Course Allocation via Stable Matching

The allocation of students to courses is a wide-spread and repeated task in higher education, often accomplished by a simple first-come first-served (FCFS) procedure. FCFS is neither stable nor strategy-proof, however. The Nobel Prize in Economic Sciences was awarded to Al Roth and Lloyd Shapley for theirwork on the theory of stable allocations. This theory was influential in many areas, but found surprisingly little application in course allocation as of yet. In this paper, different approaches for course allocation with a focus on appropriate stablematchingmechanisms are surveyed. Two such mechanisms are discussed in more detail, the Gale- Shapley student optimal stable mechanism (SOSM) and the efficiency adjusted deferred acceptance mechanism (EADAM). EADAM can be seen as a fundamental recent contribution which recovers efficiency losses from SOSM at the expense of strategy-proofness. In addition to these two important mechanisms, a survey of recent extensions with respect to the assignment of schedules of courses rather than individual courses is provided. The survey of the theoretical literature is complemented with results of a field experiment, which help understand the benefits of stable matching mechanisms in course allocation applications

Characterization of human DNGR-1+ BDCA3+ leukocytes as putative equivalents of mouse CD8α+ dendritic cells

In mouse, a subset of dendritic cells (DCs) known as CD8α+ DCs has emerged as an important player in the regulation of T cell responses and a promising target in vaccination strategies. However, translation into clinical protocols has been hampered by the failure to identify CD8α+ DCs in humans. Here, we characterize a population of human DCs that expresses DNGR-1 (CLEC9A) and high levels of BDCA3 and resembles mouse CD8α+ DCs in phenotype and function. We describe the presence of such cells in the spleens of humans and humanized mice and report on a protocol to generate them in vitro. Like mouse CD8α+ DCs, human DNGR-1+ BDCA3hi DCs express Necl2, CD207, BATF3, IRF8, and TLR3, but not CD11b, IRF4, TLR7, or (unlike CD8α+ DCs) TLR9. DNGR-1+ BDCA3hi DCs respond to poly I:C and agonists of TLR8, but not of TLR7, and produce interleukin (IL)-12 when given innate and T cell–derived signals. Notably, DNGR-1+ BDCA3+ DCs from in vitro cultures efficiently internalize material from dead cells and can cross-present exogenous antigens to CD8+ T cells upon treatment with poly I:C. The characterization of human DNGR-1+ BDCA3hi DCs and the ability to grow them in vitro opens the door for exploiting this subset in immunotherapy