Hoping to improve the systems for identifying and classifying normal and malignant lymphoid subpopulations, frozen and paraffin sections of nonmalignant lymphoid tissue and of malignant lymphomas were immunostained for surface (S) and cytoplasmic antigens using the peroxidase-antiperoxidase method. Primary follicle cells and follicle mantle cells known to be part of the recirculating B-cell pool were found to be constantly Ia and C3 receptor (C3R) positive, mostly SIgM and SIgD positive and cytoplasmic immunoglobulin (CIg) negative. The light zone of germinal centers (GC), which is rich in centrocytes, contained a large number of T cells and showed the well-known intercellular Ig network pattern; the dark zone, containing densely packed centroblasts, was usually free of T cells, but was bordered ay a mantle-like accumulation of T cells. Usually only some of the GC cells were definitely positive for SIg and CIg of different classes. All cells reacted positively for Ia and C3R. In areas described by other authors as containing marginal zone cells, cells densely bearing SIgM and deficient in SIgD were detected. The immunoblasts of the hyperplastic plasma cell reaction usually contained CIg. Cells from chronic lymphoid leukemia sections that immunostained for SIgM and SIgD were interpreted as representing a neoplasm of recirculating B cells expressing SIgM and SIgD. The immunohistologic architecture of follicular centroblastic/centrocytic lymphoma showed a more or less close similarity to the organization of secondary follicles. Lymphomas whose cells resembled reactive centrocytes were strongly SIgM positive and SIgD negative or only weakly SIgD positive. CIg was demonstrable in nearly 90% of the lymphomas whose cells resembled centroblasts and in 70% of the lymphomas whose cells resembled immunoblasts of the plasma cell reaction. Finally, immunohistologic staining results from a T-zone lymphoma are presented, which confirm that this lymphoma was composed of a neoplastic T zone and a non-malignant B zone.

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The activity of alpha-naphthyl acetate esterase at an acid pH (ANAE) was investigated in 10 cases of hairy cell leukemia. All 10 cases, including two cases with only a few tartrate-resistant acid phosphatase-reactive cells, revealed a moderate or strong ANAE reaction. There was a characteristic pattern of activity consisting of small, medium-size, or large distinct granules often distributed in a semicircle in the cytoplasm, but sparing the nucleus of hairy cells. This reaction pattern was not found in T cells, T cell-derived leukemias, normal B cells, a number of B-cell lymphomas, myeloid cells, myeloid leukemias (including monocyte-derived leukemias), reticulum cell sarcoma, or malignant reticulosis. The cells from some B-cell lymphomas and plasmacytoma showed a relatively homogeneous pattern of fine or moderately coarse ANAE-positive granules that was similar to that of hairy cells only in some cases of plasmacytoma. Thus, fine to coarse granular ANAE reactivity is characteristic of hairy cells and is of potential diagnostic value for hairy cell leukemia.

The aim of the present study was to present further evidence of the specific reactivity of an anti-C3 receptor serum (AC3RS), to demonstrate membrane-bound C3 receptors by using this AC3RS in different serological an immunohistological methods, and to investigate the relationship between membrane-bound C3 receptors and alpha1-antitrypsin. The AC3RS, or F(ab')2 fragments of the IgG fraction of this antiserum, stained a percentage of various viable cell populations roughly equivalent to the number of cells that bound EAC3b and/or EAC3d; C3 receptor-negative T cells and thymocytes were not stained. On frozen sections of tonsils and kidneys it was found that the AC3RS stained area to which EAC3b adhered. After absorption with neutrophils or Ehu, the AC3RS inhibited the agglutination of EAC3d with tonsil cells, but not the agglutination of tonsil cells or neutrophils with EAC3b; this absorbed AC3RS still stained tonsil cells but not neutrophils, and in frozen tonsil sections it stained only those areas to which EAC3d adhered. The absorbed AC3RS did not stain glomeruli. Antisera to alpha1-antitrypsin failed to inhibit EAC agglutination with C3 receptor-bearing cells or to stain C3 receptor-positive cells either in suspension or in frozen sections. Absorption of th AC3RS with purified alpha1-antitrypsin did not affect its specific reactivity.