The levels of beta 1H and C3bINA were estimated in sera from human fetuses, cord and maternal samples. Both components of complement were detected in fetuses more than 12 weeks old. The serum concentrations tended to increase with the gestational age. The mean levels of beta 1H and C3bINA in cord sera were near 54 and 61% of the mean values in sera from normal adults. Elevated levels of beta 1H were observed in maternal sera at the end of the gestational period. When the levels of beta 1H and C3bINA were compared with those of two other components of complement, it was confirmed that the mean levels of C9 were low in fetal and newborn sera, while the serum concentrations of both C9 and Factor B were elevated in maternal samples. Newly synthesised beta 1H was detected in the culture fluids of fetal liver and peritoneal cells, as judged by the incorporation of labelled aminoacids and the autoradiography of he specific immunoprecipitates in agar gel.

Peripheral blood and bronchoalveolar lavage lymphocyte subpopulations have been evaluated in 14 patients with pulmonary sarcoidosis and eight normal subjects, monoclonal antibodies of the leu series being used. No significant alterations of T lymphocyte subpopulations were found in the peripheral blood of sarcoidosis patients. There was, however, a significantly greater proportion of T suppressor-cytotoxic cells (36.0 (SD 17-6%)) in the bronchoalveolar lavage fluid of patients than of normal subjects (15% (5.6%); p < 0.01), but a decrease in the proportion of T helper-inducer cells (51.1% (18%) v 79.3% (9%). These changes correlated with the duration of the disease but not with other clinical, radiological, physiological, or biochemical criteria. Patients were followed up for six to 20 months and five patients had a repeat bronchoalveolar lavage and lymphocyte subpopulation evaluation after three to 14 months. The initial pulmonary T lymphocyte subset proportions were not predictive of clinical, physiological, or radiological alterations during follow up. There was also no consistent pattern in the relationship between change in T subset proportions and change in clinical physiological, and radiological features in the five patients having a repeat lavage. Lymphocyte surface marker studies may indicate immunopathogenetic mechanisms in sarcoidosis but do not appear to be good predictors of clinical outcome.

It has been shown that the activation of T cells by an anti-idiotypic antibody (anti-Id) TB71 containing an internal image of the corresponding mycobacterial antigen (38 kDa) was achieved by the interaction of anti-Id TB71 with the T cell receptor complex (CD3/Ti). The accessory cell requirement in this response could not be replaced by anti-Id TB71 coupled to Sepharose beads and was not inhibited by Fc receptor blockade. When taken together with the finding that anti-Id TB71-induced proliferation of a T cell clone was restricted by determinants encoded by the major histocompatibility complex, these findings suggested that anti-Id TB71 was presented to 38-kDa antigen-reactive T cells by the same mechanisms as conventional antigenic determinants. That is, both stimulated T cells through the CD3/Ti complex and had to be presented in the context of class II molecules on accessory cells. The finding that the disruption of the integrity of the anti-Id TB71 combining site did not affect T cell responsiveness although antibody binding was ablated implied that anti-Id TB71 may be partially degraded and re-expressed with MHC class II determinants.

Supernatants from clones of human T lymphocytes that were responding to a purified Mycobacterium tuberculosis antigen were able to activate macrophages and macrophage-like myeloma cells (U937) to release increased amounts of the microbicidal agent hydrogen peroxide. The activity was not neutralized by monoclonal antibody against interferon-gamma (IFN-gamma), was greater than could be accounted for by the IFN-gamma activity in the supernatants, and was separated from IFN-gamma by high performance liquid chromatography. It is evident that IFN-gamma is not the only macrophage activator released by T lymphocytes responding to microbial antigen, and may not even be the main one to enhance antimicrobial activity in infections such as tuberculosis.