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Graft-versus-host (GVH) reaction in chick embryos was suppressed by pretreating allogeneic donor lymphocytes with a noncytotoxic antithymus globulin. This effect showed direct quantitative correlation with the extent of opsonization measured in embryos by the diversion assay. ATG-F(ab')2failed to suppress GVH reaction and was also ineffective in the diversion test. The results suggest that opsonization mediated by Fe fragments may play a major role in the functional elimination of GVH-reactive cells from allogeneic bone marrow grafts.

Graft-versus-host (GVH) reaction was induced by allogeneic blood lymphocytes in chick embryos and measured by the resulting splenomegaly. Prior to injection into embryos, lymphocytes were incubated in vitro in the presence of complement with rabbit antisera raised against chicken thymus (ATS), bursa cells (ABS), or immunoglobulin (AGS). Selective elimination of GVH-reactive lymphocytes was achieved by ATS but not by ABS. Cross absorption of ATS with bursal cells further increased its specificity. The antiserum concentration was critical: 10 was inhibitory but 1 enhanced the response. Treatment of lymphocytes with AGS under various conditions failed to inhibit the GVH reaction. Treatment of bone marrow cells with ATS eliminated GVH-reactive lymphocytes but preserved the erythropoietic cells. A possible application of this approach to clinical bone marrow transplantation is apparent.

Cell-mediated and humoral immune responses to Herpesvirus hominis type 1 (HVH1) and Candida albicans were studied in patients with leukoplakia, showing a histological spectrum of changes from epithelial keratosis to acanthosis and atypia, and in patients with carcinoma. The results were ranked according to increasing values of stimulation indices of lymphocyte transformation to HVH1, and the corresponding macrophage migration inhibition indices, and complement fixing antibody titres of each patient were correlated. This revealed that most patients with epithelial atypia were clustered to that end of the spectrum which had the highest stimulation and migration indices to HVH1; this relationship was not evident with C. albicans. In patients with keratosis and acanthosis there was a significant lack of correlation between lymphocyte transformation and migration inhibition to both HVH1 and C. albicans. In carcinoma the indices of lymphocyte transformation and migration inhibition to HVH1 and C. albicans were depressed. Furthermore, a significant negative correlation was found between lymphocyte transformation and migration inhibition to HVH1, unlike the positive correlation in control subjects. Complement fixing antibodies to HVH1, HVH2, cytomegalovirus and adenovirus, and fluorescent antibodies to C. albicans failed to show a significant change in titre in any one group of subjects tested. The results suggest a cell-mediated immune defect in leukoplakia, with a dissociation between lymphocyte transformation and macrophage migration inhibition to HVH1 and C. albicans in cases of keratosis or acanthosis. A specific increase in cell-mediated immunity to HVH1 in leukoplakia with epithelial atypia and the sequential changes argue in favour of a possible participation of HVH1 in carcinomatous transformation of some leukoplakias.

Rabbits immunized to different antigens (bacteriophage T4, bovine serum albumin, and keyhole limpet hemocyanin), in which presence of antibodies in serum had been proved, were checked for presence of antibodies in tears. Using different techniques, the presence of antibodies in tears was found in all rabbits checked. The most sensitive technique was passive hemagglutination with five positive results out of five animals checked. Passive cutaneous anaphylaxis showed three positive results out of five. Ouchterlony showed zero positive out of four and phage neutralization assay showed one out of one.

THERE is currently a great deal of interest in binding sites (receptors) on lymphocytes with respect to their role: (a) for recognition of antigens, (b) as “trigger sites” for lymphocyte differentiation and proliferation, (c) as markers of the type and specificity of antibodies that the progeny of the cell will produce if stimulated, and (d) in regulating whether immunity or tolerance is induced by exposure to the antigen1–3. The well defined antigenic structure of immunoglobulins makes it possible to look for the presence of immunoglobulin-type receptors using anti-immuno-globulin sera. The interaction of anti-immunoglobulin antibodies with small lymphocytes in cell culture stimulates nucleic acid synthesis and the transformation of lymphocytes to blast cells5. We have used this approach to investigate the phenotypic expression of H-chain controlling genes in lymphocytes. Stimulation of nucleic acid synthesis in vitro by specific anti-H-chain sera was used as a criterion for the presence of receptors with μ or γ-chain specificity on lymphocytes.