PubMed Health⌕ Search

Biomedical subjects

H Lassmann

Publications and source records attributed to H Lassmann.

295 records · Page 17Linked to original sources
PubMedDate not supplied

APP peptides stimulate lymphocyte proliferation in normals, but not in patients with Alzheimer's disease.

We hypothesized that metabolic products of the Alzheimer beta amyloid precursor protein (APP) might be targets for cells of the immune system. To test this hypothesis, peripheral blood lymphocytes from young and old healthy blood donors and patients with Alzheimer's disease were analysed for their responsiveness upon stimulation with amyloid beta protein as well as with four other synthetic peptides corresponding to parts of the APP sequence. Stimulation of resting blood lymphocytes from young and old healthy blood donors resulted in IL-2 receptor expression and proliferation in both age groups. In contrast, lymphocytes from the majority of patients with Alzheimer's disease did not proliferate, when stimulated with APP peptides, while their proliferative response to anti-CD3 was unimpaired. This lack of proliferative responsiveness to APP peptides was not due to apoptosis, but could reflect T cell anergy, as it was accompanied by unimpaired IL-2 receptor expression. The results suggest that autoreactive lymphocytes with specificity for metabolic products of APP occur in healthy individuals. These cells may be of relevance for the elimination of potentially amyloidogenic substances. This mechanism could be impaired in patients with Alzheimer's disease.

Adolescent↗
PubMedDate not supplied

A shared antigenic determinant between natural killer cells and nervous tissue.

Considerable evidence for shared antigenic determinants between nervous elements and lymphocytes has accumulated. It has also been suggested that this cross-recognition may be involved in the pathogenesis of human neurological diseases such as myasthenia gravis and multiple sclerosis. We report here evidence that a marker for natural killer (NK) cells, anti-Leu-7 (HNK-1), specifically binds to components of human and rodent central nervous tissue as well as peripheral nervous tissue, especially to myelin sheaths. In contrast, another NK-cell marker (VEP13) did not react with nervous tissue. Since NK-cell function is impaired in a population of multiple sclerosis patients, the observed cross-reactivity indicates that autosensitization against myelin may simultaneously cause a defect of NK-cell function. Furthermore, the shared antigenic determinant may help to identify a hitherto undefined nervous tissue antigen and simultaneously increase the knowledge about the nature of NK-cell antigens.

Animals↗
PubMedDate not supplied

The development of periventricular lesions in chronic relapsing experimental allergic encephalomyelitis in guinea-pigs: a light and scanning electron microscopic study.

Periventricular lesions in the centrum semiovale are the most frequent changes in the brain in chronic relapsing experimental encephalomyelitis in guinea-pigs. They are generally distributed symmetrically at the lateral angle of the ventricular wall. The number of lesions and their size increases in anterior-posterior direction. Typically periventricular lesions in the later chronic stages are similar to those in multiple sclerosis. Earlier lesions generally originate in the depth of the white matter and secondarily, by extension, reach the ventricular surface. Lesions developing at later stages after sensitization may also originate from the ventricular wall and extent into the centrum semiovale. In these latter, severe structural changes in the ventricular ependyma may generally be found. Increased intracranial pressure in these animals may be one of the possible mechanisms leading to the peculiar topographical distribution of the periventriuclar lesions.

Animals↗
PubMedDate not supplied

Antisera against ganglioside GM2: immunochemical and immunohistological studies.

Antisera against ganglioside GM2 were raised in rabbits and tested by immunodiffusion, complement fixation and immunohistology. The presence of precipitating antibodies was demonstrated by immunodiffusion techniques (Ouchterlony and reversed Mancini). GM2-antibody titres were determined by a quantitative microcomplement fixation assay. The GM2-antibodies were shown to be specifically directed against GM2 and did not cross-react with the major brain gangliosides. Application of GM2-antiserum to brain sections from a case of GM2-gangliosidosis (Sandhoff's disease) in an immunofluorescence study produced a specific fluorescence of the granular GM2-storage material within the cytoplasm of cortical neurons. With immunoperoxidase staining by electron microscopy, labelling of the surface of the membraneous cytoplasmic bodies was obtained.

Brain↗
PubMedDate not supplied

Dynamics of IgG+, IgA+, and IgM+ plasma cells in the central nervous system of guinea pigs with chronic relapsing experimental allergic encephalomyelitis.

IgG+, IgA+, and IgM+ plasma cells (PC) were investigated by quantitative immunocytochemistry in the central nervous system (CNS) of guinea pigs with chronic relapsing experimental allergic encephalomyelitis (crEAE) and in the CNS of controls. Frequencies of Ig+ PC in crEAE were, on average, 30-130 times higher than in controls. At all stages of crEAE, IgG was the dominant isotype of CNS PC. In the course of crEAE there was an increase in the proportion of IgG+ PC and a decrease in the proportions of IgM+ and, to a lesser extent, of IgA+ PC. Accumulation of IgM+ PC appears to be related to the acuteness of the disease. Our studies also indicate that IgA, in addition to IgG and IgM, is involved in the immunological response of crEAE in the CNS, and demonstrate that the time course of crEAE is characterized by isotype-specific differences in the immune responses of IgG+, IgM+, and IgA+ PC in the CNS.

Animals↗
PubMedDate not supplied

[Pathology of the cytoskeleton in Alzheimer's disease and disorders related to this disease].

The reported findings suggest that ubiquitination of pathological proteinaceous intracytoplasmic inclusions is not at all specific of AD. On the contrary it appears to be a general biochemical marker for disorders in the degradation of a variety of cytoskeletal and other cytoplasmic proteins. The pattern of affected cytoskeletal components is not specific of AD/SDAT tangles. Tau definitely is present also in PSP tangles and possibly in Pick bodies but not in Lewy bodies. Furthermore, reactivity to tau, although not associated with ubiquitin but with Actin has been described in Hirano bodies. Therefore it has to be considered that the intracytoplasmic accumulation of cytoskeletal protein/ubiquitin complexes in itself is a rather unspecific cellular reaction pattern, possibly a secondary reaction to cell injury of any type especially, however, of neuronal aging. Nevertheless, the manifestation of NFT in an excessive quantity, intensity, and dynamics with severe concomitant lesions as in AD/SDAT undoubtedly is a true pathological and in this sense a disease-specific change.

Aged↗