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Biomedical subjects

A M Solinger

Publications and source records attributed to A M Solinger.

28 records · Page 2Linked to original sources
PubMed1982

Exfoliative dermatitis from captopril.

Captopril, an angiotensin converting enzyme blocker, has recently been released for limited clinical use in the treatment of refractory congestive heart failure and severe hypertension. The only major dermatologic side effects from this medication have been either an urticarial or an erythematous, maculopapular eruption. This paper presents what I believe to be the first reported case of exfoliative erythroderma associated with the use of captopril. Although this medication may be lifesaving with its minimal side effects, close attention should be paid to the dermatologic side effects of this drug.

Captopril↗
PubMed1981

Regulation of immune reactivity to collagen in human beings.

Denaturated beef collagen was tested for its ability to induce the production of leukocyte inhibition factor among the peripheral blood mononuclear cells from patients with rheumatoid arthritis and normal individuals. Responsiveness, defined as the production of leukocyte inhibition factor sufficient to cause greater than 20% inhibition of leukocyte migration, was significantly (P less than 0.001, X2 = 31.1) associated with HLA-DR4. All HLA-DR4 positive individuals, including subjects without any evidence of synovitis, were collagen responders. There was no significant (P = 0.3) difference in the absolute reactivity of HLA-DR4+ versus HLA-DR4- individuals to respond to another antigen, Candida albicans. Collagen reactivity required interactions between macrophages and T cells and was directed against determinants inherent in the linear polypeptide, (Gly-Pro)n. In 5 normal HLA-DR4- nonresponders tested, absence of discernable reactivity to collagen was associated with the presence of antigen-specific, radiosensitive suppressive T cells. These studies suggest that during the physiologic metabolism of collagen all individuals are exposed to Gly-Pro determinants normally buried in the interstices of the collagen triple helix. In individuals whose major histocompatibility complex contains genes linked to those coding for HLA-DR4, this results in the activation of reactive T cells. Conversely, in individuals lacking these genes, collagen-specific suppressive cells predominate.

Animals↗
PubMed1981

Cellular, molecular, and genetic characteristics of T cell reactivity to collagen in man.

Rheumatoid arthritis is significantly associated with the HLA determinant HLA-DRw4 and cell-mediated reactivity to collagen. To determine if genes linked to those coding for HLA-DRw4 constituted immune response genes for collagen reactivity, peripheral blood mononuclear cells from 20 individuals with rheumatoid arthritis, 13 individuals with other arthropathies, and 41 normal individuals were compared for their ability to synthesize the lymphokine leukocyte inhibition factor in response to denatured bovine collagen. All individuals were responsive to the control antigen Candida albicans. While 90% of the patients with rheumatoid arthritis responded to collagen, so did 30% of the individuals without rheumatoid arthritis. This included 15 normal individuals without any evidence of arthritis. Collagen responsiveness was dependent on interactions between T cells and macrophages was dependent on interactions between T cells and macrophages and was directed against determinants expressed by primary amino acid sequences in the synthetic polypeptide (Gly-Pro)n. HLA-DRw typing of 59 individuals revealed a highly significant relationship (P less than 0.0001, chi 2 = 33.7) between HLA-DRw4 and collagen responsiveness, irrespective of whether or not rheumatoid arthritis was present. All normal individuals who were HLA-DRw4-positive were collagen responders. These studies demonstrate that the cellular, molecular, and genetic characteristics of collagen reactivity in man parallel those documented for the T cell-dependent response to antigens under immune response gene control in rodents.

Arthritis, Rheumatoid↗
PubMed1981

Severe pulmonary involvement in mixed connective tissue disease.

Pulmonary involvement in mixed connective tissue disease has been considered a benign manifestation that is easily treated with corticosteroids. We followed 5 patients who had mixed connective tissue disease and severe, rapidly progressive, lung disease. Two types of lung disease were found, interstitial lung disease and pulmonary hypertension. Histologic sections from our patients were compared with sections from patients who had interstitial lung disease and systemic lupus erythematosus or pulmonary hypertension and scleroderma. Although clinical presentations were similar, the immunofluorescent and electron microscopic findings for interstitial lung disease were somewhat different in patients with systemic lupus erythematosus. Histologic findings for pulmonary hypertension appeared different in patients with mixed connective tissue disease and patients with scleroderma. For patients with either type of lung disease, corticosteroid therapy proved inadequate, but nearly cytotoxic therapy may be beneficial.

Adult↗
PubMed1980

The T lymphocyte proliferative response to poly-L-Glu-poly-D,L-Ala--poly-L-Lys.

The immune response to several antigens has been shown to be under the control of two complementing major histocompatibility-linked immune response (Ir) genes. In most cases, one gene has been mapped to the I-A subregion and the other to the I-E/C subregion. However, in some cases F1 complementation has been described between two alleles in the I-A subregion, so called beta-beta complementation. In these examples, complementation has been seen at the antibody level but not in a T lymphocyte proliferation assay. In the present work, we studied the T cell proliferative response to poly-L-Glu-poly-D,L-Ala--poly-L-Lys (G-A--L). Peritoneal exudate, T lymphocyte-enriched subpopulations (PETLES) from F1 hybrids between C57BL/10 and B10.A, C57BL/10, and B10.A(4R), or B10.A and B10.A(3R) or (5R) mice responded well to G-A--L. In contrast, PETLES from F1 hybrids between C57BL/10 and B10.A(5R) or B10.A and B10.A(4R) mice, as well as from all inbred strains tested, failed to respond to G-A--L. These results demonstrate for the first time an example of Ir gene complementation at the T cell level in which both genes map to the left of the I-J subregion presumably in I-A. This system should now allow us to determine whether alpha-beta and beta-beta complementation take place through the same biologic mechanism.

Animals↗
PubMed1979

T-lymphocyte response to cytochrome c. I. Demonstration of a T-cell heteroclitic proliferative response and identification of a topographic antigenic determinant on pigeon cytochrome c whose immune recognition requires two complementing major histocompatibility complex-linked immune response genes.

The T-lymphocyte proliferative response to pigeon cytochrome c was studied in the mouse. H-2a and H-2k strains were responders to this antigen whereas H-2b, H-2d, H-2f, H-2ja, H-2p, H-2q, H-2r, H-2s, and H-2u strains were low or nonresponders. Genetic mapping demonstrated that two major histocompatibility complex (MHC)-linked Ir genes control the response, one in I-A, the other in I-E/I-C. The major antigenic determinant recognized in this response was localized by cross-stimulations with species variants and cyanogen bromide cleavage fragments of cytochrome c. It was found to be a topographic surface determinant composed of an isoleucine for valine substitution at residue 3, a glutamine for lysine substitution at residue 100 and a lysine for glutamic acid substitution at residue 104. Tobacco hornworm moth cytochrome c, which contains a glutamine at residue 100 but a terminal lysine at residue 103 (one amino acid closer to the glutamine), stimulated pigeon cytochrome c immune T cells better than the immunogen. This result demonstrates for the first time a functional T-cell heteroclitic proliferative response in a system under Ir gene control. Immunization with the cyanogen bromide cleavage fragments revealed that only pigeon cytochrome c fragment 81-104 was immunogenic. This fragment primed for a T-cell proliferative response whose specificity was nearly identical to that of the T-cell response primed for by the whole molecule, suggesting that the glutamine at 100 and the lysine at 104 form the immunodominant portion of the antigenic site. Furthermore, mixing experiments using the two cross-reacting antigens, hippopotamus cytochrome c and Pekin duck or chicken cytochrome c fragment (81-104), each of which contains only one of the two immunodominant substitutions, demonstrated that the T lymphocytes responding to the major antigenic determinant comprise a single family of clones that recognize both amino acids as part of the same determinant. Thus, two complementing MHC-linked Ir genes can control the immune response to a single antigenic determinant.

Animals↗
PubMed1978

Genetic control of the T-lymphocyte proliferative response to cytochrome c.

Cytochromes c have been used as antigens in a murine T-lymphocyte proliferation assay in order to characterize the nature of determinants whose recognition is under immune response (Ir) gene control. The cytochromes are advantagous as antigens because 1) they have well-characterized primary and tertiary structures, 2) they are antigenically simple, differing from mouse cytochrome c at only a small number of amino acid residues, and 3) there exist a large number of evolutionary variants which can be used to locate antigenic sites by cross-stimulation. In the present studies, the T-lymphocyte proliferative response to pigeon cytochrome c was shown to be under the control of two complementing major histocompatibility (MHC)-linked Ir genes in mice of the H-2a and H-2k haplotypes. Mice of the H-2b, H-2d, H-2p, H-2q, H-2s, and H-2u haplotypes were low or nonresponders. Complementation was demonstrated by showing that an F1 hybrid between two nonresponder recombinant strains, B10.A(4R) and B10.A(5R), could respond to pigeon cytochrome c. The determinant on the cytochrome recognized in this immune response was located to the C-terminal portion of the molecule around residues 89 and/or 100. This was shown by the failure of closely related cytochromes from the Pekin duck and chicken to cross-stimulate T lymphocytes immune to pigeon cytochrome; position 89 and 100 carry the only residues different from those in mouse cytochrome c that are unique to pigeon cytochrome among the three bird cytochromes tested. This localization was further substantiated by demonstrating that the cyanogen bromide cleavage-fragment (residues 81-104) from pigeon cytochrome, but not the same fragment from Pekin duck cytochrome, was as good a stimulant of T cells immune to the whole molecule as the intact cytochrome. These results identify the immunogenic site on the molecule as one which differs from mouse cytochrome c by only one or two amino-acid residues. Thus, T-cell immune responses, which are under MHC-linked Ir gene control, are as capable as antibody responses of recognizing subtle differences in protein structure. However, the ability of T cells to respond equally well to stimulation with polypeptide fragments or with the whole molecule suggests either that T-cell recognition involves certain differences from B cell recognition or that in some cases the fragments possess a similar spatial structure to that of the corresponding segment in the native protein.

Animals↗