A cytokine was identified that stimulated the proliferation of T lymphocytes, and a complementary DNA clone encoding this new T cell growth factor was isolated. The cytokine, designated interleukin-15 (IL-15), is produced by a wide variety of cells and tissues and shares many biological properties with IL-2. Monoclonal antibodies to the beta chain of the IL-2 receptor inhibited the biological activity of IL-15, and IL-15 competed for binding with IL-2, indicating that IL-15 uses components of the IL-2 receptor.

The development and spread of antibiotic resistance in bacteria is a universal threat to both humans and animals that is generally not preventable, but can nevertheless be controlled and must be tackled in the most effective ways possible. To explore how the problem of antibiotic resistance might best be addressed, a group of thirty scientists from academia and industry gathered at the Banbury Conference Centre in Cold Spring Harbor, New York, May 16-18, 2011. From these discussions emerged a priority list of steps that need to be taken to resolve this global crisis.

No abstract

SummaryPurified CD4 + lymph node T cells were sorted into two populations on the basis of their expression of CD45RB (CD45RB hi and CD45RB 1~ and injected into congenic severe combined immunodeficient (SCID) mice. After a period of time that was dependent on the number of cells injected, the SCID mice that received CD45RBhi/CD4 + T cells developed a wasting disease that was not seen in SCID mice that received the CD4+/CD45RB 1~ cells or whole lymph node cells. At death, SCID mice that received the CD4 +/CD45RB hi cells had increased spleen and lymph node cellularity compared with normal SCID mice and SCID mice that received the CD4+/CD45RB 1~ T cells. The spleen and lymph node contained CD4 + cells and neither CD8 + nor surface immunoglobulin M-positive cells, plus a population of cells that did not express any of those markers. At necropsy, the SCID mice that received the CD4 +/CD45RB hi cells had significant hyperplasia of the intestinal mucosa with significant lymphoid cell accumulation in the lamina propria. Interestingly, mice that received mixtures of whole lymph node or purified CD4 * cells with CD4 +/CD45RB ~ cells did not develop weight loss, indicating that the unseparated CD4 + population contained cells that were capable of regulating the reactivity of the CD4 +/CD45RB hi cells. utoaggressive immunological reactivity can be driven by CD4 § thymus-derived lymphocytes. For instance, it has been demonstrated that experimental autoimmune encephalomyelitis and diabetes can be induced in normal animals by injecting them with CD4 + T cell clones or lines derived from animals with autoimmune disease of that particular tissue (1-5). Also, T cell reactivity to self-antigens can be demonstrated in normal animals by immunizing them with a closely related antigen in a unique way or by depleting them of a regulatory population (6-8). These data indicate that T cells with specificity for self-antigens exist normally, but that their reactivity is controlled by immunoregulatory mechanisms.It is well appreciated that thymus-derived lymphocytes can be categorized according to the cell surface antigens they express. This has allowed the classification ofdass I or II MHCrecognizing T cells based on their expression of CD8 or CD4 (9). Also, recent data indicate that virgin and memory T cells can be distinguished by their expression of other cell surface markers such as CD44 or CD45 (10-12). The ability to associate T cell function with the expression of a unique array of cell surface determinants is useful in studying the function of these populations in isolation as well as in defined combinations. For instance, Powrie and Mason (13) have separated CD4 + T cells based on their expression of CD45R and injected the resultant subpopulations into congenic, athymic (nude) animals. They found that nude rats injected with congenic CD45Rhi/CD4 + T cells developed wasting disease characterized by inflammatory infiltrates in many organs. Rats injected with unfractionated CD4 + cells (a mixture of CD45R hi and CD45R l~ cells) did n...

In this era of complete genomes, our knowledge of neuroanatomical circuitry remains surprisingly sparse. Such knowledge is critical, however, for both basic and clinical research into brain function. Here we advocate for a concerted effort to fill this gap, through systematic, experimental mapping of neural circuits at a mesoscopic scale of resolution suitable for comprehensive, brainwide coverage, using injections of tracers or viral vectors. We detail the scientific and medical rationale and briefly review existing knowledge and experimental techniques. We define a set of desiderata, including brainwide coverage; validated and extensible experimental techniques suitable for standardization and automation; centralized, open-access data repository; compatibility with existing resources; and tractability with current informatics technology. We discuss a hypothetical but tractable plan for mouse, additional efforts for the macaque, and technique development for human. We estimate that the mouse connectivity project could be completed within five years with a comparatively modest budget.