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Biomedical subjects

G B Ferrara

Publications and source records attributed to G B Ferrara.

At least 145 records · Page 8Linked to original sources
PubMed1978

Immunological dissection of human Ia molecules.

The immunochemical analysis of Daudi Ia molecules by a variety of alloantisera led to the recognition of at least three molecular species carrying different antigenic determinants: DRw6, DC-1, and DC-2. Genetic as well as structural evidence indicates that DRw6 and DC-1 molecules are controlled by separate, HLA-linked loci, rather than by alleles at the same locus. The alloantigenic determinants appear to be expressed on the small Ia subunit. DC-1 and DC-2 determinants discussed had not been defined by serological analysis at the population level, but were demonstrated to be present by immunochemical analysis at the molecular level.

Antigen-Antibody Reactions↗
PubMed1978

A safe blood transfusion procedure for immunization against major histocompatibility complex determinants in man.

A standardized procedure is proposed for deliberate immunizations against human major histocompatibility complex determinants. The data presented demonstrate its effectiveness and, by using a number of necessary precautions, this procedure has proven to be very safe. The following points are especially important: (1) exclusive utilization of regular blood donors as immunizers; (3) use of whole blood as an immunizing agent; and (3) use of small immunizing stimuli rather than large transfusions. This procedure can be recommended for the production of monospecific anti-HLA antisera and it may be useful if and when a deliberate transfusion policy for prospective kidney recipients is adopted.

Blood Transfusion↗
PubMed1978

Serological inhibition of blast transformation to purified streptococcal antigens by planned immunization in HLA (A,B) compatible unrelated individuals.

Sera obtained from planned immunizations between unrelated donors and recipients, identical or compatible at HLA-A and B, were assessed for their capacity to alter the in vitro response of a test panel of lymphocytes to PHA and a purified streptococcal antigen (PAS). In the case of PHA, no serum effects were apparent. The response to PAS, however, significantly inhibited by two sera. When tested for their complement-dependent cytotoxicity on enriched populations of T and B lymphocytes, none of the sera manifested cytotoxicity against T cells nor did serological inhibition correlate with the capacity to lyze B cells. The data suggest that inhibition of the PSA response is mediated by blocking antibodies specific for a subset of lymphocytes, possibly T cells. While the precise mechanism governing the response to PSA is not known, the data are compatible with the idea that an HLA-linked Ir gene, expressed on a subset of T lymphocytes, controls immune responsiveness to PSA.

Antibody Specificity↗
PubMed1977

New groups and segregant series among B-cell alloantigens of the Merrit system. A study of leukemia cells, peripheral B cells, and lymphoblastoid cell lines.

On the basis of reactions with a chronic lymphatic leukemia cell panel, evidence for 6 new specificities of the Merrit B-cell alloantigenic system in man is presented, bringing the number of provisionally defined specificities to 19. These can be roughly divided into two segregant series. The system is well represented on both homozygous and heterozygous B-type lymphoblastoid cell lines. In the cell lines some specificities show a suggestive but inexact correlation with HLA-D locus factors. This correlation is represented also on peripheral blood B cells, on the non-T variety of acute lymphatic leukemia cells, and on acute myeloid leukemia cells. Although great similarities exist, each of the cell populations may manifest differences other than or in addition to mere differences in B-cell antigen frequencies.

B-Lymphocytes↗
PubMed1976

The merrit alloantigenic system of human B lymphocytes: evidence for thirteen possible factors including one six-member segregant series.

An analysis of the typing results of a 70-member chronic lymphatic leukemia B cell panel revealed evidence for 13 possible groups of the Merrit alloantigenic system. Six of these appeared possibly allelic and may represent a segregant series. The CLL panel was also fully typed for HLA and some degree of linkage dysequilibrium between Merrit and HLA seemed apparent from the data. Merrit antibodies can be absorbed out with selected surface membrane immunoglobulin (SMIG)-positive normal lymphocytes and less so or not at all with E rosette-forming T cells or Fc-positive SMIG-negative lymphocytes.

Absorption↗
PubMedDate not supplied

The pattern of HLA antigens in two Italian regions.

The HLA antigen and gene frequencies (A, B and C loci) in the populations of the Bergamo area and of the Campania region are compared. Significant discrepancies were found between the two sets of data, as regards the distribution of single genes and the haplotype frequencies and deltas as well. Stone of the frequencies diverge significantly also from accepted data on European Caucasoid populations.

Biometry↗
PubMedDate not supplied

Loss of polymorphic restriction fragments of class I and class II MHC genes in a malignant melanoma.

DNAs from human malignant melanoma cells and autologous peripheral blood lymphocytes were evaluated by Southern blot analysis with probes for class I and II HLA genes. DNA of melanoma cells digested with PvuII, EcoRI and BglI and hybridized with a DR beta probe showed a loss of several fragments when compared with DNA from lymphocytes. The same DNAs were not distinguishable when hybridized with a DQ beta probe. Analysis of melanoma and autologous lymphocyte DNAs from the same patient with a class I cDNA, after digestion with several endonucleases, revealed a further loss of fragments in melanoma cells. Comparison of restriction fragment patterns of melanoma and lymphocytes with those of homozygous, serologically-typed cell lines indicated that melanoma cells have lost fragments diagnostic of DR2 and A1 antigens. A densitometric analysis of signals of several oncogenes in comparison with that of DR indicated that a duplication of the remaining DR allele had occurred in melanoma cells.

DNA, Neoplasm↗