It is not uncommon for some B-lineage non-Hodgkin lymphomas (NHLs) to aberrantly coexpress T-cell markers, particularly CD5, as well as CD7, CD2, CD4, and/or CD8 in rare cases. Cases of CD3-positive B-cell NHL, however, have not previously been described in the literature. We present 4 cases of large B-cell lymphoma aberrantly coexpressing T-cell marker CD3 and B-lineage markers as well as demonstrating clonal rearrangement of the immunoglobulin genes but not the gamma T-cell receptor gene. To our knowledge, this represents the first series report of B-cell NHL coexpressing T-lineage-specific marker CD3. The identification of such cases indicates that the use of CD3 antibody alone in paraffin sections may lead to an incorrect determination of cell lineage in some B-cell NHL. Immunohistochemistry using additional cell lineage specific markers or molecular analysis for antigen receptor gene rearrangements are necessary for correct determination of the cell lineage in such cases.

We carried out studies with Escherichia coli to determine the site at which the methylation-independent pathways for taxis to oxygen and to sugars of the phosphoenolpyruvate:sugar phosphotransferase transport system converge with the methylation-dependent chemotaxis pathways. Using genetic reconstitution of the pathways in a null strain, we determined that all pathways examined required the products of the genes cheA, cheW, and cheY. Thus, we conclude that both the methylation-independent and methylation-dependent pathways converge at CheA, the histidine kinase product of cheA.In Escherichia coli and Salmonella typhimurium, taxis to either oxygen (aerotaxis) or substrates of the phosphoenolpyruvate phosphotransferase transport system (PTS) does not require chemoreceptor methylation and demethylation for adaptation (4,8,13). In contrast, chemotactic adaptation to certain amino acids, dipeptides, or non-PTS sugars requires methylation and demethylation. (For a review of chemotaxis see references 2, 7, and 14.) In E. coli, the tsr, tar, trg, and tap genes encode the methylation-dependent chemoreceptors (in S. typhimurium, tip substitutes for tap) while the genes cheR, cheB, cheA, cheW, cheY, and cheZ encode the cytoplasmic proteins that make up the methylation-dependent pathway. Of these cytoplasmic proteins, CheR and CheB catalyze chemoreceptor methylation and demethylation, respectively (12, 17). CheW, in association with the signaling domain located on the cytoplasmic surface of each chemoreceptor, modulates the rate of CheA autophosphorylation of the CheA residue His-48 (2). Phospho-CheA then serves as the phosphodonor for CheY autophosphorylation of the CheY residue Asp-57. PhosphoCheY binds to the flagellar motor switch, increasing the probability of clockwise (CW) rotation (5). Finally, the CheZ protein accelerates dephosphorylation of phospho-CheY, a process that restores counterclockwise (CCW) rotation (5). Whereas bacteria swim in gently curved paths when their motors rotate CCW, they abruptly change direction by tumbling chaotically when some of the motors rotate briefly in a CW direction (7).Aerotaxis in both E. coli and S. typhimurium requires an electron transport system (11). Chemotaxis to a PTS substrate requires both a functional PTS and the transport of that substrate (9, 16). The signal transduction pathways by which the electron transport system and the PTS communicate with the flagellar motors remain unknown, although evidence that the former involves the proton motive force exists (10). Since all chemotaxis pathways utilize the same motor and flagellar structures, the aerotaxis and phosphotransferase pathways must converge with the methylation-dependent pathway at, or before, the flagellar motor switch. We have investigated this point of convergence, determining which signal transduction components of the methylation-dependent pathways are also required for aerotaxis and PTS chemotaxis. Table 1 lists the strains, plasmids, and phages used in the present study. Cells were grown at 30ЊC in trypt...

Escherichia coli and Salmonella typhimurium show positive chemotaxis to glycerol, a chemical previously reported to be a repellent for E. coli. The threshold of the attractant response in both species was 10 ؊6 M glycerol. Glycerol chemotaxis was energy dependent and coincident with an increase in membrane potential. Metabolism of glycerol was required for chemotaxis, and when lactate was present to maintain energy production in the absence of glycerol, the increases in membrane potential and chemotactic response upon addition of glycerol were abolished. Methylation of a chemotaxis receptor was not required for positive glycerol chemotaxis in E. coli or S. typhimurium but is involved in the negative chemotaxis of E. coli to high concentrations of glycerol. We propose that positive chemotaxis to glycerol in E. coli and S. typhimurium is an example of energy taxis mediated via a signal transduction pathway that responds to changes in the cellular energy level.Chemotaxis has been extensively investigated in the enterobacteria Escherichia coli and Salmonella typhimurium (reviewed in references 6, 23, 24 and 42). Four chemotaxis receptors (methyl-accepting chemotaxis proteins [MCPs]) recognize most attractants and some repellents and transmit a signal to the interior of the cell (reviewed in references 13 and 30). In E. coli and S. typhimurium, adaptation to an attractant stimulus occurs when the CheR methyltransferase transfers methyl groups from S-adenosylmethionine to the ␥-carboxyl group of glutamyl residues in the cytoplasmic domain of the receptor (39).In contrast to methylation-dependent chemotaxis, chemotaxis to oxygen and redox molecules, and to substrates of the phosphoenolpyruvate:sugar phosphotransferase transport systems in E. coli and S. typhimurium, does not require an MCP or methylation of a transmembrane receptor for adaptation (5,27). Chemotaxis to proline in E. coli is another energy-dependent (10), methylation-independent (26) process. The phosphotransferase signaling pathway and the MCP signaling pathway converge at the CheA protein, the central chemotaxis regulator (22,35). Adaptation to phosphotransferase sugars may occur by restoring the prestimulus level of unphosphorylated enzyme I or by stimulating CheA to offset enzyme I inhibition of CheA (22). Convergence of the aerotaxis signaling pathway and the MCP signaling pathway also occurs at the level of CheA (35). Aerotaxis and related responses, such as electron acceptor taxis (44) and redox taxis (5), are dependent on the sensing of changes in electron transport and proton motive force (5, 37, 38). However, the mechanism of adaptation in energy-dependent behavioral responses remains unknown.Glycerol is a widely used carbon and energy source for growth of E. coli and S. typhimurium. Early studies of chemotaxis reported that glycerol is not an attractant for E. coli (1, 2). Later, it was demonstrated that high glycerol concentrations repel E. coli cells (28). Negative glycerol taxis requires any one of the MCPs, and demethylation of MCPs is obs...

Although Hodgkin lymphoma-like posttransplantation lymphoproliferative disorder (HL-like PTLD) has been grouped with classic Hodgkin lymphoma type PTLD (HL-PTLD), controversy remains as to whether it is truly a form of HL or whether it should be more appropriately classified as a form of B-cell PTLD. Because only few cases of HL-like PTLD have been reported, their pathologic nature and clinical behavior have not been well defined. This report characterized 5 cases of HL-like PTLD with respect to their immunophenotype, EBV status, clonality, and clinical outcome. All of the patients were male, with ages ranging from 1.5 to 55 years at diagnosis. PTLD developed from 4 months to 6 years following solid organ transplantation (3 hearts, 1 kidney, 1 liver), and involved both nodal and extranodal sites. All were EBV-related (EBER+) with the large neoplastic cells CD20/CD79a positive but CD15 negative. Immunoglobulin gene rearrangements were detected in 3 of 5 tested. All patients were managed by initial reduction/withdrawal of immunosuppression, with 2 also receiving chemotherapy for non-HL. Three patients died of progressive disease within 2 to 3 months after diagnosis, 1 is alive and well 2 years later, and the fifth was disease free but died of unrelated causes (graft coronary disease) 2 years later. We conclude that, although HL-like PTLD morphologically simulates classic HL PTLD, there are important immunophenotypic, molecular genetic, and clinical differences, suggesting it is in fact most often a B-cell PTLD. Distinction between HL and HL-like PTLD may be important for clinical management and prognosis.

. Chem. 257:7969-7975, 1982). The site of the ATP requirement was investigated. The times required for S. typhimurium ST23 (hisF) to adapt to a step increase in serine, phenol, or benzoate were similar in cells depleted of ATP and in cells with normal levels of ATP. This established that ATP was not required for the chemotactic signal to cross the inner membrane or for adaptation to the transmembrane signal to occur. Depletion of ATP did not affect the probability of clockwise rotation in E. coli cheYZ scy strains that were defective in the cheY and cheZ genes and had a partially compensating mutation in the motor switch. Strain HCB326 (cheAWRBYZ tar tap tsr trg::TnlO), which was deficient in all chemotaxis components except the switch and motor, was transformed with the pCK63 plasmid (ptac-cheY+). Induction of cheY in the transformant increased the frequency of clockwise rotation, but except at the highest levels of CheY overproduction, clockwise rotation was abolished by depleting ATP. It is proposed that the CheY protein is normally in an inactive form and that ATP is required for formation of an active CheY* protein that binds to the switch on the flagellar motors and initiates clockwise rotation. Depletion of ATP partially inhibits feedback regulation of the cheB product, protein methylesterase, but this may reflect a second site of ATP action in chemotaxis.