תרומתי לרפואה

נוגדנים כנגד אנטיגנים שונים

 

עבודות מחקר בנושא נוגדנים לאנטיגנים שונים, ניתן למצוא ברשימת המאמרים המלאה, במאמרים הבאים:    12, 14, 26, 36, 47, 64, 116, 118, 142, 163, 165, 218, 423, 500, 509, 520,   (לרשימת המאמרים המלאה). להלן, מובאים תקצירים של 5 מאמרים נבחרים:

 

1.  Clin Immunol Immunopathol. 1988 Aug;48(2):119-31.
Antibodies against acetylcholinesterase and low levels of cholinesterases in a patient with an atypical neuromuscular disorder.
Livneh A, Sarova I, Michaeli D, Pras M, Wagner K, Zakut H, Soreq H.

 

Abstract
Antibodies against acetylcholinesterase were found in the serum of a patient presenting dyspnea, generalized muscle paresis, diminished tendon reflexes, and fasciculations. Electrodiagnostic studies showed a decremental response, an incomplete interference pattern, and reduced motor nerve conduction velocity. Edrophonium administration resulted in extreme cholinergic crisis. Biopsies displayed muscle atrophy and nervous tissue degeneration. Recurrent acute respiratory failure ended in death. The patient's serum pseudocholinesterase and red blood cells acetylcholinesterase levels were generally very low, with periodical fluctuations. Minute quantities of the patient's serum inhibited the activity of cholinesterases from normal human serum and from various fetal tissues. Enzyme inhibition was abolished following preadsorption of the serum immunoglobulins with goat antihuman Fab, and radioiodinated acetylcholinesterase from human erythrocytes was precipitated by the patient's serum, confirming that anticholinesterase antibodies were present. Acetylcholinesterase extracted from fetal striated muscle with detergent and salt was inhibited to a larger extent than the enzymes similarly prepared from other fetal tissues and more efficiently than buffer-soluble muscle enzyme. These findings suggest that the patient's serum contained antibodies which interacted preferentially with the membrane-associated forms of muscle acetylcholinesterase and indicate that autoantibodies against acetylcholinesterase could play a role in the pathogenesis of the disease.

 

2. Immunol Lett. 1997 Feb;55(2):79-84.
Clinically insignificant (natural) autoantibodies against acetyl cholinesterase in the sera of patients with a variety of neurologic, muscular and autoimmune diseases.
Lidar T, Christian A, Yakar S, Langevitz P, Zeilig G, Ohry A, Bakimer R, Sorek H, Livneh A.

 

Abstract
Acetyl cholinesterase (AChE) antibodies were shown to be associated with myasthenia-like neuromuscular disease. However, it is not clear whether they cause the disease, or their presence is secondary to the disease or an unrelated epiphenomenon. Therefore, AChE antibodies were studied in the sera of 135 patients with neurologic, muscular and autoimmune diseases, using enzyme linked immunosorbent assay (ELISA), immunoblotting and enzyme inhibition assay. In 12 sera the AChE binding by ELISA was greater than 2 standard deviations (SDs) above the mean value of the 20 healthy controls. However, this increased binding was not disease-specific, had no clinical correlates and could not be demonstrated using Western blotting and AChE enzyme inhibition assay, suggesting that these antibodies are naturally occurring, pathogenically unimportant autoantibodies. The finding also supports a possible pathogenic role for the previously reported, high titer, high affinity, inhibitory AChE antibodies in the neuromuscular disease.

 

3. Isr J Med Sci. 1997 Jan;33(1):30-5.
Lymphocytotoxic antibodies in Israeli patients with rheumatoid arthritis.
Livneh A, Renert A, Avishai O, Langevitz P, Gazit E.

 

Abstract
The presence, antigenic specificity, and clinical role of lymphocytotoxic antibodies (LCAs) were studied in 72 Israeli patients with rheumatoid arthritis (RA). Using the microlymphocytotoxicity assay on a cell panel of 47 donors, LCAs were found in 55% of the 72 RA sera, each displaying a distinct pattern of anti-lymphocytic reactivity, mostly against B lymphocytes. Human lymphocytic antigens (HLA) analysis of donors' lymphocytes suggested that activity of LCA-positive RA sera is HLA directed in 60% of cytotoxic sera. The anti-HLA antibodies found were not autoreactive and were not restricted to a particular class I or class II antigen. Relating the presence of LCAs to selective clinical features revealed that LCAs are inversely associated with the presence of an erosive disease (P <0.01) and with the patients' HLA-DQw1 (P <0.01). These findings suggest that LCAs in Israeli patients with RA are very common, multispecific and may have a protective role not mediated through interaction with self-HLA antigens.

 

4. Lupus. 2001;10(2):81-6.
Anti-insulin antibodies and the natural autoimmune response in systemic lupus erythematosus.
Lidar M1, Braf A, Givol N, Langevitz P, Pauzner R, Many A, Livneh A.

 

Abstract
Systemic lupus erythematosus (SLE) is characterized by the finding of ample serum autoantibodies. The role and the origin of many of these antibodies are still obscure. The aim of this work was to study the occurrence of anti-insulin antibodies (AIA) in SLE, and to postulate, based on AIA determination, on the mechanisms involved in the production of some autoantibodies in SLE. IgG and lgM AIA, anti-DNA antibodies (ADA) and anti-tetanus toxoid antibodies (ATA) were determined using ELISA in sera and B-lymphocytes culture media of 24 SLE patients, 10 healthy controls and 19 insulin-dependent diabetes mellitus (IDDM) patients. B- and T-lymphocytes were isolated using Ficoll gradient, depleted of T-cells using cyclosporin A, EBV infected and grown in medium. The frequencies of IgM-AIA and IgG-ADA were higher in SLE patients than in healthy controls (P < 0.02 and P < 0.05, respectively). The rate of IgM-AIA in SLE and IDDM was comparable, while IgG-AIA was significantly less common in SLE than in IDDM (P < 0.05). The prevalence of ATA in SLE patients and healthy controls was similar. These findings increase the spectrum of the humoral autoimmune response in SLE and suggest that part of it (natural autoantibodies) is independent of antigen driven response.

 

5. Immunology. 2010 Jul;130(3):337-43. 
An antibody profile of systemic lupus erythematosus detected by antigen microarray.
Fattal I, Shental N, Mevorach D, Anaya JM, Livneh A, Langevitz P, Zandman-Goddard G, Pauzner R, Lerner M, Blank M, Hincapie ME, Gafter U, Naparstek Y, Shoenfeld Y, Domany E, Cohen IR.

 

Summary 
Patients with systemic lupus erythematosus (SLE) produce antibodies to many different self-antigens. Here, we investigated antibodies in SLE sera using an antigen microarray containing many hundreds of antigens, mostly self-antigens. The aim was to detect sets of antibody reactivities characteristic of SLE patients in each of various clinical states--SLE patients with acute lupus nephritis, SLE patients in renal remission, and SLE patients who had never had renal involvement. The analysis produced two novel findings: (i) an SLE antibody profile persists independently of disease activity and despite long-term clinical remission, and (ii) this SLE antibody profile includes increases in four specific immunoglobulin G (IgG) reactivities to double-stranded DNA (dsDNA), single-stranded DNA (ssDNA), Epstein-Barr virus (EBV) and hyaluronic acid; the profile also includes decreases in specific IgM reactivities to myeloperoxidase (MPO), CD99, collagen III, insulin-like growth factor binding protein 1 (IGFBP1) and cardiolipin. The reactivities together showed high sensitivity (> 93%) and high specificity for SLE (> 88%). A healthy control subject who had the SLE antibody profile was later found to develop clinical SLE. The present study did not detect antibody reactivities that differentiated among the various subgroups of SLE subjects with statistical significance. Thus, SLE is characterized by an enduring antibody profile irrespective of clinical state. The association of SLE with decreased IgM natural autoantibodies suggests that these autoantibodies might enhance resistance to SLE.

​הסבר לחולים

 

התוכן בבניה...

03-6224040