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R L Yowell

Publications and source records attributed to R L Yowell.

8 recordsLinked to original sources
PubMed1979

Ir gene defects may reflect a regulatory imbalance. I. Helper T cell activity revealed in a strain whose lack of response is controlled by suppression.

A singular responsiveness to HEL was revealed in a peripheral lymphoid compartment of the genetically nonresponsive H-2b mouse. Although i.p. injection of HEL induces suppression and a lack of anti-HEL production, following footpad injection there is an early emergence in the popliteal lymph node (P-LN) of HEL-specific helper activity and plaque-forming cells. Furthermore, the early P-LN transiently expresses one of two T cell types needed for initiation of suppression. Delayed recruitment of the second required cell-type permits the induction of efficient suppression. There is only a short period during which there is concurrent representation of the two T cell subpopulations, and by mixing early and late deficient P-LN T cells, suppression could be established. The general implication of these results is that although a vigorous helper cell potential may exist in a strain nonresponsive to a multideterminant antigen, it can be obscured by a regulatory cell imbalance that results in the manifestation of a generalized Ir gene "defect."

Animals↗
PubMedDate not supplied

The role of electron microscopy in evaluating ciliary dysfunction: report of a workshop.

This report summarizes the proceedings of a workshop organized with the purpose of bringing together many of those with substantial experience in this troublesome area of pathology for an active interchange of ideas, opinions, problems, and solutions. Recognition was given the fact that current knowledge and technical capabilities are woefully inadequate for dealing with the diagnostic questions now being asked. Until such time as these inadequacies can be remedied, a very conservative approach to the interpretation of ultrastructural studies is advocated.

Adolescent↗
PubMedDate not supplied

Vascular rejection and its relationship to allograft coronary artery disease.

We have prospectively monitored 268 patients by our previously described method of routine immunofluorescence of endomyocardial biopsy specimens. We have classified these patients according to their rejection pattern: cellular, vascular, and mixed. The criteria for these designations have been previously described. In this study we retrospectively reviewed coronary angiograms of these patients to assess the presence and time-course of developing allograft coronary artery disease. All available explanted hearts and postmortem hearts were also assessed by light microscopic examination for acute coronary vasculitis and allograft coronary artery disease and by immunofluorescent microscopy for vascular immune complex deposition in a manner identical to immunofluorescent microscopic examination of endomyocardial biopsy specimens. Patients were also monitored for sensitization to immunoprophylactically administered murine monoclonal CD3 antibody (OKT3) and those demonstrated to be sensitized were separately analyzed. Clinical features and treatment of patients were retrospectively reviewed. We found that 141 patients could be classified as having cellular rejection, 76 as having vascular rejection, and 52 as having a mixed rejection pattern. The allograft survival in vascular rejection patients was significantly worse than in allografts of patients with cellular or mixed rejection, confirming our earlier results. Most importantly, we found a significant difference in the time to the development of allograft coronary artery disease based on the rejection pattern. This difference existed whether or not patients sensitized to OKT3 were excluded from evaluation. Patients with mixed rejection had an intermediate time to the development of allograft coronary artery disease between that of patients with cellular and vascular rejection.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Disease↗
PubMedDate not supplied

Sensitization to OKT3 monoclonal antibody in heart transplantation: correlation with early allograft loss.

Because administration of murine monoclonal anti-CD3 antibody (OKT3) may result in the formation of human antimouse antibody, which complexes with OKT3, we conducted this study to assess the incidence and effect of human antimouse antibody formation during prophylactic administration of OKT3 in heart transplantation. Human antimouse antibody developed in eight of 55 (14%) cardiac allograft recipients receiving OKT3 prophylaxis as measured by enzyme-linked immunosorbent assay. Additionally, two recipients had an inexplicable rise in CD3+ lymphocytes during therapy without detectable antibody. The outcome of these 10 sensitized recipients was compared with that of 45 nonsensitized recipients. Age, preoperative diagnosis, hemodynamics, and the need for intravenous inotropes or mechanical assistance before transplantation were similar in both groups. No female patients were in the sensitized group, whereas 33% of the nonsensitized group were female patients. A trend toward greater sensitization when prophylaxis was extended to 21 days (28%) compared with the more conventional 14-day administration (10%) was not statistically significant. Retransplantation because of rejection was required in a single patient in each group. Allograft survival was significantly lower by 3 months in the sensitized group, and allograft loss caused by rejection selectively accounted for that difference. In survivors, rejection frequency and infectious complications were similar. These findings suggest that sensitization to OKT3 occurs at low frequency after prophylactic administration in heart transplantation but is associated with an increased frequency of graft loss because of rejection.

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