Bernard Chatelain

From health locus of control to immune control: internal locus of control has a buffering effect on natural killer cell activity decrease in major depression.

Decreased immunity in depressive as compared with control subjects has been well documented, although some depressed patients have severe alterations whereas others have milder ones or not at all. Since for equal severities of depression, there may be individual differences in the degree of perceived control over ones condition, we investigated the interaction of perceived control with immunological variations. Immune function (T and B lymphocytes, lymphocyte proliferation and natural killer cell activity (NKCA)) were evaluated in 34 adult major depressives and in 18 healthy controls. Lymphocyte proliferation did not differ between the two groups, but NKCA was significantly lower in the depressed patient group. Among the depressed subjects, those who experienced less subjective control also showed significantly lower NKCA. An internal locus of control appears to act as a buffer against the decrease in cellular immunity observed in major depression. Further studies should focus on methods of coping and on degree of perceived control rather than on diagnostic and nosographic variables alone.

Presence of Fc Receptors for IgA on Rat Alveolar Macrophages but not Peritoneal Macrophages

Different blood cells, including lymphocytes, polymorphonuclear leukocytes and monocytes, possess a receptor for the Fc portion of IgA (FcaR) on their surface (1–4). Recently, an FcaR has also been demonstrated on mouse alveolar marcrophages (AM) but not peritoneal macrophages (PM) (5), and the IgA-mediated phagocytosis correlated with the presence of FcaR (6). Despite early studies reporting the absence of FcaR on rat and human AM (7,8), up to 17% of human AM can ingest sIgA-opsonized Pseudomonas (9). Further, a possible role of AM has been suggested in a rat model of IgA-induced lung injury (10). Therefore, the present study was designed to assess by flow cytometry the issue of FcaR on rat AM and PM and to investigate whether the molecular size of IgA could influence its binding to the cells.

Blunted rise in intracellular calcium in CD4+ T cells in response to mitogen following autologous bone marrow transplantation.

Summary. Following autologous bone marrow transplantation (ABMT), both impaired T cell activation and defective production of the principal T cell growth factor, interleukin‐2 (IL‐2), has been observed. These processes are dependent on a rise of intracellular calcium ([Ca2±]i), a step which follows binding of T cell receptor (TCR) and transduction of signal via the generation of cytoplasmic second messengers. In order to better understand the nature of defective cellular immunity in ABMT, in the present study we investigated the rise of [Ca2±]i in T cells of recipients of ABMT. By concomitant labelling lymphocytes with anti‐CD4 antibody and addition of fluo‐3 as fluorescent calcium indicator, we have selected for the T cell subset which is the principal source of IL‐2. Short‐term (less than 1 year post‐transplantation) recipients of ABMT show a statistically significant blunted rise in [Ca2±]i in response to concanavalin A as compared to normal controls not accounted for solely by a decreased percentage of CD4± cells in these patients. The [Ca2±]i response of CD4± cells from long‐term (greater than 1 year post‐transplant) recipients was lower than that of the normal group although not to a statistically significant level. These findings suggest that following ABMT is a defect in the early stages of T cell activation involving either T cell receptor binding or early signal transduction ultimately resulting in depressed transcription of IL‐2 mRNA. These defects are analogous to findings in both allogeneic transplantation where factors of histoincompatability and graft‐versus‐host disease (GVHD) come into play, as well as in the defective T cell activation of the normal ageing process.

Fc-receptor mediated phagocytosis of IgA- and IgG-coated red cells by human alveolar macrophages

Receptors for the Fc portion of IgG subclasses and IgA are present on the cell surface of alveolar macrophages (AM) from mice, rat, and humans (1–5). Fc-receptors for IgG (Fcγ-R) are known to induce a series of phagocyte functions including the respiratory burst, degranulation and phagocytosis (6). By contrast, there is little information on the function of Fc-R for IgA (Fcα-R). In the present in vitro study, we evaluate the Fc-αR mediated phagocytosis in normal human AM and compare it to the Fcγ-R mediated phagocytosis. Furthermore, the effect of in vivo macrophage activation on the Fc-R is investigated by studying AM from patients with pulmonary sarcoidosis.