T-cell dysregulation in patients with hyperprolactinemia: effect of bromocriptine treatment

We studied four patients with tumoral hyperprolactinemia and normal ovarian function before and after prolactine levels had become normal with treatment with bromocriptine (BrC), a dopamine agonist that inhibits prolactin release. Their proliferative responses to concanavalin A, pokeweed mitogen, and, to a lesser extent, phytohemagglutinin, their spontaneous and concanavalin A-induced suppression, and their production of interleukin 2 were found to be decreased and to correct partially or completely after bromocriptine treatment. The T-cell response to interleukin 2 was low in two patients in whom it increased after BrC treatment. These findings give insight on the immunomodulatory role of prolactin in vivo.     

Hyperprolactinemia inhibits natural killer (NK) cell functionin vivo and its bromocriptine treatment not only corrects it but makes it more efficient

We studied NK cell function in eight patients with pathological hyperprolactinemia by measuring⁵¹Cr release by K562 cells exposed to their mononuclear cells and found it decreased compared to normal controls (P<0.01). Bromocriptine (BrC) treatment corrected NK function but also made it more efficient at 12:1 than at 25:1 or 50:1 effector:target ratios (ANOVA;P=0.01). The study of NK cell function in agarose revealed that its decrease in hyperprolactinemia is due to their low active binding to target cells, active killing, and recycling capacity. BrC tended to correct them but also increased recycling capacity to levels higher than those of controls (P<0.05). Sequential studies in three hyperprolactinemic patients before and after BrC showed correction of NK function within 1 week but its increased efficiency at the 12:1 effector:target ratio required 8 weeks. We conclude that hyperprolactinemia decreases NK cell function. BrC corrects this by decreasing prolactin levels but also makes NK function more efficient by increasing the capacity of NK cells to recycle after killing.     

In vivo electrical characteristics of human skin, including at biological active points

The aim is to compare the mean values of the in vivo electrical characteristics of bioiogical active points (BAPs) with those of the surrounding human skin. The impedance measurements at BAPs and on the surrounding skin are carried out in vivo on ten young, healthy people. The results of the measurements show that the BAP resistance R_P is smaller, and the capacitance C_P is higher, than the corresponding values for skin, R_S and C_S, respectively, these differences are larger at low frequencies (at f=3 Hz, R_S/R_P=3.19 and C_P/C_S=3.2). The mean values of the impedance measurements at the BAPs are different from those measured on the skin. The dependence of R_P and C_P on the pressing force, in the range of about 1–5 N, for the BAPs, has a smaller slope than that observed for the surrounding skin. An equivalent circuit for the BAPs is proposed that describes sufficiently well the experimental results obtained. These results show that the large dispersion in the observed impedance characteristics of the human body measurements in different body regions can be related to the influence of the BAPs present under the electrodes.     

The role of intrahepatic lymphocytes in mediating protective immunity induced by attenuated Plasmodium berghei sporozoites

Summary: Exposure to irradiated Plasmodium sporozoites (g‐spz) results in protection against malaria. Like infectious spz, g‐spz colonize hepatocytes to undergo maturation. Disruption of liver stage development prevents the generation of protection, which appears, therefore, to depend on liver stage antigens. Although some mechanisms of protection have been identified, they do not include a role for intrahepatic mononuclear cells (IHMC). We demonstrated that P. berghei g‐spz‐immune murine IHMC adoptively transfer protection to naive recipients. Characterization of intrahepatic CD4+ T cells revealed an immediate, albeit transient, response to g‐spz, while the response of CD8+ T cells is delayed until acquisition of protection. It is presumed that activated CD8+ T cells home to the liver to die; g‐spz‐induced CD8+CD45RBloCD44hi T cells, however, persist in the liver, but not the spleen, during protracted protection. The association between CD8+CD45RBloCD44hi T cells and protection has been verified using MHC class I and CD1 knockout mice and mice with disrupted liver stage parasites. Based on kinetic studies, we propose that interferon‐g, presumably released by intrahepatic effector CD8+ T cells, mediates protection; the persistence of CD8+ T cells is, in turn, linked to Plasmodium antigen depots and cytokines released by CD4+ T cells and/or NK T cells.     

Foramen Thyroideum: A Comparative Study in Embryos,Fetuses, and Adults

The incidence and characteristics of foramen thyroideum (FT) in embryonic and/or fetal larynges have not been established. In the present study, 90 adult larynges and 53 embryonic-fetal larynges were studied. The incidence of FT during the embryonic-fetal period (57%) was statistically different from the adult period (31%) (P = 0.005). All the FT found in the adult period contained vessels and/or nerves, while in the embryonic and fetal period only 63% presented neurovascular elements (P < 0.001). The origin of FT in the embryonic period and its persistence during adult life is discussed.