T cell malignancy in Richter's syndrome presenting as hyper IgM. Induction and characterization of a novel CD3, CD4^‐, CD8 T cell subset from phytohemagglutinin‐stimulated patient's CD3, CD4, CD8 leukemic T cells

Abstract

A patient is described, having Richter's syndrome and immunodeficiency with hyper IgM, who developed suppressor T cell lymphoma (CD3+, CD4-, CD8+) following untreated helper-suppressor T cell chronic lymphocytic leukemia (CD3+, CD4+, CD8+). The neoplastic T cells in both malignancies expressed interleukin (IL) 2 receptors but were deficient in typical CD2+ and CD5+ pan T antigens. Additionally, a large percentage of malignant lymph node T cells expressed HLA-DR+ activation antigens. In vitro immunoglobulin-production experiments demonstrated that the patient's leukemic blood T cells had an excess helper function for IgM synthesis but a suppressor function for IgG and IgA synthesis by normal B and T cells. The leukemic blood T cells demonstrated a poor response to phytohemagglutinin (PHA). A defect in IL 2 receptor expression was evident in PHA-stimulated leukemic blood T cells. Of interest was the observation that PHA stimulated the induction of a novel CD3+, CD4-, CD8+ T cell subset from patient's CD3+, CD4+, CD8+ leukemic blood T cells. These PHA-induced CD3+, CD4-, CD8+ T cell subsets produced an elevated proliferative response to PHA and concanavalin A, had a helper cell function for IgM synthesis and produced highly elevated amounts of IL 2.

γδ T cells and the immune response in visceral leishmaniasis

“…CD3+ T cells (96 YO OKT3 mAb reactive) were incubated with the saturating concentrations of anti-TcR ciP or antiTcR y6 mAb, washed twice, and then added to petri dishes previously coated with affinity-purified F( ab')2 anti-mouse Ig as shown [19]. After incubation of mAb-coated T cells on the petri dishes for 1 h at room temperature, the nonadherent cells were gently washed with RPMI 1640 medium.…”

“…PBMC were separated into T and non-T cell fractions by sheep erythrocyte rosetting technique and Histopaque-1077 density gradient centrifugation method [19]. The T cell preparation contained 92 YO-96 % CD3+ cells, whereas the non-T cells contained 68 YO -76 YO CD24+ B cells.…”

“…The non-T cells were further treated with anti-CD3 (OKT3) mAb and rabbit complement to remove residual T cells. B cells (94 "0-96 YO CD24+) were purified from non-Tcells by removal of CD11+ (OKMI+) monocytes (adherent cells) on petri dishes [19].…”

“…The CD4+ and CD8+ Tcell subsets were isolated by an immunoadsorption (panning) technique using OKT8 and OKT4 mAb solutions, respectively, as described recently [19]. Petri dishes were coated with affinity-purified goat anti-mouse IgG (Ortho Diagnostics), and the mAb-treated cells were incubated on these dishes for 1 h at room temperature.…”

“…A standard indirect immunofluorescence technique as described earlier [19] was used to label cells with a series of mAb. The following mAb were employed: CD3 (OKT3, total T cells), CD4 (OKT4, helpedinducer T cells), CD8 (OKT8, suppressor/cytotoxic T cells), CD25 (anti-IL-2R), CD38 (OKT10, activation antigen), CD71 (OKT9, transferrin receptor), HLA-DR (OKIal, activation antigen), CD24 (OKB2, B cells), CD11 (OKMI, monocytes), CD45R (2H4), CDw29 (4B4),TcR ~$3 (TcR-1 WT31+ and PFl), and TcR y6 (TcR 61 WT31-).…”