A rapid method for skin grafting in mice that greatly enhances graft and recipient survival.

A streamlined method of skin grafting in mice is described. This procedure eliminates bandages, sutures, and dressings. The elimination of bandages renders the overall procedure fast and easy to learn. More importantly, the elimination of bandaging results in an increased survival of engrafted mice and a drastic reduction in graft displacement. Finally the lack of bandages also makes it possible to monitor the graft even in the earliest stages after engraftment.

Short class I major histocompatibility complex cytoplasmic tails differing in charge detect arbiters of lateral diffusion in the plasma membrane.

Directed and Brownian movement of class I major histocompatibility complex (MHC) molecules on cell membranes is implicated in antigen presentation. Previous studies indicated that the class I MHC cytoplasmic tail imposes constraints on the molecule's diffusion. Here we used single particle tracking to study the mobility of the wild-type mouse H-2L(d) class I MHC molecule and of seven cytoplasmic tail variants. Six of the variants have cytoplasmic tails of four or seven residues (differing in net charge), and one is tailless, yet all are susceptible to confinement in membrane domains. However, truncation of the cytoplasmic tail to 0-4 residues decreases the proportion of particles exhibiting confined diffusion and increases the proportion exhibiting simple diffusion. Particularly for the truncated mutants (tail length of 0-7 residues), many of the particles have complex trajectories and do not move at a constant speed or in the same mode of diffusion throughout the observation period. Several particles of the tailless H-2L(d) mutant display a type of directed diffusion that is rarely observed for other H-2L(d) mutants. Taken together, these data show that even short cytoplasmic tails can influence markedly class I MHC mobility and that cytoplasmic tail length and sequence affect the molecule's diffusion in the membrane.

Lessons in détente or know thy host: the immunomodulatory gene products of myxoma virus.

The poxvirus, myxoma virus, encodes within its genome at least eleven different proteins that compromise, skew, or disable the innate and adaptive responses of its hosts. In the laboratory rabbit, Oryctolagus cuniculus, these effects result in myxomatosis, a fatal condition characterized by skin lesions and systemic immunosuppression. Interestingly, while myxoma infection also causes skin lesions in its natural host and in natural populations of O. cuniculus in Australia where this novel host and the virus have co-evolved, the condition of myxomatosis does not ensue and infection is not fatal. In this review I discuss the biochemical properties of the characterized immunomodulatory proteins of myxoma virus, and their pathogenic effects in laboratory rabbits. Disruption of any one myxoma immunomodulatory gene diminishes the severity of the infection without compromising infectivity. Thus, the characterized immunomodulatory genes appear not to be required for a productive infection in vivo. The differences in the severity of their effects in laboratory-bred versus wild O. cuniculus suggest that the outcome of myxoma infection is a consequence of the interplay between the viral immunomodulatory gene products and the cells and molecules of the host immune system.

A pox on thee! Manipulation of the host immune system by myxoma virus and implications for viral-host co-adaptation.

The poxviruses have evolved a diverse array of proteins which serve to subvert innate and adaptive host responses that abort or at least limit viral infections. Myxoma virus and its rabbit host are considered to represent an ideal poxvirus-host system in which to study the effects of these immunomodulatory proteins. Studies of laboratory rabbits (Oryctolagus cuniculus) infected with gene knockout variants of myxoma virus have provided compelling evidence that several myxoma virus gene products contribute to the pathogenic condition known as myxomatosis. However, myxomatosis, which is characterized by skin lesions, systemic immunosuppression, and a high mortality rate, does not occur in the virus' natural South American host, Sylvilogus brasiliensis. Moreover, in Australia where myxoma virus was willfully introduced to control populations of O. cuniculus, myxomatosis-resistant rabbits emerged within a year of myxoma virus introduction into the field. In this review I discuss the characterized immunomodulatory proteins of myxoma virus, their biochemical properties, their pathogenic effects in laboratory rabbits, the role of the host immune system in the susceptibility or resistance to myxomatosis, and the evidence that immunomodulatory genes may have been attenuated during the co-adaptation of myxoma virus and O. cuniculus in Australia.