Publications

The kinetics of cell-mediated immunity developed during the course of Leishmania major infection in resistant (C57BL/6) and susceptible (BALB/c) mice were determined by using in vitro bioassays. Cells isolated from the lymph nodes draining the infected footpads were assayed for their proliferative responses to leishmania antigens (promastigote and amastigote) or to concanavalin A (Con A). Although lymph node cells (LNC) from both mouse strains proliferated to mitogen and antigen early after infection, both C57BL/6 and BALB/c mice developed diminished in vitro proliferative reactivity within 3 to 5 wk after infection. LNC from both mouse strains recovered lymphoproliferative reactivity to Con A (week 6), but only C57BL/6 mice regained reactivity to leishmania antigens. BALB/c cells remained unresponsive to leishmania antigens throughout the subsequent course of the infection. Supernatants derived from cultures of LNC that had been stimulated with Con A or leishmania antigens were assayed for interferon-gamma (IFN-gamma) by analyzing three distinct activities associated with IFN-gamma. Culture supernatants derived from leishmania antigen stimulation of LNC from infected C57BL/6 mice, but not BALB/c mice, were able to induce surface Ia on murine P388D1 cells. Ia-inducing activity was detectable in supernatants from C57BL/6 cells as early as 3 wk, and peaked by 5 wk after infection. Although cells from infected BALB/c mice never produced detectable IFN-gamma in response to leishmania antigens, LNC from both mouse strains produced readily detectable IFN-gamma in response to Con A throughout the course of infection. Culture supernatants that induced Ia on P388D1 cells were also capable of activating resident peritoneal macrophages to display leishmanicidal activity and of inhibiting encephalomyocarditis virus replication in murine fibroblasts. Each of these activities could be removed by prior incubation of the supernatants with rabbit heterologous anti-murine IFN-gamma sera or monoclonal rat-anti-murine IFN-gamma. The correlation of healer status with the capacity to generate IFN-gamma in vitro in response to leishmania antigens was examined in BALB/c mice that had been exposed to sublethal irradiation (550 rad) before infection. These animals have been previously shown to effectively resist L. major infection. Consistent with observations in the genetically resistant C57BL/6 mice, LNC from these animals demonstrated the capacity to respond to in vitro leishmania antigen stimulation with lymphoproliferation, and more importantly, by producing IFN-gamma.(ABSTRACT TRUNCATED AT 400 WORDS)

The authors conducted a retrospective hospital-based chart review of cases of hemolytic-uremic syndrome among children less than or equal to 18 years of age, hospitalized in Oregon during the four-year period from January 1979 to December 1982. Thirty children with hemolytic-uremic syndrome living in Oregon were hospitalized during this period, for an average annual incidence of 0.97 cases per 100,000 children. Seventy per cent of cases occurred in children under five years of age, for an incidence of 2.65 cases per 100,000 children. Twenty-seven (90%) of the 30 children were white, and 17 (57%) were female. Twenty-four (80%) had a diarrheal prodromal illness including 20 who had bloody diarrhea. Twelve children (40%) acutely required peritoneal dialysis, and two (7%) developed chronic renal failure. Three children died, for a case fatality ratio of 10%. Sixty per cent of the 30 cases occurred during the summer and early fall months. Geographic clustering was also evident. Hemolytic-uremic syndrome is a rare but endemic disease in Oregon and may occur in small clusters. Although descriptions of several large series of patients have been published, this study describes the first statewide population-based study of this syndrome.

Cholecystokinin (CCK) and substance P (SP) were measured in discrete areas of the rat brain at different stages of the estrous cycle. Significantly higher levels of CCK were found in the lateral septum during diestrus as compared to proestrus. In the parietal cortex, CCK concentrations were significantly higher in diestrus than in proestrus. In the amygdala, estrous levels of CCK were significantly higher than proestrous levels. SP concentrations were significantly higher in diestrus than in proestrus in the medial and lateral septum, and the medial and lateral preoptic area. In the amygdala and ventral tegmental area, SP concentrations were significantly higher in estrus than in proestrus. These data suggest that certain CCK and SP neuronal systems may play a role in regulating the hypothalamo-pituitary-gonadal axis and/or be involved in steroid-dependent behavior.

Ig and T cell antigen receptor genes in their germ line form are separated DNA segments that are joined by recombinations during lymphocyte development. The analysis of Ig and T cell receptor gene arrangements has been of value in the study of lymphoid neoplasms. The identification of T cell receptor gene rearrangements taken in conjunction with studies of Ig gene rearrangements aids in the elucidation of the lineage (T cell or B cell) and the clonality of lymphoid populations of all series. The application of this molecular genetic approach has great potential for complementing conventional marker analysis, cytogenetics, and histopathology, thus broadening the scientific basis for the classification, diagnosis, and monitoring of the therapy of lymphoid neoplasia. IL 2 is a lymphokine synthesized by some T cells following activation. Resting T cells do not express IL 2 receptors, but receptors are rapidly expressed on T cells following the interaction of antigens, mitogens, or monoclonal antibodies with the antigen-specific T cell receptor complex. Normal resting T cells and most leukemic T cell populations do not express IL 2 receptors; however, the leukemic cells of all patients with HTLV-I-associated adult T cell leukemia examined expressed the Tac antigen. The constant display of large numbers of IL 2 receptors that may be aberrant may play a role in the uncontrolled growth of these leukemic T cells. Patients with the Tac antigen positive adult T cell leukemia are being treated with the anti-Tac monoclonal antibody directed toward this growth factor receptor.