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Biomedical subjects

M L Rose

Publications and source records attributed to M L Rose.

122 records · Page 7Linked to original sources
PubMed1978

The accumulation of immunoblasts in extravascular tissues including mammary gland, peritoneal cavity, gut and skin.

The migration of [125I]UdR labelled mesenteric (MLN) and peripheral T immunoblasts (PLN) has been followed in mice with multiple sites attractive to immunoblasts. The sites studied were the inflamed gut (produced by Trichinella spiralis infection), inflamed skin, the peritoneal cavity and the mammary glands of lactating mice. PLN were capable of assembling in all of the four sites and in the presence of both inflamed gut and inflamed skin, PLN accumulated preferentially in the skin. MLN, in contrast migrated only to the gut and mammary glands and not to the skin or peritoneal cavity, and could not be diverted from one site to another. Time course experiments revealed that whereas PLN migrate rapidly through the inflamed gut, they are retained in the skin for at least 3 days.

Animals↗
PubMed1976

Factors which determine the accumulation of immunoblasts in gut and skin.

The capacity of immunoblasts from two sources (1) peripheral lymph nodes draining the site of application of a contact sensitizer and (2) mesenteric lymph nodes from mice infected with the gut parasite T. spiralis to migrate to the gut and to inflamed skin sites were compared. The peripheral lymph node blasts readily entered skin sites in a non-specific way but failed to migrate to the gut even when inflammation was induced. By contrast, the mesenteric lymph node blasts readily migrated to the gut in normal mice and in increased amounts to the gut of mice infected with T. spiralis or inflamed with oral turpentine. A small proportion of mesenteric lymph node blasts did, however, migrate, non-specifically to the skin but in much smaller amounts than peripheral lymph node blasts. We conclude that the migration of immunoblasts to the gut has some specificity related to the source from which the cells were taken but little specificity with regard to intraluminal antigen.

Animals↗
PubMed1976

75SeL-selenomethionine: a new isotopic marker for lymphocyte localisation studies.

L-selenomethionine (SeM), an analogue of methionine containing Se, is incorporated by mouse and rat lymphocytes in vitro: labelled with 75Se (75SeM) it emits gamma-rays distinguishable in energy from those of 125I and 51Cr. The usefulness of 75SeM for lymphocyte localisation studies was investigated. Both B and T cells incorporated 75SeM. Reutilization of the isotope in the mouse after injection of killed cells or allogeneic cells into immunized recipients was 1-2% of the injected dose. The immunocompetence of labelled mouse T and B cells was assessed in irradiated recipients, no effect of 75SeM incorporation being found. The distribution of labelled lymphocytes from various tissues in syngeneic recipients was found to be comparable to that previously obtained with 51Cr.

Animals↗
PubMed1976

I. Effect of Trichinella spiralis infection on the migration of mesenteric lymphoblasts and mesenteric T lymphoblasts in syngeneic mice.

The migration of [125I]UdR-labelled mesenteric lymph node cells in NIH strain mice at various times after inis produced an enhanced accumulation of mesenteric immunoblasts in the small intestine at 2 and 4 days after infection but not at later times. The enhanced migration occurred when using cells from both uninfected and infected donors, denoting an absence of antigenic specificity. This effect is not secondary to a reduced arrival of cells at sites away from the gut in infected mice, but to a primary increase of the arrival in the small intestine. Mesenteric T lymphoblasts (separated on a nylon-wool column) migrated to the small intestine of uninfected recipients and appear to be a major portion of the population which migrate to the gut of infected recipients. Our results were confirmed using 51Cr to label mesenteric cells. We conclude that the parasite causes the small intestine to become more attractive or retentive for mesenteric blast cells early during infection.

Animals↗
PubMedDate not supplied

Association of pretransplantation antiheart antibodies with clinical course after heart transplantation.

METHODS: Sera from 129 patients awaiting heart transplantation were assayed for the presence of IgM and IgG antiheart antibodies by means of sodium dodecyl sulphate-polyacrylamide gel electrophoresis and Western blotting. The patients' posttransplantation clinical course was assessed with regard to the amount of methylprednisolone, rabbit antithymocyte globulin, and OKT3 anti-T cell antibody, and the number of biopsy-confirmed rejection episodes. Before undergoing heart transplantation, approximately half the patients had weak IgM (45%) and weak IgG (48%) antiheart antibodies. However, 22.5% of the patients had strong IgM antiheart antibodies before transplantation, and they required more methylprednisolone than those who were negative and weak and approximately twice as much rabbit antithymocyte globulin as those who were negative, weak, or moderate. Six of the patients in this group required OKT3 therapy, and additionally they had a significantly greater number of rejection episodes than those patients who were negative (p = 0.006), or who had weak antiheart antibodies before transplantation (p = 0.001). RESULTS AND CONCLUSIONS: Analysis of the pattern of banding of strong IgM antiheart antibody sera showed antiheart antibodies most frequently against myocardial proteins of 35, 42, 50, 60, 70, 110, 120, 150, 180, and 200 kDa. Several of these proteins were characterized by two-dimensional polyacrylamide gel electrophoresis and Western blotting as tropomyosin (35 kDa), actin (42 kDa), heat shock protein 60 (60 kDa), and heat shock protein 70 (70 kDa). All strong antiheart antibody sera showed reactivity against a 200 kDa protein corresponding to myosin heavy chain.

Adult↗
PubMedDate not supplied

Antiendothelial antibodies after heart transplantation: the accelerating factor in transplant-associated coronary artery disease?

Although the precise cause of transplant-associated coronary artery disease is unknown, immune mechanisms have been implicated. Using the techniques of SDS-PAGe and Western immunoblotting, we have previously shown that a strong positive correlation exists between the development of coronary artery disease and the presence of antiendothelial antibodies reactive with a doublet of polypeptides of approximately 60 and 62 kDa. We have now extended this study to investigate the temporal pattern of antiendothelial antibody formation after transplantation and its association with cellular rejection episodes. The original study used patients in whom coronary artery disease had developed early after transplantation, that is at 1 or 2 years. Here we investigate whether antiendothelial antibodies are also made in patients in whom the disease does not develop until 5 to 10 years after heart transplantation and whether the antibodies are found in patients with severe nontransplant atherosclerosis. We confirm the 60 to 62 kDa antigens are membrane bound, and recalculation of their molecular mass makes the doublet 56 and 57.5 kDa. The results show that antibodies specific for the doublet of endothelial antigens are rarely produced by patients other than those in whom rapidly progressing coronary artery disease develops early after transplantation. The antibodies are unrelated to cellular rejection episodes. We believe their production may be an accelerating factor for the rapid development of transplant-associated coronary artery disease.

Adolescent↗