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1.
Spine (Phila Pa 1976) ; 26(5): 499-500, 2001 Mar 01.
Article in English | MEDLINE | ID: mdl-11242377

ABSTRACT

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.


Subject(s)
Cervical Vertebrae , Discitis/etiology , Endocarditis, Bacterial/complications , Adult , Aged , Anti-Bacterial Agents , Aortic Valve/surgery , Cervical Vertebrae/diagnostic imaging , Cervical Vertebrae/pathology , Discitis/diagnosis , Discitis/drug therapy , Drug Therapy, Combination/therapeutic use , Echocardiography, Transesophageal , Endocarditis, Bacterial/diagnosis , Endocarditis, Bacterial/drug therapy , Endocarditis, Bacterial/surgery , Humans , Magnetic Resonance Imaging , Male , Middle Aged , Mitral Valve/surgery , Radiography , Streptococcal Infections/complications , Streptococcal Infections/diagnosis , Streptococcal Infections/therapy , Streptococcus/isolation & purification
2.
Viral Immunol ; 11(1): 9-17, 1998.
Article in English | MEDLINE | ID: mdl-9586693

ABSTRACT

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.


Subject(s)
Autoimmunity , CD4 Antigens/immunology , CD4-Positive T-Lymphocytes/immunology , HIV Infections/immunology , Adult , Antibodies, Monoclonal/immunology , Antigen-Presenting Cells/immunology , Autoantibodies/immunology , Down-Regulation , Female , HIV Envelope Protein gp120/immunology , Histocompatibility Antigens Class II/immunology , Humans , Leukocytes, Mononuclear/immunology , Lymphocyte Activation , Male , Middle Aged , Tetanus Toxoid/immunology , Tuberculin/immunology
3.
J Exp Med ; 181(6): 2253-7, 1995 Jun 01.
Article in English | MEDLINE | ID: mdl-7760011

ABSTRACT

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.


Subject(s)
Antigens, CD/immunology , CD4 Antigens/chemistry , CD4 Antigens/immunology , HIV Envelope Protein gp120/pharmacology , Lymphocyte Activation/drug effects , T-Lymphocytes/immunology , Amino Acid Sequence , Animals , Antigen-Presenting Cells/immunology , Antigens, CD/chemistry , Antigens, CD/drug effects , B-Lymphocytes/immunology , CD4 Antigens/drug effects , CHO Cells , Clone Cells , Cricetinae , Humans , Molecular Sequence Data , Recombinant Proteins/drug effects , Recombinant Proteins/immunology , T-Lymphocytes/drug effects , Transfection
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