The origins of the enigmatic Falkland Islands wolf.

The origins of the extinct Falkland Islands wolf (FIW), Dusicyon australis, have remained a mystery since it was first recorded by Europeans in the seventeenth century. It is the only terrestrial mammal on the Falkland Islands (also known as the Malvinas Islands), which lie ~460 km from Argentina, leading to suggestions of either human-mediated transport or overwater dispersal. Previous studies used ancient DNA from museum specimens to suggest that the FIW diverged from its closest living relative, the South American maned wolf (Chrysocyon brachyurus) around 7 Ma, and colonized the islands ~330 ka by unknown means.

Polyspecific self-reactive antibodies in individuals infected with human immunodeficiency virus facilitate T cell deletion and inhibit costimulatory accessory cell function.

Self-reactive polyspecific IgG antibodies (PSAs) arise in human immunodeficiency virus (HIV)-seropositive subjects before they develop AIDS. Self-reactive PSA levels correlate with the destruction of CD8 T cells in HIV-infected individuals and mediate the antibody-dependent cellular toxicity-based destruction of human T cells in tissue culture. PSAs react across the species barrier and bind to T cell antigens in mice.

MHC class I molecules on CD4 T cells regulate receptor-mediated activation signals.

Three T cell populations can be distinguished based on their response to antigen receptor engagement. A sizable fraction dies within hours of TCR ligation, a smaller fraction enters the mitotic cycle, and the remaining T cells merely upregulate the expression of certain cell surface markers. An MHC-I-controlled regulatory mechanism has been identified.

Elevated major histocompatibility complex class I expression protects T cells from antibody- and macrophage-mediated deletion.

Macrophages are capable of destroying T cells with which they form cellular conjugates. The deletion can be prevented by the simultaneous transmission of costimulatory signals. We show here that T cells with elevated major histocompatibility complex (MHC) class I expression are resistant against macrophage-mediated cytotoxicity.

Staphylococcal enterotoxin B-induced T-cell anergy is mediated by regulatory T cells.

Naive T cells mount a vigorous proliferative response to superantigen (SAg) stimulation in vivo. The proliferative response is followed by a partial deletion of responder T cells. Part of the deletion process has recently been attributed to the action of regulatory cytotoxic T cells that recognize major histocompatibility complex (MHC) class I-associated antigen receptor determinants on the target cell surface.

Macrophages may activate or destroy T cells with which they form antigen- or coreceptor-mediated cellular conjugates.

The formation of antigen- or mitogen-mediated cellular conjugates with T cells enables macrophages to trigger in T cells costimulatory signals and to facilitate T cell clonal expansion and differentiation. The present study describes T cell death as an alternative consequence of T cell interaction with macrophages. Macrophages initiate the deletion of T cells which they target for conjugate formation through CD4 coreceptors.

Evidence for progenitors of chronic lymphocytic leukemia B cells that undergo intraclonal differentiation and diversification.

Peripheral blood mononuclear cells from five patients with IgG+ B-type chronic lymphocytic leukemia (B-CLL) were analyzed for the presence of clone-specific Ig H chain variable region gene mRNA transcripts linked to C mu and/or C alpha. This was assessed by (1) comparing the lengths of portions of the VHDJH of the IgG+ CLL clones with those of the mu and alpha isotype-expressing B cells, (2) performing clone-specific endonuclease digestion studies, and (3) determining the DNA sequences of the mu and alpha isotype-expressing cDNA. Thus, when B-cell mRNA from these five patients were reverse transcribed with C gamma-specific primers and then amplified by polymerase chain reaction, dominant cDNA were found with lengths corresponding to those of the IgG+ CLL B cell.

X chromosome inactivation patterns correlate with fetal-placental anatomy in monozygotic twin pairs: implications for immune relatedness and concordance for autoimmunity.

Background: Monozygotic (MZ) twinning is a poorly understood phenomenon that may result in subtle biologic differences between twins, despite their identical inheritance. These differences may in part account for discordant expression of disease in MZ twin pairs. Due to their stochastic nature, differences in X chromosome inactivation patterns are one source of such variation in female MZ twins.

What is the significance of the presence of MHC molecules on the surface of parasites in human neurocysticercosis?

Sixteen cysticerci excised from 15 surgery patients were examined for the presence of HLA molecules on their surface, to confirm the role of these molecules in parasite damage and to investigate if HLA products are host specific or perhaps host-like antigens synthesized by the parasite. MoAbs against monomorphic and polymorphic HLA were chosen according to the patients HLA phenotypes. MoAbs against host and non-host antigens were selected and tested on cyst slides by indirect immunofluorescence assays.