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Biomedical subjects

R A Gatti

Publications and source records attributed to R A Gatti.

At least 19 recordsLinked to original sources
PubMed1979

HLA-D locus typing in ankylosing spondylitis and Reiter's syndrome.

HLA-D typing of 44 patients with ankylosing spondylitis (AS) and 31 patients with Reiter's syndrome (RS) did not show increased frequency of any particular Dw allele in either population of patients as compared to controls. Such studies also allowed each patient's general response to be compared with other general responses within each experiment. Contrary to reports of diminished lymphocyte responses in AS patients, hyperresponsiveness in both AS and RS patients was found.

Alleles↗
PubMed1979

Sézary syndrome. Tartrate-resistant acid phosphatase in the neoplastic cells.

Tartrate-resistant acid phosphatase has been known to be of diagnostic value in hairy cell leukemia. However, occasionally neoplastic cells of other varieties of lymphoproliferative disorders may contain tartrate-resistant acid phosphatase. The authors have studied four patients with Sézary syndrome who had typical cutaneous lesions with extensive lymphoid infiltrates and circulating atypical E-rosetting lymphoid cells. The abnormal Sézary cells accounted for 23-69% of the peripheral mononuclear cells and often showed convoluted or folded nuclei. These cells in all four patients were strongly positive for acid phosphatase resistant to tartaric acid inhibition. Enzymatic cytochemical studies for acid phosphatase with and without tartrate may be helpful in the differential diagnosis of cutaneous T-cell lymphomas from variants of chronic dermatitis.

Acid Phosphatase↗
PubMed1979

HLA-D typing with lymphoblastoid cell lines. VI. Rationale and goals of data reduction.

This report documents various characteristics of HLA-D typing by mixed leukocyte culture reactions when lymphoblastoid cell lines (LCLs) are substituted for peripheral blood lymphocytes as the stimulator cells. It also provides the rationale for designing the computer program described in the subsequent report. In such experiments, each donor to be HLA-D typed is stimulated with a panel of 30-50 HLA-D homozygous LCLs, each defined HLA-D allele being represented by several different human homogygous typing cells (LCT-HTCs). Variability in the strength of eahc donor's general response and in the strength of stimulation by each LCL-HTC makes it necessary to normalize raw data before the responses of various combinations can be compared and typing responses distinguished from non-typing responses. The autologous response and its equivalent effect among allogenetic combinations, the so-called "autologous-stimulation" effect, must also be distinguished from true allogeneic responses. The latter has been accomplished by "modelling," as described in the subsequent report. EBV-negative donors can also be HLA-D typed by this method despite the EBV-positivity of the LCL-HTCs. Preliminary analyses suggest that the HLA-D alleles defined by this method appear to segregate with appropriate haplotypes in family studies.

Alleles↗
PubMed1979

HLA-D typing with lymphoblastoid cell lines. VII. A computer program for data analysis.

When lymphoblastoid cell lines (LCL) are substituted for peripheral blood lymphocytes from human typing cell donors in HLA-D typing experiments, a data analysis program must be designed to distinguish the effect of allo-reactivity from those peculiar to LCL, mainly the "autologous-stimulation" effect. The computer program described in this report was created specifically for such an analysis. The rationale for the design of this program is presented in the preceding report (see this issue).

Cell Line↗
PubMed1979

Suppression of lymphoblastoid cell line proliferation by antisera to HLA-DR and other HLA antigens.

We have observed that certain antisera to HLA antigens suppress the in vitro proliferation of lymphoblastoid cell lines. An antiserum to HLA-B8 demonstrated suppressor activity associated with the presence of B8 antigen on the target LCLs; this activity was removed by absorption with platelets or with B8-positive LCLs. An antiserum to HLA-DRw7 suppressed proliferation of all six DRw7-positive LCLs and none of 12 DRw7-negative LCLs; this activity was removed by absorptions with three DRw7-positive LCLs, each representing a different HLA-D allele (i.e. Dw7, 10 and 11); it could not be removed by triple serial absorptions with platelets from multiple-donor pools. These experiments indicate that the suppressor activity of this serum is specifically associated with antibodies to DRw7. Our model of LCL growth suppression by HLA antisera is easily manipulated and provides a definitive tool for further characterizing HLA antigens and antisera in a complement-independent system.

B-Lymphocytes↗
PubMed1979

HLA--D typing with lymphoblastoid cell lines. IV. Allelic relationships.

Responses of approximately 200 persons were measured by mixed leukocyte cultures against 41 lymphoblastoid cell lines which were thought to be homozygous for HLA--D (i.e. LCL-HTCs). These responses were standardized by computer analysis and the resultant Interaction Indices for each LCL-HTC were compared with those of every other LCL-HTC in a correlation matrix of 861 independent analyses. Only those analyses involving LCL-HTCs of defined HLA--D types are reported here. In general, these studies confirmed many allelic relationships of reputedly similar LCL-HTCs; however, several unexpected groups of correlations suggested that groups Dw1 and 3 overlap to form Groups "1a-3," "1b-3" and "true 3." The "1b-3" group also included Dw8. Segregation of the "1b-3" allelic group was also observed in a family study. These preliminary analyses suggest a working model for further investigation of HLA--D allelic relationships (Fig. 3). On the other hand, they may also be interpreted to suggest that "typing" with LCL-HTCs may be controlled by a separate HLA locus which is closely related to, but distinct from, HLA--D.

Alleles↗
PubMed1979

Membrane receptors and their redistribution in lymphoproliferative disorders.

Lymphoid cells from 20 patients with lymphoproliferative disorders, including chronic lymphocytic leukemia, hairy cell leukemia, Sezary syndrome, lymphoma, and lymphadenitis, were studied for redistribution of surface membrane immunoglobulins (SmIg) and concanavalin A (Con-A) receptors. Fluorescein-labeled polyvalent goat anti-human immunoglobulin and fluoresceinated concanavalin A were used as ligands. Results were similar with both ligands. The highest percentage of capping of ligand-membrane receptors was noted in mononuclear cells from patients with "hairy" cell leukemia: from 24% to 90%. These cells showed moderate to marked fluorescein activity and were able to cap within 15 min at 4 degrees C. Chronic lymphocytic leukemia cells showed a weak fluorescein stain with a very low percentage of cells (0%--16%) capping. Lymph node cells from patients with lymphoma demonstrated moderate to strong fluorescein activity with only an average of 3% of the cells capping; while lymphoid cells from patients with lymphaedenitis showed an average of 27.5% capping and moderate fluorescein activity. Capping of Con-A receptors in mononuclear cells from patients with Sezary syndrome was poor (0%--14%) with moderate fluorescein intensity. This report demonstrates difference in density and mobility of binding sites for SmIg and Con-A on the surface membrane of lymphoid cells from various subclasses of lymphoproliferative disorders. These differences may assist in the differential diagnosis and classification of these conditions.

Cell Membrane↗
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↗
PubMed1977

Simplification of B-cell antisera of the Merrit system with platelets and lymphoblastoid cell lines.

Human sera with anti-HLA and anti-Merrit B-cell reactivities were absorbed with different volumes of a pool of packed outdated human platelets obtained from 237 donors. After absorption, each serum was tested against a panel of CLL cells and normal unfractionated peripheral blood lymphocytes that had given positive reactions with the same serum prior to absorption. The optimal platelet volume for complete absorption of anti-HLA and full preservation of anti-Merrit B-cell activities in these sera was found to be 1/10 to 1/5 of the volume of serum. Higher volumes of packed platelets, especially over 1/1, in most instances reduced anti-B-cell activity "nonspecifically." Among the platelet absorbed sera, those showing no HLA and strong anti-Merrit B-cell cytotoxicity were used for cross-absorption studies with cultured human lymphoid cell lines. Multi-specific anti-Merrit sera could be simplified by this method. Cultured lymphoblastoid cell lines represent a valuable resource, since large volumes of cells may be needed for absorption and simplification of human sera containing allogeneic B-lymphocyte antibodies.

B-Lymphocytes↗