The surface and cytoplasmic expressions of the transducing chain (IFN-γR2) of the heterodimeric IFN-γ receptor on human T lymphocytes have been investigated. We show that its surface expression is low, whereas high cytoplasmic levels are found in both resting and PHA-activated T lymphocytes. This low expression does not prevent activated T cells from responding to IFN-γ, because it induces IFN-regulatory factor 1 expression. Low surface IFN-γR2 expression appears to be due to recycling between cytoplasmic stores and the cell surface, which does not depend on signals mediated by endogenous IFN-γ, because IFN-γR2 surface expression is low, and its internalization is equally observed in patients with inherited IFN-γR1 gene deficiency and in healthy donors. Moreover, IFN-γR2 internalization in T lymphoblasts from healthy donors was not affected by the presence of anti-IFN-γ-neutralizing or anti-IFN-γR1-blocking mAb. In conclusion, these data illustrate a new mechanism whereby human T cells limit the surface expression of IFN-γR2 in a ligand-independent manner.
A careful search for groups of nerve cell bodies enclosed within a common connective envelope was made in the spinal ganglia of the lizard and rat using a serial-section technique. Nerve cell bodies sharing a common connective envelope were found to be more common in the lizard (9.4%) than in the rat (5.6%). These nerve cell bodies were arranged in pairs, or, less frequently, in groups of three. At times, they appeared to be in immediate contact, with no intervening satellite cells; at others, they remained separated from one another by a satellite cell sheet. The clusters of nerve cell bodies enclosed within a common connective envelope probably result from the arrest of developmental processes in the spinal ganglion. It is possible that, as a result of the cell arrangement here described, certain neurons electrically influence other sensory neurons at the level of the ganglion.
The treatment of anterior cruciate ligament (ACL) injuries in children and adolescents is challenging. Preclinical and clinical studies investigated ACL repairing techniques in skeletally immature subjects. However, intra-articular bioenvironment following ACL tear has not yet been defined in skeletally immature patients. The aim of this study was to measure cytokine concentrations in the synovial fluid in adolescent population. Synovial levels of IL-1β, IL-1ra, IL-6, IL-8, IL-10, and TNF-α were measured in 17 adolescent patients (15 boys) with ACL tears who underwent ACL reconstruction including acute (5), subacute (7), and chronic (5) phases. Femoral growth plates were classified as “open” in three patients, “closing” in eight, and “closed” in six. Eleven patients presented an ACL tear associated with a meniscal tear. The mean Tegner and Lysholm scores (mean ± SD) of all patients were 8 ± 1 and 50.76 ± 26, respectively. IL-8, TNF-α, and IL-1β levels were significantly greater in patients with “open” physes. IL-1ra and IL-1β levels were significantly higher in patients with ACL tear associated with a meniscal tear. Poor Lysholm scores were associated with elevated IL-6 and IL-10 levels. IL-10 levels positively correlated with IL-6 and IL-8 levels, whereas TNF-α concentration negatively correlated with IL-6 levels. Skeletally immature patients with meniscal tears and open growth plates have a characteristic cytokine profile with particularly elevated levels of proinflammatory cytokines including IL-8, TNF-α, and IL-1β. This picture suggests that the ACL tear could promote an intra-articular catabolic response in adolescent patients greater than that generally reported for adult subjects. The study lacks the comparison with synovial samples from healthy skeletally immature knees due to ethical reasons. Overall, these data contribute to a better knowledge of adolescent intra-articular bioenvironment following ACL injuries.
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