For the laboratory confirmation of cellular hypersensitivity responses the inhibition of cell migration is widely used. This procedure is based upon the observations of Rich and Lewis (1932), who found a reduced radial migration of macrophages from spleen explants of tuberculin-sensitive guinea-pigs in the presence of tuberculin, in contrast to those originating from Mantoux-negative animals. The inhibition of macrophage migration is nowadays most frequently examined in the manner described by George and Vaughan (I962): from a capillary tube containing the peritoneal exudate of guinea-pigs its cells migrate out in the same way as do the motile cells of the spleen explant, and this cell migration also may be inhibited by specific antigens. According to the investigations of David, Al-Askari, Lawrence, and Thomas (I964) the cell migration is inhibited by antigens causing delayed hypersensitivity only, and this phenomenon is unrelated to humoral immunity. The inhibition is due to a soluble protein (migration inhibitory factor, MIF) synthesized by the immunocompetent lymphocytes found between the peritoneal cells when the former come in contact with the specific antigen, MIF decreasing the motility of macrophages (David, I966; Bloom and Bennett, I966).The studies of S0borg and Bendixen (1967) and S0borg (i 967) demonstrated the migration of the leucocytes separated from the peripheral blood leaving the capillary tube container in the same way as the peritoneal macrophages; the migration of leucocytes can also be inhibited by antigens causing delayed hypersensitivity. The inhibition of leucocyte migration has since become widely used to investigate antimicrobial, antitumour, and antitransplant immunity of the delayed type, and also autoimmune diseases and drug allergy (Revillard, 1971;Dobozy, Hunyadi, and Simon, 1973).The present paper gives an account of our investigations in performing leucocyte migration tests with uveal pigment as antigen from the blood of patients suffering from sympathetic ophthalmitis and the Vogt-Koyanagi-Harada syndrome, respectively. In both diseases, earlier anti-uveal antibodies and lymphocytes hypersensitive to uveal antigen were demonstrated in the peripheral blood (Kahan, Sztanojevits, Szabados, Vass, and Szabo, I964; Mills and Shedden. I965; Hammer, 197I; Wong, Anderson, and O'Brien, I97I)e Marak, Font, Johnson, and Alepa (I 97 I) and Marak, Aye, and Alepa (I 973) prepared separately uveal and pigment epithelial antigens and found blastogenic activity of the latter only in sympathetic ophthalmitis.

Many studies have characterized the phenotypic features of individuals who are likely to develop cutaneous melanoma. One of the major items included in melanoma risk assessment has been the presence of clinically atypical nevi (dysplastic nevi). This study assessed the number of subjects with dysplastic nevi in groups of patients with uveal melanoma or cutaneous melanoma and in a group of volunteer controls. The SPSS program was used to calculate the odds ratios (hereafter called relative risks; RR) and 95% confidence intervals (C) in melanoma patients and controls. The RR was 4.36 for uveal melanoma (95% Cl 1.84-10.36) and 4.22 for cutaneous melanoma (95% Cl 1.81-9.84). These results suggest that cutaneous dysplastic nevi are a significant risk factor for uveal melanoma.

The lymphocyte transformation test (LTT) has been shown to be a reliable method of demonstrating the antigen of delayed-type allergic responses. The test is based upon the process of gradual enlargement, transformation into lymphoblasts, and mitotic activity of small mature lymphocytes in the peripheral blood which occurs when they come into contact with an antigen to which the organism has previously been sensitized (Pearman, Lycette, and Fitzgerald, I963; Marshall and Roberts, I963; Daniels, Ritzmann, and Levin, I968; Ling, I968). The mechanism of this blastic transformation appears to be identical with that of lymphocyte activation observed in the course of homograft rejection. Blastogenesis will not take place if no antigen has been added to the lymphocyte cultures, or if the donor organism has not been previously sensitized to the antigen tested.Phytohaemagglutinin (PHA) is known to stimulate aspecifically the blastic transformation of lymphocytes cultured from healthy subjects (Hungerford, Donelly, Nowell, and Back, I959; Nowell, I960), but this stimulation does not occur if the subject suffers from a disease damaging the immune apparatus or is receiving immunosuppressive treatment (Daniels and others, I968; Bozsoky, I969).In this paper the effects of uveal pigment and PHA on lymphocyte cultures from patients with sympathetic ophthalmitis (SO) or the Vogt-Koyanagi-Harada syndrome (VKHS) are compared. Methods LYMPHOCYTE CULTURESThese were taken from two patients suffering from the VKHS and three with SO. Cultures from five ophthalmologically healthy subjects served as controls. Diagnosis was based on the histories and typical clinical signs as well as the histological findings. ANTIGENSUveal pigment not containing soluble proteins prepared from bovine eyes according to the method of Woods (I925) was used for specific stimulation. Phytohaemagglutinin M (o-oI U/ml.) manufactured by Difco was used for aspecific transformation. CULTIVATION OF LYMPHOCYTESLymphocytes isolated from citrated venous blood by sedimentation were cultured in a 5-fold volume of Parker igg solution (Simon, Dobozy, and Hunyadi, I969). The lymphocytes were not separated

Lysosomal serine and cysteine proteases are reported to play a role in collagen degradation. In this study, the activities of the lysosomal cysteine proteases cathepsin B and H, dipeptidyl peptidase I, and the serine protease tripeptidyl peptidase I and dipeptidyl peptidase II, all ascribed a role in collagen digestion, were compared with those of the aspartate protease cathepsin D, and lysosomal glycosidases in leukocytes from rheumatoid arthritis patients at different stages of the disease. In all patients the activities of cysteine protease cathepsin B, dipeptidyl peptidase I, aspartate protease cathepsin D, and two glycosidases were elevated, but the activities of the serine proteases tripeptidyl peptidase I, dipeptidyl peptidase II, and the cysteine protease cathepsin H was unchanged. The magnitude of the increased activity was correlated with the duration of the disease. Patients with long-standing RA (10 years or more) had higher cysteine protease activity in their leukocytes than did those with disease of shorter duration. This tendency suggests that elevated lysosomal cysteine protease activities, together with aspartate protease cathepsin D and lysosomal glycosidases (but not serine proteases), are associated with progression of rheumatoid arthritis.

There is a growing body of evidence supporting the theory that cutaneous dysplastic naevus syndrome patients are at increased risk of developing not only skin but also uveal melanoma. The relationship between dysplastic naevus syndrome and ocular naevi needs to be clarified. In this study we investigated the ocular pigmented findings in patients with dysplastic naevus syndrome and compared the results with a control group (subjects without atypical moles) in order to investigate the frequency of ocular naevi among dysplastic naevi-bearing patients. A total of 152 dysplastic naevus syndrome patients were enrolled in our investigation. The control group consisted of 142 sex-, age- and skin type-matched healthy volunteers without cutaneous dysplastic naevi or skin melanoma. Conjunctival and uveal pigmented findings and iris colour were recorded during a detailed ophthalmic examination. A greater number of conjunctival naevi (3.2% versus 0%), iris naevi (5.2% versus 1.4%), iris freckles (17% versus 5.6%) and choroidal naevi (5.2% versus 0.7%) were detected in the dysplastic naevus syndrome group compared with the controls. The difference reached statistical significance in the case of conjunctival naevi, choroidal naevi and iris freckles. Our results confirm the hypothesis that dysplastic naevus syndrome patients might have overstimulation of their melanocytic system not only in the skin but also in the uvea, leading to increased benign (as well as rarely malignant) melanocytic proliferation. Dysplastic naevus syndrome patients should be screened by ophthalmologists because of the increased frequency of different ocular pigmented alterations.