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M L Mahowald

Publications and source records attributed to M L Mahowald.

46 records · Page 3Linked to original sources
PubMed1983

The cellular basis of adjuvant arthritis. I. Enhancement of cell-mediated passive transfer by concanavalin A and by immunosuppressive pretreatment of the recipient.

Two reliable systems for the cell-mediated passive transfer of adjuvant arthritis have been developed. Donor rats were sensitized with Mycobacterium butyricum in mineral oil. In the first system, intravenous injection of adjuvant-sensitized donor lymph node or spleen cells into adult-thymectomized, lethally irradiated, bone marrow cell-reconstituted syngeneic rats induced arthritis in the recipients. In the second system, adjuvant-sensitized donor lymph node or spleen cells were cultured in vitro with concanavalin A; these cells induced arthritis in normal recipients as well as in thymectomized, irradiated, bone marrow cell-reconstituted recipients. The passively transferred disease in both systems resembled classical adjuvant-induced arthritis clinically, radiographically, and histologically. Neither irradiated, adjuvant-sensitized donor cells nor cells from donors not injected with complete adjuvant could passively transfer arthritis.

Animals↗
PubMed1983

The cellular basis of adjuvant arthritis. II. Characterization of the cells mediating passive transfer.

It has previously been reported that lymph node or spleen cells from rats with adjuvant-induced arthritis can transfer the disease to normal recipients after being cultured with concanavalin A (Con A). In this report, it is shown that a subpopulation of cells that (1) lack surface Ig and the antigen reactive with the monoclonal antibody OX8, (2) are largely nonadherent and esterase negative, and (3) are predominantly marked by the monoclonal antibody W3/25 can transfer arthritis after stimulation with Con A. Adjuvant-sensitized lymph node or spleen cells stimulated with Con A but not PHA transfer arthritis, and this difference correlates with relatively higher levels of interleukin 2 secretion by Con A-stimulated cells. A synthetic adjuvant, CP-20961, a substituted propanediamine, induces arthritis that is passively transferable under the same conditions as arthritis induced by classical mycobacterium-containing adjuvant. The data support the hypothesis that adjuvant inoculation in the rat results in the induction of a unique subpopulation of T cells that initiate the inflammatory joint disease.

Animals↗
PubMed1983

Endogenous inhibition of autologous lymphocyte antibody-dependent cellular cytotoxicity.

Previous reports have indicated that prostaglandins can inhibit certain immune mechanisms, particularly mitogen responsiveness and cell-mediated cytotoxicity of virus-infected or tumor cells. In this study an endogenous self-inhibitory mechanism for antibody-dependent cellular cytotoxicity (ADCC) with normal human peripheral blood mononuclear cells is described. This inhibition could be abrogated by the prostaglandin synthetase inhibitor indomethacin or by removing nylon wool-adherent cells but not platelets. ADCC inhibition was restored by adding exogenous PGE1, PGE2, or supernatant fluid from cultured plastic-adherent mononuclear cells. In contrast, supernatant fluid from adherent mononuclear cells cultured with indomethacin was not inhibitory for ADCC. These results suggest that peripheral blood mononuclear cells contain adherent cells, probably monocytes, which produce prostaglandins that inhibit the ADCC effector activity of normal peripheral blood lymphocytes. This may explain, in part, the wide variability of ADCC effector cell activity that has been reported previously. Monocyte proportions and/or activity may have profound effects on tests of ADCC effector cell activity in various disease states.

Animals↗
PubMed1983

Acute polyarticular gout.

We report here on 41 male patients with acute polyarticular gout seen in 3 years. Acute polyarticular gout continues to masquerade as other commoner rheumatological disorders such as septic arthritis, rheumatoid arthritis, degenerative joint disease, and even hemiparesis. Almost all of these patients had clues to the diagnosis of acute gout in their medical history. These clues included a past history of intermittent acute gout, prior attacks of polyarticular arthritis, previous hyperuricaemia, and/or obvious tophi. The patients all responded promptly to nonsteroidal anti-inflammatory drugs. We observed serious toxic drug reactions in 8 patients.

Acute Disease↗
PubMed1982

Lymphocyte destruction by antibody-dependent cellular cytotoxicity mediated in vitro by antibodies in serum from patients with systemic lupus erythematosus.

Sera from patients with systemic lupus erythematosus (SLE) were tested for the presence of IgG antilymphocyte antibodies that are capable of mediating antibody-dependent cellular cytotoxicity (ADCC) of peripheral blood lymphocytes (PBL) from normal donors. The effector cells employed were PBL autologous with the target PBL. Positive ADCC responses were obtained with serum from 5 SLE patients with severe active diseases. It is possible that ADCC is a mechanism by which IgG antilymphocyte antibodies in patients with SLE may mediate in-vivo lymphocytolysis.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1979

Linkage relationship of C2 deficiency, HLA and glyoxalase I loci.

Immunogenetic analysis of a homozygous C2-deficient individual and family members demonstrated linkage of HLA-A25, B18 and C2o. HLA-D typing showed that 5 members typed with homozygous Dw2 typing cells from an individual with C2 deficiency but not with Dw2 typing cells from 2 individuals with normal C2. The homozygous C2-deficient propositus and brother were HLA-A and B homozygous but heterozygous at the HLA-D and glyoxalase I loci. Therefore, in this family, the C2o gene is linked with two distinct haplotypes: HLA-A25, B18, Dw2, GLO1 and HLA-A25, B18, D unknown, GL02. These results could be explained by an ancestral recombinant event, which occurred between the C2o locus and HLA-D locus in which C2o segregated with HLA-B. This would suggest that the locus for the C2o gene maps between HLA-B and HLA-D on the sixth chromosome.

Chromosome Mapping↗
PubMed1977

A comparative study of procedures for sheep erythrocyte-human-T-lymphocyte rosette formation.

A comparative study of several published methods for sheep red blood cell-T-lymphocyte rosette formation was performed. Maximum SRBC-rosette formation occurred with AET treated SRBC in medium supplemented with 20% FCS or with untreated SRBC in 100% FCS. Prolongation of the 4 degrees C incubation period from 4 to 18 h enchanced rosette formation. Fluorescein diacetate staining significantly increased calculated percentage of rosette formation. Fluorescein diacetate staining significantly increased calculated percentage of rosette-forming lyphocytes by allowing accurate indentification of the central lymphocytes in morulas.

Animals↗
PubMedDate not supplied

Isolated Candida parapsilosis arthritis in a heroin addict.

A case of isolated Candida parapsilosis arthritis involving the shoulder of a heroin addict is described. Amphotericin B successfully eradicated the infection after failure of flucytosine. Optimal therapy for this condition has not been determined.

Amphotericin B↗
PubMedDate not supplied

Amyloid in a patient with Reiter's syndrome - secondary or coincidental? Differentiation with potassium permanganate.

A patient with Reiter's syndrome developed a pulmonary nodule composed of amyloid. Reiter's syndrome has been reported as 1 of the diseases associated with secondary systemic amyloidosis. Isolated nodular pulmonary amyloid has not been reported to become systemic. Potassium permanganate treatment of amyloid abolishes congo red stain affinity for amyloid of unknown origin found in secondary amyloidosis. However, the amyloid of immunoglobulin origin, characteristic of primary amyloid, is resistant to KMnO4. The amyloid deposit from our patient was resistant to KMnO4 which suggested that the pulmonary amyloid was a coincidental nodular amyloid deposit in the lung rather than secondary amyloidosis.

Amyloidosis↗