212 research outputs found
Human T lymphocyte cell line (Mo) and its subclone (J) produce colony stimulating activity on normal and malignant T cell precursors
No full textConditioned medium from a T-lymphoblastic cell line (Mo) is known to produce factors promoting CFU-GM, BFU-E and CFU-MK In our study we investigated the potential CSA of conditioned media obtained from Mo and its subclone J on normal and malignant lymphoid progenitors of both T and B lineage. Both cell lines release factors inducing a significant increase in number and size of T-lymphoid colonies when compared to standard source of factors (PHA-LCM). On the contrary, they, presented a low CSA on B cell precursors confirming the difficulties in identifying a source of growth and differentiation factors for human B cell ontogeny. This study contributes to the knowledge of biological properties of these tumor cell lines, suggesting the possibility to employ Mo- and J-derived supernatants in vitro for improving growth potential of normal and malignant T cell progenitors
Generation of anti NAG-2 Mab from patients memory B cells: implication for a novel therapeutic strategy in systemic sclerosis
No full textSerum levels of granulocyte-macrophage colony-stimulating factor and granulocyte colony-stimulating factor in treated patients with chronic myelogenous leukemia in chronic phase.
No full textHuman parvovirus B19 infection and autoimmunity.
No full textHuman parvovirus B19 infection is responsible for a wide range of human diseases ranging from mild erythema infectiosum in immunocompetent children to fetal loss in primary infected pregnant women and aplastic anemia or lethal cytopenias in adult immunocompromised patients. Since persistent viral infection is responsible for an autoimmune response and clinical symptoms can mimic autoimmune inflammatory disorders, parvovirus B19 is the object of intense efforts to clarify whether it is also able to trigger autoimmune diseases. Indeed the virus has been implicated as the causative or the precipitating agent of several autoimmune disorders including rheumatoid arthritis, systemic lupus, antiphospholipid syndrome, systemic sclerosis and vasculitides. Molecular mimicry between host and viral proteins seems to be the main mechanism involved in the induction of autoimmunity. By means of a random peptide library approach, we have identified a peptide that shares homology with parvovirus VP1 protein and with human cytokeratin. Moreover the VP peptide shares similarity with the transcription factor GATA1 that plays an essential role in megakaryopoiesis and in erythropoiesis. These new data sustain the role played by molecular mimicry in the induction of cross-reactive (auto)antibodies by parvovirus B19 infection
A subset of anti-rotavirus antibodies directed against the viral protein VP7 predicts the onset of celiac disease and induces typical features of the disease in the intestinal epithelial cell line T84.
No full textAdult human circulating CD34-Lin-CD45-CD133- cells can differentiate into hematopoietic and endothelial cells
No full textA precise identification of adult human hemangioblast is still lacking. To identify circulating precursors having the developmental potential of the hemangioblast, we established a new ex vivo long-term culture model supporting the differentiation of both hematopoietic and endothelial cell lineages. We identified from peripheral blood a population lacking the expression of CD34, lineage markers, CD45 and CD133 (CD34-Lin-CD45 -CD133- cells), endowed with the ability to differentiate after a 6-week culture into both hematopoietic and endothelial lineages. The bilineage potential ofCD34-Lin-CD45-CD133 - cells was determined at the single-cell level in vitro and was confirmed by transplantation into NOD/SCID mice. In vivo,CD34 -Lin-CD45-CD133- cells showed the ability to reconstitute hematopoietic tissue and to generate functional endothelial cells that contribute to new vessel formation during tumor angiogenesis. Molecular characterization of CD34-Lin -CD45-CD133- cells unveiled a stem cell profile compatible with both hematopoietic and endothelial potentials, characterized by the expression of c-Kit and CXCR4 as well as EphB4, EphB2, and ephrinB2. Further molecular and functional characterization of CD34-Lin -CD45-CD133- cells will help dissect their physiologic role in blood and blood vessel maintenance and repair in adult life
Identification of autoantibodies against inner ear antigens in a cohort of children with idiopathic sensorineural hearing loss.
No full textImmune-mediated pathogenesis has been suggested for idiopathic sensorineural hearing loss. Recent studies have investigated the relationship between idiopathic sensorineural hearing loss and autoantibodies against inner ear antigens. We conducted a prospective, observational study in a series of pediatric patients affected by idiopathic sensorineural hearing loss. Autoantibodies against inner ear (anti-Cogan peptide, anti-connexin 26, anti-DEP1/CD148 and anti-reovirus), previously described in the serum of patients with Cogan's syndrome, were detected in our population. The characteristics of children whose results were positive were also evaluated to verify if clinical data, disease progression and response to treatment could confirm an immune-mediated pathogenesis. Eleven patients were enrolled and 9 of them were positive for inner ear antibodies. Non-organ specific autoantibodies were present in 5 children out of 9. An immune-mediated condition was diagnosed in 2 cases and minor immune manifestations were found in 2 additional patients. In 5 cases hearing loss remained stable without therapy, while 4 children developed progression. Two subjects were treated with corticosteroids and methotrexate, achieving hearing improvement. Another subject showed stabilization on methotrexate. Inner ear autoantibodies can be positive in children with autoimmune sensorineural hearing loss, and in conjunction with clinical data may assist the clinician in identifying a subset amenable for immune modulation therapy. Large prospective studies are needed to investigate usefulness, diagnostic and prognostic role of these autoantibodies
Identification of tear lipocalin as a novel autoantigen target in Sjogren’s syndrome
No full text.Sjögren's syndrome (SS) is an autoimmune disease characterized by lymphocytic infiltration and tissue damage mainly confined to the salivary and lacrimal glands, resulting in dryness of mouth and eyes. Since different epithelial cells of exocrine and non-exocrine tissues are primarily affected, an autoimmune reaction against antigens commonly expressed in epithelial cells is believed to play a pathogenic role. To identify novel autoantigen targets associated with the systemic involvement in SS, we screened a random peptide library with pooled IgG immunoglobulins derived from patients with primary SS. Among the identified peptides, one was recognized by the majority of patients' sera, but not by sera of normal donors and of patients with other autoimmune diseases. The peptide showed homology with an Epstein-Barr Virus (EBV) derived protein and with tear lipocalin, a protein highly expressed in tears and saliva, and with alpha-fodrin, a cytoskeleton protein considered an important autoantigen target in SS. Anti-peptide antibodies affinity purified from patients' sera recognize the viral protein, tear lipocalin and alpha-fodrin. Our findings suggest that EBV infection may be linked to the pathogenesis of SS and that tear lipocalin can be considered a novel and yet unidentified autoantigen in SS
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