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Twenty-six cases of high-grade lymphomas with activation markers (CD30) classified and immunophenotyped according to the Kiel classification were studied to determine their fine structural features. Transmission electron microscopy showed in 17 cases anaplastic nuclear and cytoplasmic changes identical to those observed in Hodgkin's disease, it being impossible to determine by the morphology a B, T, or null nature. Four high-grade B-centroblastic and immunoblastic cases and five T-pleomorphic cases showed nuclear changes and cytoplasmic differentiation that suggested a T or B nature. An immunogold-labeling technique showed CD30-positive particles primarily in the Golgi complex and occasionally in the cell membrane.

Seven cases of gastric B-cell low-grade lymphomas were characterized by morphology, immunohistology and electron microscopy. All them were immunophenotyped with a panel of monoclonal antibodies against immunoglobulins and other B-cell determinants. Histologic study of gastric B-cell low-grade lymphomas showed germinal centers of lobated shape and polyclonal nature, mainly polyclonal subepithelial plasma cell (except in one case) and neoplastic interfollicular B-cells of monoclonal character. Light-chain restriction supports the neoplastic nature of gastric lymphoma of low-grade malignancy, a distinctive tumour of extranodal B-cell origin. Interfollicular B-cells share with marginal zone cells a perifollicular localization, morphology and phenotype, suggesting a possible relation between these two cellular subtypes. In two cases, the tumour appears constituted by monocytoid B-lymphocytes (MBL), which suggests a relation of tumoral interfollicular B-cells with this subpopulation.

The proliferation of characteristic cells in expanded sinuses and in the perivenular area of the paracortex of lymph nodes with patients with toxoplasmosis, and homosexual and drug abusers with lymphadenopathy is referred to as 'immature sinus histiocytosis' (ISH). In a study of nine cases we have shown that these cells are monocytoid B-cells with an immunological phenotype differing from that of other node-based B-cells. The function of these cells is not known.

HLA class I and II expression was studied on 244 (177 primary and 67 metastatic) solid human tumours of different origin. Alkaline immunophosphatase (APAAP) and immunoperoxidase were used on cryostatic sections to stain MHC antigens. Monomorphic MoAbs were used against class I heavy chain, beta 2-microglobulin, DR, DQ and DP molecules. Class I expression was homogeneous on colon, melanoma and epidermoidal primitive tumours. Loss of HLA class I antigens was more frequent on basal cell carcinomas and sarcomas and was related to tumour differentiation on larynx carcinoma. Class I expression was heterogeneous on breast, larynx and stomach primitive neoplasias. Class I negative tumours were more frequent on metastatic than on primitive melanomas. Divergence of class I between primary tumours and autologous metastases was observed on melanomas, larynx and colorectal carcinomas. Class II expression was heterogeneous on all tumours and in a large number of cases was associated with high intensity of leukocytic infiltrate. HLA-DR expression was higher than HLA-DP and HLA-DQ (DR greater than DP greater than DQ) and was related to tumour progression. Four human tumour cell lines were modulated with recombinant interferon-gamma for HLA class I and II antigens. Different HLA profiles were obtained: increased class I and II expression, increased class II or a low response. Finally, class I genes from 22 tumours were compared with autologous normal cells by Southern blot analysis: 12 tumours were class I positive and 10 negative. No clear differences in RFLP were observed that could be associated with class I rearrangement. The results are discussed in relation to the role that histocompatibility antigens may play in tumour progression and invasiveness.

An immunohistochemical and ultrastructural study of 14 cases of persistent and generalized lymphadenopathy (PGL), acquired immune deficiency syndrome (AIDS) related, revealed florid follicular hyperplasia, follicular dendritic cell (FDC) lysis, lymphoid follicle invaginations, increased presence of T8 cells in germinal center, immature sinus histiocytosis (monocytoid B-cells), and inversion of T4/T8 ratio in the paracortical area. Electron microscopic examination showed viral particles of morphologic characteristics consistent with human immunodeficiency virus (HIV) virions attached to the processes of FDC in three of the nine cases studied. Lesions of the germinal center dendritic cell network are the cardinal feature of PGL. This finding lends support to the idea of a viral aggression directed against FDC as the cause of disregulation of the B-cells.

Monocytoid B-lymphocytes are a B-cell subset present in subcapsular sinuses in some cases of lymphadenitis. We describe a case of lymphoma of this cell type. The tumour shows a distinctive morphology characterized by concentric strands of tumour cells around lymphoid follicles with hyperplastic germinal centres and conserved mantle zones. Electron microscopy of these cells shows short cellular processes as well as moderate development of endoplasmic reticulum. The phenotype of the tumour was monoclonal IgM-kappa, distinct from other node-based B-cell subpopulations and suggesting a possible relationship to the lymphocytes of the marginal zone present peripheral to lymphoid follicles of the spleen. Morphological features that suggest a relationship with hairy cell leukaemia are contrasted by phenotypic differences and the ultrastructural absence of ribosomic lamellar complexes.

We have compared the expression of the common leucocyte antigen (CD45) and the restricted leucocyte antigen (CD45R) on normal haematopoietic cells, cell lines, and a total number of 136 cases of myeloid and lymphoid proliferative syndromes. CD45, the conventional leucocyte antigen, presents a generalized distribution along the lymphoid and myeloid maturation pathway with the exception of some myelomas and pre-B leukaemias. In contrast, the expression of the CD45R determinant is more limited. Although it is found in the majority of the differentiation stages of B cells and monocytes, it is present only in the early stages of myeloid differentiation. On T cells it is expressed on mature thymocytes and in the majority of CD8+ lymphocytes and a subset of CD4+ cells on peripheral blood. Finally, our results also indicated that CD4+ T lymphoproliferative syndromes are derived from the CD4+ CD45R- subset (20/20 cases).