IL-12 is required for differentiation of pathogenic CD8+ T cell effectors that cause myocarditis.

Cardiac antigen-specific CD8(+) T cells are involved in the autoimmune component of human myocarditis. Here, we studied the differentiation and migration of pathogenic CD8(+) T cell effector cells in a new mouse model of autoimmune myocarditis. A transgenic mouse line was derived that expresses cardiac myocyte restricted membrane-bound ovalbumin (CMy-mOva).

Beta-galactoside alpha2,3-sialyltransferase-I gene expression during Th2 but not Th1 differentiation: implications for core2-glycan formation on cell surface proteins.

Biosynthesis of core2 O-glycans on T cell surface glycoproteins is essential for their interactions with selectins expressed by activated endothelium, and may also regulate susceptibility to apoptosis. Beta-galactoside alpha2,3-sialyltransferase-I (ST3Gal-I) is a major inhibitor of core2 O-glycan formation on CD43 and CD45 in naive T cells. Here we show that ST3Gal-I mRNA is extensively expressed during Th2, but not Th1 differentiation.

Tob is a negative regulator of activation that is expressed in anergic and quiescent T cells.

During a search for genes that maintain T cell quiescence, we determined that Tob, a member of an anti-proliferative gene family, was highly expressed in anergic T cell clones. Tob was also expressed in unstimulated peripheral blood T lymphocytes and down-regulated during activation. Forced expression of Tob inhibited T cell proliferation and transcription of cytokines and cyclins.

CD8+ T cell subsets TC1 and TC2 cause different histopathologic forms of murine cardiac allograft rejection.

Background: CD4+ T cell effector function is sufficient to mediate allograft rejection, and it is suggested that CD8+ T cell-mediated effects are dependent on CD4+ T cell help. CD8+ T cells can be classified into at least two functional subsets: Tc1, producing high amounts of interferon (IFN)-gamma and Tc2, producing interleukin (IL)-4, -5, -10, and -13 and low levels of IFN-gamma. Because these subsets express different chemokine receptors, they may have different capabilities of migrating into grafts.

Do urinary tract infections trigger chronic kidney transplant rejection in man?

Purpose: Urinary tract infections are frequent after kidney transplantation but little is known about the impact on long-term survival. As chronic rejection is the major cause of graft loss in the long term, we retrospectively analyzed the role of urinary tract infections in this process.

Materials And Methods: We included in the study all adult patients who received kidney transplants at our unit between 1972 and 1991, which ensured followup of at least 5 years, and we focused on the relationship between urinary tract infections and the incidence of chronic rejection episodes.