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Cell electrophoresis was performed on peripheral-blood lymphocytes obtained from 11 patients with rheumatoid arthritis (R.A.) and 16 normal controls. On the basis of cell frequency/mobility histograms each subject's lymphocyte electrophoretic profile was resolved into a bimodal distribution of fast and slow cells. The mean electrophoretic mobility (E.P.M.) of the fast-cell population was similar in controls and in R.A. patients but the mean E.P.M. of the slow population was significantly slower in R.A. than in the controls. In the R.A. patients the E.P.M. of the polymorphonuclear cell population was significantly slower than that of P.M.N. cells in the peripheral blood of controls.

The unaffected skin of eighteen patients with dermatitis herpetiformis (D.H.), twenty-two patients with cœliac disease (C.D.), and eight controls were examined using direct immunofluorescence and class-specific fluorescein-conjugated anti-human IgA, IgM, and IgG antisera. All eighteen patients with D.H. showed IgA deposits in the skin: in seventeen the deposits were only found in the dermal papillae, whilst in one it was found in a continuous line below the basement membrane, confirmed by immuno-electronmicroscopy. IgM deposits were also found in the dermal papillae in three patients with D.H. and IgG deposits below the basement membrane in one patient. In cœliac disease, however, only one of the twenty-two patients showed papillary IgA deposits and one had continuous IgM deposits. These immunoglobulin deposits in D.H. and C.D. seem to be on the reticulin of the dermal papillae. It is suggested that in D.H. there is a fault of the reticulin in the skin and small intestine, whilst in cœliac disease it is present in the small intestine but not in the skin. The reticulin cross-reacts with gluten complexes to give rise to an immunological reaction. In support of this hypothesis we have demonstrated cross-reactivity between gluten and reticulin.

Immunoglobulin levels in cyst-fluids from 19 odontogenic cysts were significantly higher than in the sera of the same patients. Mean cyst/serum ratios for IgA, IgG, and IgM were 3.0, 2.1, and 1.8 respectively. Immunofluorescent staining of sections of cyst walls showed that the characteristic cellular mural aggregates contained many cells forming immunoglobulins; IgA plasma cells were preponderant, but IgG and IgM cells were also seen. In some cases plasma cells were seen penetrating the epithelial lining of the cyst and entering the cavity. It seems that immunoglobulins reaching the cyst cavity are transported by the cells that make them.

Without prior knowledge of the diagnosis or clinical status, sera from patients with various arthritides were screened for antibody against rheumatoid-arthritis-associated nuclear antigen (RANA) with indirect immunofluorescence on cytocentrifuged Raji cell preparations. 93% of 103 seropositive rheumatoid patients had anti-RANA antibody, in contrast to 16% of 50 normal controls and a mean of 19% (10-29%) of 122 patients with other arthritides. Anti-RANA antibody was also demonstrated in 95% of 21 patients with seronegative rheumatoid arthritis characterised by symmetrical erosive peripheral polyarthritis. No correlation was found in rheumatoid arthritis between anti-RANA antibody and disease activity, duration of disease, drug therapy, or extra-articular manifestations. RANA staining was absent in a non-Epstein-Barr-virus (EBV) cell line (Ramos). In 10 rheumatoid patients, discordance between the presence of antibodies to EBV antigens (viral capsid antigen [VCA] and EBNA) ANd RANA antibody was demonstrated. Anti-RANA antibody could be a useful marker for rheumatoid arthritis.

The peripheral-blood lymphocytes from eight patients with infectious mononucleosis (I.M.) included an abnormally high proportion (45·4%) of cells forming spontaneous rosettes with sheep red blood-cells (mean normal 30·3%). The rosette-forming cells were preponderantly the atypical lymphocytes characteristic of the acute stage. In one patient with numerous circulating atypical cells (84%) the rosette-forming cells were equally numerous, and phytohaemagglutinin (P.H.A.) responsiveness was much depressed, on serial study a fall in rosetted cells paralleled the loss of atypical cells, while P.H.A. responsiveness returned. It is concluded that the atypical cells of I.M. are derived from the T lymphocyte population.

A new antibody of IgG class reacting with connective tissue in rat and human organs was found in 17% of 29 patients with dermatitis herpetiformis and in 36% of 31 patients with adult coeliac disease. The antibody appeared to be directed against reticulin rather than basement membrane. In 34% of the dermatitis-herpetiformis patients antinuclear factors of IgG or IgM class were present.

A method for the detection in human sera of precipitating antibody specific for D.N.A. by two-stage electroimmunodiffusion is described. The results obtained in a pilot study on 351 sera indicate that the significance of this antibody may be different from that attributed to D.N.A. antibodies detected by other procedures, since development of nephropathy in cases of systemic lupus erythematosus was associated with absence of the antibody, while its presence correlated with the occurrence of cutaneous vasculitic lesions.

It is firmly established that erythroblastosis fetalis (hemolytic disease of the newborn) is a blood disease of the fetus and newborn resulting from isosensitization of the mother to an antigen on the red cells of the fetus which is lacking from her own blood, and the transplacental transfer of the maternal antibody into the fetal circulation, where it combines with the red cells of the fetus (Levine et al. 1941). Thus, there necessarily is a strong association between blood groups and this disease, so much so that Rh typing and Rh antibody testing have become a routine part of the prenatal care of expectant mothers, in order to predict before birth the occurrence of the disease in the fetus and newborn baby. While the purpose of this article is primarily to discuss the numerous investigations that have been carried out on the association of blood groups with diseases and conditions other than erythroblastosis fetalis, it will be necessary to compare these two kinds of investigations for the proper development of the argument. The pathogenesis of erythroblastosis fetalis was elucidated when it was realized that the expectant mother could be isosensitized either by an injection of blood having the agglutinogen lacking from her red cells, or as a result of leakage of fetal blood into her circulation across the ordinarily impervious placenta. The presence in the mother's serum of the isoantibody produced in response to such stimulation and also coating the red cells of the newborn baby is pathognomonic of erythroblastosis. This is true both in the classic cases caused by Rho sensitization* and in atypical types due to sensitization to other Rh-Hr blood factors such as rh", hr', etc., or blood factors like S. M, etc., of other blood group systems. In the vast majority of cases of ABO hemolytic disease, the mother belongs to group 0, and the baby, to subgroup Al or group B (Wiener 1961). Thus, the reason for the association between blood groups and hemolytic disease of the newborn is crystal clear and can be demonstrated in every individual case. The rationale underlying the claimed associations between blood groups and other diseases, on the other hand, is not at all apparent. In such investigations (reviewed by Wiener 1943, pp. 361-379; Bourdel 1960; Race and Sanger 1962, pp. 385400; Muschel 1966; Chakravartti 1967; Prokop and Uhlenbruck 1969, pp. 690-722), as large a series as possible is compiled of examples of a particular disease or a condition selected more or less at random (e.g., syphilis, malaria, feeblemindedness, skin