An allometric approach to quantify the extinction vulnerability of birds and mammals.

Methods to quantify the vulnerability of species to extinction are typically limited by the availability of species-specific input data pertaining to life-history characteristics and population dynamics. This lack of data hampers global biodiversity assessments and conservation planning. Here, we developed a new framework that systematically quantifies extinction risk based on allometric relationships between various wildlife demographic parameters and body size. These allometric relationships have a solid theoretical and ecological foundation. Extinction risk indicators included are (1) the probability of extinction, (2) the mean time to extinction, and (3) the critical patch size. We applied our framework to assess the global extinction vulnerability of terrestrial carnivorous and non-carnivorous birds and mammals. Irrespective of the indicator used, large-bodied species were found to be more vulnerable to extinction than their smaller counterparts. The patterns with body size were confirmed for all species groups by a comparison with IUCN data on the proportion of extant threatened species: the models correctly predicted a multimodal distribution with body size for carnivorous birds and a monotonic distribution for mammals and non-carnivorous birds. Carnivorous mammals were found to have higher extinction risks than non-carnivores, while birds were more prone to extinction than mammals. These results are explained by the allometric relationships, predicting the vulnerable species groups to have lower intrinsic population growth rates, smaller population sizes, lower carrying capacities, or larger dispersal distances, which, in turn, increase the importance of losses due to environmental stochastic effects and dispersal activities. Our study is the first to integrate population viability analysis and allometry into a novel, process-based framework that is able to quantify extinction risk of a large number of species without requiring data-intensive, species-specific information. The framework facilitates the estimation of extinction vulnerabilities of data-deficient species. It may be applied to forecast extinction vulnerability in response to a changing environment, by incorporating quantitative relationships between wildlife demographic parameters and environmental drivers like habitat alteration, climate change, or hunting.

Glomerulopathy induced by graft-versus-host reaction in the rat. Requirement of donor CD4+ T lymphocytes and MHC class II incompatibility at the lymphoid compartment.

Graft-versus-host reactions (GVHR) can be associated with several autoimmune phenomena involving the kidney as a target organ. By transferring lymphocytes of AO rats into complete Freund's adjuvant-pretreated (AO x BN)F1 hybrids, a dose-dependent GVHR with glomerulopathy was experimentally induced. IgM, IgG1, and IgG2a were deposited in the mesangial area and along the glomerular basement membrane. Eluted immunoglobulins from diseased kidneys bound to normal basement membranes and especially to laminin. Anti-laminin reactivity was also present in sera from F1 recipients with GVHR. Parental CD4+ T lymphocytes were required and sufficient to induce GVHR and glomerulopathy in sublethally irradiated F1 hybrids. Using various F1 hybrids, MHC class II incompatibility was shown to be required for the induction of GVHR-associated glomerulopathy. Across MHC class I incompatibility, GVHR without glomerulopathy could be induced, provided that both CD4+ and CD8+ donor T lymphocytes were administered. Finally, MHC incompatibility between donor T lymphocytes and the recipient non-lymphoid compartment was found to be sufficient for the induction of GVHR, but not for GVHR-associated glomerulopathy. The results indicate that alloreactive donor CD4+ T lymphocytes have to interact directly with MHC class II alloantigen bearing host B lymphocytes in order to stimulate the latter to produce (auto-)antibodies. GVHR-induced glomerulopathy shares several immunopathological features with HgCl2-induced autoimmune glomerulopathy in the rat.

Thymus localization of monoclonal antibodies circumventing the blood-thymus barrier.

The binding in the rat thymus of mouse monoclonal antibodies which recognize determinants present on class II major histocompatibility complex antigens (HIS 19) and all T cells (HIS 17) was studied at several intervals after in vivo injection of a single dose (8 mg) of the monoclonal antibodies (MoAb). The MoAb, injected either intravenously or intraperitoneally, penetrated the thymus initially across the thymic capsule from the extravascular space. The extent to which the MoAb penetrated both cortex and medulla correlated with serum presence of the monoclonal antibody. These results suggest that the thymus cortex and medulla are permeable to MoAb present in the extravascular compartment. If this situation is a general phenomenon, which applies to circulating self non-major histocompatibility complex antigens under physiological conditions, the current dogma relating to self-tolerance needs to be reviewed.