodular lymphocyte predominance Hodgkin's lymphoma, previously called nodular paragranuloma, which share distinct clinical aspects. The definition of diagnostic criteria has also been helpful to separate Hodgkin's lymphoma from other lymphomas which can mimick Hodgkin's disease such as anaplastic large cell lymphomas, T-cell/histiocyte rich diffuse large B-cell lymphoma, and some peripheral T-cell lymphomas, mainly angioimmunoblastic-type. Reed-Sternberg cell, the neoplastic cell of "classical" Hodgkin's lymphoma, still retains some secrets. Despite some controversies, there is more and more evidence for a lymphoid B cell origin. The involvement of Epstein-Barr virus, cytokines and/or oncogenes expression in the pathogeny can be suggested, although the precise mechanisms leading to transformation and/or accounting for tumour progression are still elusive. Recently, the roles of the pathway implicating the activation of NFkappaB as well as the autocrine secretion of interleukin-13 have been demonstrated.     

Aberrant FHIT protein expression in classical Hodgkin's lymphoma: a potential marker

AIMS: The fragile histidine triad (FHIT) gene is frequently inactivated in human cancers; however, the FHIT gene remains unexplored in Hodgkin's lymphoma. The aim of this study was to investigate the role of FHIT expression in classical Hodgkin's lymphoma. METHODS: Classical Hodgkin's lymphomas were analysed for FHIT gene expression by two-step non-biotin immunohistochemical method and Western blotting. RESULTS: Thirty of the 33 (91%) cases of Hodgkin's lymphoma tested were positive for FHIT protein by immuohistochemistry. The expression of FHIT was mainly located in cytoplasm of Reed-Sternberg (HRS) cells. The protein expression was also documented by Western blotting. The non-Hodgkin's lymphomas were negative for FHIT protein. CONCLUSIONS: The results indicate that abnormal FHIT expression is noted frequently in classical Hodgkin's lymphoma and the expression can give insight into the pathogenesis of the disease. The protein may serve as a marker to localise HRS cells in classical Hodgkin's lymphoma.     

Immunohistochemical determination of CD23 expression in Hodgkin's disease using paraffin sections

The leukocyte antigen CD23 is expressed during B-cell development, and functions as an IgE receptor and a lymphocyte growth factor. We studied the expression of CD23 in paraffin sections of lymphoid tissue using the monoclonal antibody BU38. Fifteen cases of Hodgkin's disease, ten reactive lymph nodes, eight B-cell, and seven T-cell non-Hodgkin's lymphomas were analysed immunohistologically. CD23 positivity was seen on follicular dendritic cells and a small number of lymphocytes in reactive nodes. Thirteen of the 15 cases of Hodgkin's disease showed CD23 expression in both neoplastic cells and reactive lymphocytic infiltrate. The antigen was demonstrated in four of the B-cell and one of the T-cell tumours. CD23 may be important in mediating the mixed cellular infiltrate characteristic of Hodgkin's lymphoma.     

Expression of enolases in T cell tumors and Hodgkin's disease

Frozen biopsy specimens taken from 30 cases with T cell tumors (8 with T cell acute lymphoblastic leukemia, 8 with T cell lymphoblastic lymphoma, and 14 with peripheral T cell lymphomas), and from 12 with Hodgkin's disease, were investigated using a direct immunohistochemical method to detect alpha-, beta- and gamma-enolases. Normal thymus and lymph node specimens with reactive lymphadenitis were also investigated. Subcortical thymocytes and the majority of deep cortical thymocytes showed reactivity of alpha-/beta-/gamma- approximately +/- -enolases, and medullary thymocytes and small lymphocytes in T zone areas of lymph node showed reactivity of alpha-/beta+/gamma- approximately +/- -enolases. Seven of the 8 cases with T cell acute lymphoblastic leukemia showed reactivity of alpha-/beta-/gamma(-)-enolases or alpha+/beta-/gamma(-)-enolases in leukemic lymphocytes, 7 of the 8 cases with T cell lymphoblastic lymphoma showed reactivity of beta(+)-enolase, and all 14 cases with peripheral T-cell lymphomas showed reactivity of alpha-/beta- approximately +/gamma(+)-enolases in lymphoma cells. All the 12 cases with Hodgkin's disease showed reactivity of alpha-/beta+/gamma(+)-enolases in Reed-Sternberg and Hodgkin's cells. These results indicate the following: (a) The neoplastic cells of T cell acute lymphoblastic leukemia, T cell lymphoblastic lymphoma and peripheral T cell lymphomas present different expressions in each of these three categories. This may imply a difference of maturation and differentiation or activation among neoplastic T lymphocytes. (b) T lymphocytes may switch from alpha- to beta-enolase and from alpha- to gamma-enolase in the course of differentiation and activation. (c) It is worth noting that the Reed-Sternberg and Hodgkin's cells of Hodgkin's disease present an identical expression of enolases.