SummaryCD40 is expressed on a variety ofcells, including B cells, monocytes, dendritic cells, and fibroblasts. CD40 interacts with CD40L, a 30-33-kD activation-induced CD4 + T cell surface molecule. CD40L-CD40 interactions are known to play key roles in B cell activation and differentiation in vitro and in vivo. We now report that normal human endothelial cells also express CD40 in situ, and CD40L-CD40 interactions induce endothelial cell activation in vitro . Frozen sections from normal spleen, thyroid, skin, muscle, kidney, lung, or umbilical cord were studied for CD40 expression by immunohistochemistry . Endothelial cells from all tissues studied express CD40 in situ. Moreover, human umbilical vein endothelial cells (HUVEC) express CD40 in vitro, and recombinant interferon y induces HUVEC CD40 upregulation. CD40 expression on HUVEC is functionally significant because CD40L+ Jurkat T cells or CD40L+ 293 kidney cell transfectants, but not control cells, upregulate HUVEC CD54 (intercellular adhesion molecule-1), CD62E (E-selectin), and CD106 (vascular cell adhesion molecule-1) expression in vitro. Moreover, the kinetics of CD40L-, interleukin 1-, or tumor necrosis factor ot-induced CD54, CD62E, and CD106 upregulation on HUVEC are similar. Finally, CD40L-CD40 interactions do not induce CD80, CD86, or major histocompatibility complex class 11 expression on HUVEC in vitro. These results demonstrate that CD40L-CD40 interactions induce endothelial cell activation in vitro. Moreover, they suggest a mechanism by which activated CD4 + T cells may augment inflammatory responses in vivo by upregulating the expression of endothelial cell surface adhesion molecules .

Marginal zone B-cell lymphomas (MZBCLs) are low-grade lymphomas that characteristically lack CD5 expression. However, rare cases of MZBCL have been described in which the lymphomatous B cells coexpress CD5 (CD5+ MZBCL). In 7 of 9 reported CD5+ MZBCLs, there was evidence of widespread disease. We report four additional cases of CD5+ MZBCL. Three cases were low-grade B-cell lymphomas of mucosa-associated lymphoid tissue (MALT) involving the lungs, the conjunctiva (bilateral), and the uterus. The remaining case represented a monocytoid B-cell lymphoma involving a posterior cervical lymph node. Southern blot hybridization did not show rearrangements of bc11 or bc12 in the three cases analyzed. All four patients had localized disease and normal peripheral blood counts. Staging of bone marrow biopsies from three patients did not show evidence of bone marrow involvement. The remaining patient had bilateral conjunctival lesions that were present for 15 years without progression. These four additional cases of CD5+ MZBCL show that this group of low-grade B-cell lymphomas occasionally may exhibit an atypical phenotype. Furthermore, in this study, the CD5+ MZBCLs were clinically localized at presentation, in contrast to most other reported cases, which have had dissemination to bone marrow or peripheral blood.

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Kaposi's sarcoma-associated herpesvirus (KSHV), which was originally detected in Kaposi's sarcoma, also has been found in primary effusion lymphomas (PELs) and some cases of multicentric Castleman's disease. We describe two transplant recipients who developed Kaposi's sarcoma and a spectrum of non-neoplastic lymphoproliferative disorders that show pronounced plasmacytic and plasmacytoid features. The first patient had recurrent pleural effusions and Castleman's disease-like changes in lymph nodes. The second patient had systemic lymphadenopathy and hepatosplenomegaly secondary to diffuse infiltration by polyclonal plasma cells and plasmacytoid B lymphocytes that clinically mimicked Epstein-Barr virus (EBV)-associated posttransplant lymphoproliferative disease. In both cases, KSHV DNA was detected by polymerase chain reaction and Southern blotting, and KSHV vIL-6 protein expression was identified in affected tissues by immunohistochemical localization. In contrast, no evidence of KSHV coinfection was detected in any of 31 EBV-related posttransplant lymphoproliferative disorders or 112 non-PEL lymphomas tested. The pathologic findings in these two patients were not representative of malignancy by morphologic, immunophenotypic, or molecular criteria. This study underscores the marked propensity for hematolymphoid proliferations associated with KSHV infections to show plasmacytic features. Additionally, this study describes use of an antibody reactive against KSHV vIL-6 that can readily detect a subpopulation of KSHV-infected hematopoietic cells.

Marginal zone B cell lymphomas (MZBCLs) represent a category of non‐Hodgkin's lymphoma which may arise in a wide variety of extranodal organs where they are termed low grade B cell lymphomas of mucosa‐associated lymphoid tissue (MALT). MZBCLs may involve primarily lymph nodes and or spleen where they are designated monocytoid B cell lymphoma or splenic marginal zone lymphoma, respectively. Recognition of this category of lymphoma, in particular, extranodal MALT lymphoma, is clinically significant in determining optimal therapy. Although there have been recent case reports describing the cytologic findings in low grade MALT lymphoma in various extranodal organs, this category of lymphoma has not been widely recognized or discussed in the cytology literature. The cytologic findings in seven fine‐needle aspirations and two bronchial washings of histologically confirmed marginal zone lymphoma (five extranodal MALT lymphomas and four nodal marginal zone lymphomas) are described. In all of the cases, the cytologic specimens showed a polymorphous proliferation comprising a predominant population of intermediate sized lymphoid cells with centrocyte‐like or monocytoid features, transformed cells, and variable numbers of plasma cells. These findings, while highly suggestive of MALT lymphoma in extranodal proliferations, may be more difficult to distinguish from reactive conditions in lymph nodes. Diagn. Cytopathol. 1999;20:190–198. © 1999 Wiley‐Liss, Inc.