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Biomedical subjects

A Wetterwald

Publications and source records attributed to A Wetterwald.

At least 19 recordsLinked to original sources
PubMed2002

Can the reverse transcriptase-polymerase chain reaction for prostate specific antigen and prostate specific membrane antigen improve staging and predict biochemical recurrence?

OBJECTIVE: To evaluate the perioperative gene-specific primed nested reverse transcription-polymerase chain reaction (RT-PCR) for prostate-specific antigen (PSA) and prostate-specific membrane antigen (PSMA) for staging patients undergoing radical prostatectomy and predicting biochemical recurrence. PATIENTS AND METHODS: In 80 consecutive patients undergoing radical prostatectomy for prostate cancer, blood samples were drawn before, during and 1 and 7 days after removing the prostate. After buffy coat and mRNA extraction, gene-specific primed nested RT-PCR was performed for PSA, PSMA and glyceraldehyde-3-phosphate dehydrogenase mRNA, and Southern blot analysis of the PCR reaction. RESULTS: The sensitivity of gene-specific RT-PCR to detect tumour cells was comparable with random primed RT-PCR. In the 80 patients the stage distribution was pT1 in two (2.5%), pT2 in 30 (37.5%) and > or = pT3 in 48 (60%); the nodal status was pN0 in 57 (71%), pN1 in 11 (14%) and pN2 in 12 (15%). The gene-specific RT-PCR reaction for PSA and PSMA was positive in no patients with pT1, 11 (37%) with pT2 and 23 (48%) with stage > or = pT3 disease. The result for PSA was positive in 12 (52%) and for PSMA in 11 (48%) of those with positive nodal status. Neither gene-specific RT-PCR for PSA or PSMA was able to predict organ-confined disease (P > 0.5). After a median (range) follow-up of 37 (11-67) months a biochemical recurrence was predicted in 65% of patients by preoperative RT-PCR for both PSA and PSMA, with a sensitivity, specificity, positive and negative predictive value of 58%, 80%, 87% and 47%, respectively; the assay after surgery predicted a recurrence in 73%, with respective values of 68%, 84%, 84% and 57%. CONCLUSIONS: Gene-specific primed nested RT-PCR for PSA and PSMA is a sensitive and simple assay; it might add substantial information for tumour staging in individual patients. RT-PCR before surgery allows the prediction of recurrence in 65% of cases and after surgery in 73%.

Blotting, Southern↗
PubMed1997

Role of CSF-1 in bone and bone marrow development.

There is a close interaction between the processes involved in osteogenesis and hemopoiesis. In developing bone, the osteoclasts, cells of hemopoietic origin, resorb and invade the calcified cartilage rudiment. As a result, the primitive marrow cavity is formed and hemopoiesis initiates. Osteogenic cells-osteoblasts and osteocytes-control the development and activity of the osteoclasts through the local release of factors. One factor responsible for this osteoblast-osteoclast interaction is colony-stimulating factor-1 (CSF-1). Studies performed on the osteopetrotic op/op mouse mutant have established that this factor is essential for proliferation and differentiation of the osteoclasts. Expression of CSF-1 receptors by mature osteoclasts and osteoclast precursors strongly suggests that CSF-1 action is exerted directly on cells of this lineage. In vivo, CSF-1 synthesis by osteoblasts is temporally and spatially related to sites of osteoclast development. Thus CSF-1 may represent one of the factors responsible for coupling hemopoiesis to osteogenesis. In vitro, osteoblasts express at least 4 transcripts encoding either a secreted or a membrane-bound form of CSF-1. At the protein level, osteoblasts in vitro synthesize the membrane-bound form and secrete the majority of CSF-1 as a proteoglycan, a small fraction of which is integrated into the matrix. These different molecular forms may locally restrict the biological action of this cytokine. Indeed, injection of recombinant human CSF-1 in op/ op mutants does not correct the osteoclast deficiency in the metaphyseal spongiosa of long bones, and sclerosis persists at this site. Similarly, the deficiency of some tissue macrophage populations in op/op mice is only partially or not at all corrected by injection of CSF-1. The expression of CSF-1 receptors by mature osteoclasts may imply that CSF-1 also influences their bone resorbing activity. Indeed, CSF-1 has been shown to induce osteoclast fusion, spreading, and survival. These findings suggest that CSF-1 is essential for the proliferation, differentiation, activity, and survival of tissue macrophages and osteoclasts, cells involved in tissue turnover. Furthermore, they corroborate the view that both osteoclasts and tissue macrophages stem from a CSF-1-dependent common precursor along the macrophage lineage.

Animals↗
PubMed1996

Synthesis of membrane- and matrix-bound colony-stimulating factor-1 by cultured osteoblasts.

Colony-stimulating factor-1 (CSF-1) is synthesized as a secreted or membrane-bound molecule. We investigated whether osteoblastic cells produce these forms of CSF-1. Glutaraldehyde-fixed cell layers supported proliferation of the macrophage cell line BAC1.2F5, suggesting the presence of membrane- or/and matrix-associated CSF-1. Furthermore, CSF-1 activity could be either extracted from the matrix or released from the cell membrane. A neutralizing antiserum against CSF-1 inhibited these activities. After labeling the cellular proteins with [35S] met/cys or [35S] SO4(2-), CSF-1 was immunoprecipitated and analyzed by SDS-PAGE. Under nonreducing conditions, bands with MW more than 200, 200, 100, and 50 kd were detected. These bands shifted to lower MW under reducing conditions. Treatment with chondroitin lyase ABC decreased the MW of the 200 kd monomer, proving the proteoglycan structure. Much smaller quantities of CSF-1 were found in the matrix extract than in the conditioned medium. Transforming growth factor beta (TGF-beta) increased both the synthesis of CSF-1 and its accumulation in the matrix. CSF-1 released with trypsin from the membrane fraction yielded on SDS-PAGE a band with MW of 60 and 30 kd under nonreducing and reducing conditions, respectively. Transcripts encoding both the secreted and the membrane-associated forms of the cytokine were detected in osteoblasts by reverse transcription polymerase chain reaction. These data indicate that osteoblastic cells produce the secreted forms, either remaining in the culture supernatant, or being associated to the matrix, and the membrane associated form of CSF-1.

Animals↗
PubMed1996

Characterization and cloning of the E11 antigen, a marker expressed by rat osteoblasts and osteocytes.

A new marker for cells of the osteoblastic lineage was identified by raising monoclonal antibodies against an immortalized rat osteoblastic cell line. Among the different antibodies one was selected which, on tissue sections, strongly reacts with osteoblasts, preosteocytes, and osteocytes. This antibody, designated E11, recognizes an antigen localized at the cell surface. The cDNA encoding the E11 antigen was cloned from a cDNA library prepared from ROS 17/2.8 cells, using a eukaryotic expression system. The E11 cDNA sequence revealed homology with the murine OTS-8/gp38 sequence. In situ hybridization confirmed that E11 mRNA expression in bone is restricted to osteoblasts and osteocytes. The tissue specificity of the E11 expression was studied by immunohistochemistry and Northern blot analysis. Apart from bone, E11-positive cells were also found in lung: namely, the alveolar cells of type I. Epithelial cells of the choroid plexus and endothelial cells of lymphatic vessels were also labeled with mAb E11. These results were confirmed by Northern blot, as the 1.8 kb E11 mRNA transcript was detected in bone and also in lung, brain, and skin. In conclusion, we describe a novel osteoblastic product which is expressed by mature osteoblasts and newly formed osteocytes.

Adenylyl Cyclases↗
PubMed1996

Expression of matrix proteins during the development of mineralized tissues.

The specific properties of mineralized tissues are defined by the composition of the fraction of the noncollagenous matrix proteins. Because these proteins play a pivotal role in the processes of cell differentiation and activation and of mineralization, their temporal and spatial expression is tightly regulated. Within this study, the expression of the enamel protein amelogenin and of the bone matrix proteins osteopontin, bone sialoprotein, osteocalcin, and osteonectin was investigated by in situ hybridization. Two models that allow observation of the formation of mineralized tissues were chosen. The development of bone and cartilage was observed on murine metatarsals from 15-day-old embryos up to 1-day-old mice. This time covers the periods of initial bone formation as well as onset of resorption of mineralized cartilage and bone. To study gene expression in the mineralized tissues of the dental organ, enamel, dentin, and cementum, developing molars ranging in age from 16-day-old embryos to 14 days after delivery were chosen. Within this time frame, the molars develop from an immature state to the differentiated organ which erupts through the mandibular bone. In the developing metatarsals, osteopontin and bone sialoprotein mRNAs were detected in osteoblasts and hypertrophic chondrocytes at the onset of mineralization. In the tooth organ, only cementoblasts expressed transcripts encoding the two proteins; odontoblasts and ameloblasts did not express these genes. Osteonectin was expressed by osteoblasts and hypertrophic chondrocytes as well, whereas in the molars it was produced exclusively by odontoblasts. Osteocalcin was expressed specifically by osteoblasts in the developing metatarsals. In tooth, osteocalcin transcripts were detected in odontoblasts. Finally, amelogenin was a specific product of ameloblasts. Thus, a sequential and cell type-restricted expression of matrix proteins takes place during the development of the mineralized tissues. The expression patterns of the transcripts encoding the bone matrix proteins suggest different biological roles depending on the time and site of expression.

Amelogenin↗
PubMed1996

T1 alpha protein is developmentally regulated and expressed by alveolar type I cells, choroid plexus, and ciliary epithelia of adult rats.

T1 alpha is the first marker gene known to be expressed in the adult lung solely by the alveolar type I epithelial cell. Previous studies showed that T1 alpha transcripts are abundant in early rat embryos where they are found in the nervous system and in the foregut and certain of its derivatives including the primitive lung. By mid- to late gestation T1 alpha messenger RNA (mRNA) expression is lost from neural tissues but appears to increase in the lung throughout fetal life. To determine whether the T1 alpha transcripts are translated into protein, especially in early embryos which sometimes express transcripts that are translationally silent, we performed immunohistochemistry on embryos and fetal tissues and analyzed certain tissues by western blotting using a monoclonal antibody against T1 alpha protein. T1 alpha protein is present at all sites that have previously been shown to express the mRNA and at similar developmental stages. As estimated from western blots, T1 alpha protein abundance peaks at about fetal day 16 in the brain and decreases thereafter to a relative level in the adult that is lower than that of the neural tube of the day 13 embryo. Relative protein abundance in the lung is very low, although detectable, on embryonic day 13 but increases slowly until fetal day 20 when there is a dramatic increase. At the time of birth, restriction to the type I cell is not complete and therefore must occur during postnatal lung development. Immunostaining reveals additional sites of expression in fetal and adult rats that had not been clearly visualized in previous in situ hybridization studies. T1 alpha is present in mesonephric tubules and apparently in primitive germ cells but is not detectable in specific cells in the adult kidney, ovary, or testis. However, cells of the choroid plexus of the central nervous system and the ciliary epithelium of the eye express T1 alpha in both fetuses and adults. The well-known functions of these epithelia are to elaborate cerebrospinal fluid and aqueous humor respectively by processes of active ion transport and water fluxes, probably through the aquaporin 1 (channel-forming integral membrane protein [CHIP] 28). We speculate therefore that T1 alpha protein may modulate or participate in these types of cellular functions in the lung.

Age Factors↗
PubMed1995

Detection of transcripts and binding sites for colony-stimulating factor-1 during bone development.

Colony-stimulating factor-1 (CSF-1), originally characterized as the growth factor for the cells of the mononuclear phagocytic system, has been shown to be essential for osteoclast formation. The aim of the present study was twofold: (i) to investigate the expression of transcripts encoding CSF-1; and (ii) to detect binding sites for CSF-1 during bone development. As a model, metatarsal rudiments from embryonic mice of different ages were used, an in vivo system allowing one to follow osteoclast formation. In 16-day-old embryos, proliferating osteoclast precursors are located on the outer surface of the rudiments. They differentiate subsequently to post-mitotic precursors. At 18 days, the precursors fuse and the mature osteoclasts invade the mineralized cartilage of the rudiments to excavate the future bone marrow cavity. Within this study, in situ hybridization on sections of whole paws from 17-day-old embryos revealed CSF-1 transcripts to be present in cells lining the outside of the midregion of the metatarsals. One day later, cells containing CSF-1 mRNA were found within the mineralized cartilage. The levels of transcripts encoding CSF-1 were further increased in the bone rudiments of newborn animals. Binding sites for CSF-1 on cells in close proximity of the metatarsals were detected at embryonic age 17 days, but not before. At this stage, cells binding CSF-1 were located on the periosteum of the midregion of the metatarsal rudiment. At 18 days, cells expressing high levels of CSF-1 binding sites had invaded the mineralized cartilage.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Role of colony-stimulating factor-1 in bone metabolism.

Colony-stimulating factor-1 (CSF-1) is a cytokine required for proliferation, differentiation, activity, and survival of cells of the mononuclear phagocytic system. The growth factor is synthesized as a soluble, matrix, or membrane associated molecule. The specific functions of these forms are not clear. However, some data suggest a dependence of the development of various populations of tissue macrophages on the locally expressed and presented cytokine. Deficiency in CSF-1, as is the case in the murine mutant strain op/op, results in low numbers of macrophages and monocytes and, most striking, leads to osteopetrosis due to a virtual absence of osteoclasts. Using the op/op mutation as a model, CSF-1 was established as one of the growth factors for osteoclasts. The expression of CSF-1 receptors, encoded by the proto-oncogene c-fms, by osteoclast precursors and osteoclasts, suggested an effect of this cytokine not only during osteoclast formation but also on the mature cells. In fact, CSF-1 was shown to inhibit the resorbing activity, to stimulate migration, and to support survival of isolated osteoclasts in vitro. By these actions on cells of the osteoclast lineage, CSF-1 induces recruitment of new osteoclasts, leading to a net increase of bone resorption, and might govern the spatial distribution of resorption sites within the bone. During these processes, locally expressed and presented forms of the growth factor may play a crucial role, as will be discussed in this article.

Animals↗
PubMed1994

Role of colony stimulating factor-1 in the establishment and regulation of tissue macrophages during postnatal development of the mouse.

Colony stimulating factor-1 (CSF-1) regulates the survival, proliferation and differentiation of mononuclear phagocytes. The osteopetrotic (op/op) mutant mouse is devoid of CSF-1 due to an inactivating mutation in the CSF-1 gene and is deficient in several mononuclear phagocyte subpopulations. To analyze more fully the requirement for CSF-1 in the establishment and maintenance of mononuclear phagocytes, the postnatal development of cells bearing the macrophage marker antigens F4/80 and MOMA-1, in op/op mice and their normal (+/op or +/+) littermates, were studied during the first three months of life. In normal mice, maximum expression of tissue F4/80+ cells was generally correlated with the period of maximum organogenesis and/or cell turnover. Depending on the tissue, the F4/80+ cell density either decreased, transiently increased or gradually increased with age. In op/op mice, tissues that normally contain F4/80+ cells could be classified into those in which F4/80+ cells were absent and those in which the F4/80+ cell densities were either reduced, normal or initially normal then subsequently reduced. To assess which F4/80+ populations were regulated by circulating CSF-1 in normal mice, op/op mice in which the circulating CSF-1 concentration was restored to above normal levels by daily subcutaneous injection of human recombinant CSF-1 from day 3 were analyzed. These studies suggest that circulating CSF-1 exclusively regulates both the F4/80+ cells in the liver, spleen and kidney and the MOMA-1+ metallophilic macrophages in the spleen. Macrophages of the dermis, bladder, bone marrow and salivary gland, together with a subpopulation in the gut, were partially restored by circulating CSF-1, whereas macrophages of the muscle, tendon, periosteum, synovial membrane, adrenals and the macrophages intimately associated with the epithelia of the digestive tract, were not corrected by restoration of circulating CSF-1, suggesting that they are exclusively locally regulated by this growth factor. Langerhans cells, bone marrow monocytes and macrophages of the thymus and lymph nodes were not significantly affected by circulating CSF-1 nor decreased in op/op mice, consistent with their regulation by other growth factors. These results indicate that important differences exist among mononuclear phagocytes in their dependency on CSF-1 and the way in which CSF-1 is presented to them. They also suggest that the prevalent role of CSF-1 is to influence organogenesis and tissue turnover by stimulating the production of tissue macrophages with local trophic and/or scavenger (physiological) functions. Macrophages involved in inflammatory and immune (pathological) responses appear to be dependent on other factors for their ontogenesis and function.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1993

Expression of tissue transglutaminase in skeletal tissues correlates with events of terminal differentiation of chondrocytes.

Calcifying cartilages show a restricted expression of tissue transglutaminase. Immunostaining of newborn rat paw bones reveals expression only in the epiphyseal growth plate. Tissue transglutaminase appears first intracellularly in the proliferation/maturation zone and remains until calcification of the tissue in the lower hypertrophic zone. Externalization occurs before mineralization. Subsequently, the enzyme is present in the interterritorial matrix during provisional calcification and in the calcified cartilage cores of bone trabeculae. In trachea, mineralization occurring with maturation in the center of the cartilage is accompanied by expression of tissue transglutaminase at the border of the hydroxyapatite deposits. Transglutaminase activity also shows a restricted distribution in cartilage, similar to the one observed for tissue transglutaminase protein. Analysis of tissue homogenates showed that the enzyme is present in growth plate cartilage, but not in articular cartilage, and recognizes a limited set of substrate proteins. Osteonectin is coexpressed with tissue transglutaminase both in the growth plate and in calcifying tracheal cartilage and is a specific substrate for tissue transglutaminase in vitro. Tissue transglutaminase expression in skeletal tissues is strictly regulated, correlates with chondrocyte differentiation, precedes cartilage calcification, and could lead to cross-linking of the mineralizing matrix.

Animals↗
PubMed1992

Detection of transcripts for the receptor for macrophage colony-stimulating factor, c-fms, in murine osteoclasts.

Macrophage colony-stimulating factor (M-CSF), whose action is restricted to the cell populations of the mononuclear phagocyte system, has recently been found to be required for osteoclastogenesis and bone resorption. To investigate the cells involved in the action of M-CSF in these processes, expression of c-fms mRNA, encoding the M-CSF receptor, was studied by in situ hybridization. Paws from murine embryos and newborn mice, tibiae from 2-day-old animals, as well as isolated osteoclasts, were hybridized with a c-fms-specific RNA probe. In bone, c-fms mRNA was detected only in cells at the late stages of osteoclastogenesis and in mature osteoclasts. The findings strengthen the relation between osteoclasts and the mononuclear phagocyte system. Furthermore, they suggest that M-CSF acts directly on osteoclast precursors and on mature osteoclasts during osteoclastogenesis.

Animals↗
PubMed1992

Expression of collagen, osteocalcin, and bone alkaline phosphatase in a mineralizing rat osteoblastic cell culture.

Rat calvaria bone cells isolated by collagenase digestion form a bone-like matrix which mineralizes in vitro in the presence of beta-glycerophosphate, in less than 2 weeks. The purpose of this work was to investigate, in this mineralizing rat osteoblastic cell culture, the synthesis of collagen, osteocalcin, and bone alkaline phosphatase (ALP). The results obtained indicate (1) After 15 days in culture, the extracellular-matrix contains collagen type I, V, and to some extent type III. Metabolic labeling at day 14, during the phase of nodules mineralization as well as new nodules formation, shows that collagen types I and type V are synthesized; (2) During the phase of cell growth, no osteocalcin could be detected in the medium, however, at the point of nodule formation, the osteocalcin level reached values of 3.55 +/- 1.39 ng/ml, followed by a 30-fold increase after nodules became mineralized. At day 14, after metabolic labeling, de novo synthesized osteocalcin was chromatographed on an immunoadsorbing column. With urea-SDS PAGE the apparent molecular weight was determined to be 9,000 daltons. (3) Specific activity of ALP was found to be 10 nmol/min/mg of proteins at cell confluence. At day 15, when nodules are mineralized, this activity was increased by 40-fold. The Michaelis constant was 1.58 10(-3) M/L. ALP was inhibited by L-homoarginine and levamisole but not by L-phenylalanine. ALP was shown to be heat sensitive at 56 degrees C with two slopes of inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed1988

Production of hemopoietic growth factors by bone tissue and bone cells in culture.

This study was carried out to determine whether bone might be a source of hemopoietic growth factors. Both neonatal murine calvaria and primary cultures of cells isolated from calvaria released, upon stimulation with lipopolysaccharide, an activity that stimulated the growth of the interleukin (IL) 3-dependent cell lines, 32D cl, 123, and NSF 60. Upon gel filtration, this activity eluted with a molecular weight of 30,000 kDa. Further characterization, however, revealed that the major activity in conditioned medium was not IL 3. Activity was absorbed by DEAE-Sephacel at low salt concentration, whereas IL 3 does not adhere. Furthermore, an IL 3-specific antiserum did not neutralize the activity from cells and only partly neutralized the activity generated by whole calvaria. After gel filtration, the 30-kDa activity stimulated the growth of very large colonies in semisolid medium consisting mainly of granulocytes with the remainder being macrophages. No colony types belonging to other hemopoietic lineages were found, indicating, again, that the activity was not identical to IL 3. Subsequently, conditioned medium was fractionated by hydrophobic chromatography on Phenyl-Sepharose CL-4B, yielding two peaks of activity. Neutralization of activity with antisera to granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL 3 and use of colony assays showed that medium conditioned by whole calvaria contained GM-CSF and granulocyte CSF (G-CSF) in similar amounts together with a little IL 3, and medium conditioned with calvaria cells contained GM-CSF and little G-CSF. We conclude that bone releases hemopoietic growth factors that could contribute both to hemopoiesis and to the recruitment of osteoclasts from progenitors resident in the adjacent marrow.

Animals↗
PubMed1988

Bisphosphonates inhibit 1,25-dihydroxyvitamin D3-induced increase of osteocalcin in plasma of rats in vivo and in culture medium of rat calvaria in vitro.

In order to test whether bisphosphonates, which are potent inhibitors of osteoclastic bone resorption, may also act upon osteoblasts, we studied the effect of dichloromethylenebisphosphonate (Cl2MBP) and 4-amino-1-hydroxybutylidene-1,1-bisphosphonate (AHBuBP) on in vivo levels and in vitro release of osteocalcin, a bone-specific protein produced by osteoblasts. In rats, 161 mumol/kg of Cl2MBP or 1.61 mumol/kg AHBuBP strongly inhibited the increase of plasma osteocalcin induced by 1,25(OH)2D3. The inhibition was measurable within 24 hours after the administration of bisphosphonate and was independent of any change in bone resorption. The effect upon osteocalcin release was also present in calvaria cultures. 250 microM Cl2MBP strongly inhibited the osteocalcin release induced by 10(-8) M 1,25(OH)2D3. In the presence of 1,25(OH)2D3, protein synthesis and DNA synthesis were also decreased, whereas in the absence of 1,25(OH)2D3, protein synthesis was increased. Thus, bisphosphonates affect the production of a bone-specific protein by osteoblasts in addition to their inhibitory action on osteoclasts.

Alendronate↗
PubMed1986

Suppression of established IgE antibody responses with isologous anti-idiotypic antibodies in guinea pigs.

Guinea pigs of strains 2 and 13 can produce isologous anti-idiotypic (aIds) antibodies against anti-benzylpenicilloyl (anti-BPO) IgG, following immunization with affinity-purified anti-BPO antibodies of the same strain. The specificity of aId was determined by inhibition of binding of aId to Fab(t) in ELISA. The results showed that the reaction of strain 2 (anti-BPO)aId can be inhibited with syngeneic anti-BPO Fab(t) and to a smaller degree with anti-BPO Fab(t) of strain 13. On the other hand, strain 13 (anti-BPO)aId reacted exclusively with syngeneic anti-BPO Fab(t). In both cases, binding of aId to anti-BPO Fab(t) could not be inhibited with BPO-epsilon-aminocaproic acid, indicating that these aId are not directed against the antigen-combining site. The effect of isologous aId on both short- and long-time established IgE responses was studied in guinea pigs of strain 13. In both situations, administration of isologous aId resulted in suppression of the anti-BPO IgE antibody response. The suppressive effect was antigen-specific and lasted for several weeks: in the case of an early-response IgE remained suppressed despite additional booster injections of antigen. In contrast to the IgE response, the production of anti-BPO IgG antibodies was only slightly affected.

Animals↗
PubMed1985

Isotypic and idiotypic characterization of anti-bee venom phospholipase A2 antibodies.

It was shown that anti-bee venom phospholipase A2 antibodies (anti-PLA) of bee keepers belong mainly to the IgG4 class. Furthermore anti-PLA of different individuals are idiotypically related to each other. This was shown by the binding of heterologous antiidiotypic antibodies, produced against anti-PLA IgG from single donors, to anti-PLA F(ab')2 of different individuals. Therefore, the anti-PLA response provides a human model to study the idiotypic regulation of isotypes in a defined system.

Antibodies↗
PubMed1984

Production and characterization of monoclonal antibodies to the myelin glycolipid sulfatide.

Sulfatide is enriched in the myelin sheath and accounts for 5% of the total lipids in this membrane. In the present work we describe the production and characterization of mouse monoclonal antibodies against sulfatide. The antibodies were detected and characterized in a previously described ELISA test system. The clone AIC3IA2 produced antibodies of the IgG3 class with high specificity for sulfatide. These antibodies showed almost no cross-reactivity with galactocerebroside or with any of the other lipids we tested. When used with the peroxidase antiperoxidase technique the antibodies stained a cell population either in fixed or unfixed brain cell cultures, indicating a surface localization of sulfatide in the respective cell population. In double-staining experiments the stained cell population was identified as myelin basic protein-positive oligodendrocytes.

Animals↗