Spondylodiscitis and infective endocarditis: case studies and review of the literature.

STUDY DESIGN: This study evaluated the association between infective endocarditis and infective spondylodiscitis and its clinical features. OBJECTIVES: To report case studies of patients with spondylodiscitis complicating infective endocarditis. SUMMARY OF BACKGROUND DATA: Early diagnosis of infective endocarditis as the source of the spondylodiscitis is often difficult because clinical and radiologic patterns are similar to those present in spondylodiscitis alone. METHODS: The case records of the patients with infective endocarditis admitted to our Department from 1991-1998 were reviewed. The diagnosis of spondylodiscitis was made on the basis of clinical features and of typical radiologic signs. RESULTS: Among 30 patients affected by infective endocarditis, three also were affected by spondylodiscitis. All patients fully recovered after appropriate antibiotic therapy. CONCLUSIONS: In all patients with spondylodiscitis, infective endocarditis should be excluded, particularly in patients with a history of heart valve disease.

Autoimmune T-cell response to the CD4 molecule in HIV-infected patients.

In a previous study, we demonstrated that by downregulating plasma membrane CD4 and increasing its processing, human immunodeficiency (HIV)-1-gp120 unveils hidden CD4 epitopes, inducing an in vitro anti-CD4-specific T-cell response. We report herein that this mechanism may potentially have important implications in HIV immunopathogenesis, because it could take part in the severe depletion of CD4+ cells that characterizes acquired immune deficiency syndrome (AIDS) and be related to disease progression. Freshly isolated peripheral blood lymphocytes (PBMC) from about 1/4 of a conspicuous cohort of HIV-infected patients responded to CD4 and this response was correlated with beta2-microglobulin levels, widely recognized as marker for progression of HIV infection. Moreover, we provide evidence that a CD4-specific T cell priming can occur in vivo, following a gp120 or anti-CD4 monoclonal antibody (mAb)-mediated CD4 molecule downregulation on antigen-presenting cells (APC). To our knowledge, this is the first study indicating that an autoimmune T-cell response is linked to HIV infection and that it could have an important impact on the immunopathogenesis of this disease.

HIVgp120 activates autoreactive CD4-specific T cell responses by unveiling of hidden CD4 peptides during processing.

T cells are made tolerant only to those self-peptides that are presented in sufficient amounts by antigen-presenting cells. They ignore cryptic self-determinants, such as either those not generated by processing machinery or generated in insufficient amounts. It is anticipated that mechanisms that either change antigen processing or increase the yield of previously "invisible" peptides may be capable of inducing T cell priming and, if they are self-maintained, may sustain autoimmune diseases. Herein, we demonstrate for the first time a mechanism by which the gp120 human immunodeficiency virus-I, by downregulating plasma membrane CD4 and increasing its processing, unveils hidden CD4 epitopes, inducing an autoimmune-specific T cell response.