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Biomedical subjects

M Trucco

Publications and source records attributed to M Trucco.

At least 217 records · Page 12Linked to original sources

A novel human lymphokine that inhibits haematopoietic progenitor cell proliferation.

T lymphocytes in culture synthesize and secrete a variety of factors that activate and guide the differentiation, replication and maturation of haematopoietic cells in vitro. Malignant T-cell lines as well as T-cell hybridomas producing several of these factors have been established. We report here a factor produced by a human cell line that exerts a potent inhibitory effect on the growth of bone marrow progenitor cells. The properties of this factor, which we have termed colony-inhibiting lymphokine ( CIL ), differ from other inhibitors of haematopoietic progenitor cell proliferation, but resemble those of a T-cell-derived factor causally linked with some cases of severe aplastic anaemia in humans. Sensitivity of cells to this factor appears to correlate positively with expression of HLA-DR surface antigens.

Bone Marrow↗

Relationship between DQ alpha and DQ beta RFLP and cell surface polymorphisms of class II HLA antigens.

DQ alpha and beta DNA probes of the human major histocompatibility complex (MHC) were hybridized to restriction enzyme-digested genomic DNA with the aim of establishing a correspondence between the polymorphisms recognized by classical serology and DNA restriction fragment length polymorphisms (RFLP). In DR homozygous human cell lines, three distinct PstI fragments were recognized by the DQ alpha probe and four PstI fragments were recognized by the DQ beta probe. Each fragment was associated with a different group of DR antigens. Three allelic forms of either DX alpha or beta genes were identified, but none showed any strong association with DR or DQ. Family segregation analysis at the DNA level further confirmed the DR linkage of the DQ alleles in estimations of gene frequencies of different alleles of DQ alpha, DQ beta, DX alpha and DX beta. Evidence was presented that the DQ alpha and DQ beta allelic forms described at the DNA level correspond to polymorphic determinants at the cell surface which can be defined serologically or in cellular assays. Our data suggest that the HLA-DQ subregion-encoded alloantigens should be defined at the individual alpha and beta chain levels.

Alleles↗

Reversal of graft-versus-host disease with infusion of autologous bone marrow.

Graft-versus-host disease (GVHD) remains a major complication of bone marrow transplantation. This report describes reversal of GVHD by infusion of stored recipient bone marrow following combined liver-bone marrow allotransplantation. Graft-versus-host disease developed at the end of the first postoperative week. The skin involvement progressively spread to approximately 80% of the body surface and was not affected by modification of the immunosuppressive treatment. On the 42nd and 43rd postoperative day 1.23 x 10(8) and 1.6 x 10(8) autologous bone marrow cells per kg of recipient body weight were infused. The skin rush began to dramatically improve and resolved within 2 wk from the autologous marrow infusion. Autologous bone marrow storage previous to allogeneic bone marrow transplantation for tolerance induction could constitute a safety net in case of occurrence of GVHD.

Biopsy↗

Exposure to superantigens as an immunogenetic explanation of type I diabetes mini-epidemics.

Insulin-dependent diabetes mellitus (IDDM) is considered to be an autoimmune disease. Autoimmune diseases result from the breakdown of self-tolerance elicited by environmental factors on a susceptible genetic background. This reduced tolerance allows immunocompetent cells to attack normal structures present on an individual's tissues. The study of the T cells present in the islets of patients who died at the onset of the disease allowed the recognition of "superantigens" as etiopathogenetic factors in the development of IDDM. Since superantigens are the product of bacteria or viruses able to quickly stimulate a large number of the peripheral T cells sharing the same T cell receptor V beta segments once presented by certain HLA class II molecules, a number of observations in genetics, immunology, virology and epidemiology can now find a unifying explanation.

Adolescent↗