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D M Parrott

Publications and source records attributed to D M Parrott.

At least 73 records · Page 4Linked to original sources

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.

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Studies of chemotaxis of lymphocytes.

Lymphoblasts migrate into filters towards chemoattractants in vitro. Human lymphoblasts maintained in continuous culture and mouse lymphoblasts from unsensitized lymph nodes show chemotactic responses and migrate towards the same chemotactic factors as neutrophils and macrophages, namely activated plasma, casein, denatured serum albumin, oxazolone. On the other hand, mouse lymphoblasts from oxazolone-sensitized lymph nodes show considerable random migration and chemokinesis but not chemotaxis. The migration of lymphoblasts to these agents appears not to be antigen-specific. These migratory properties of lymphoblasts are probably relevant to their migration into inflammatory sites in vivo.

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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.

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The different migratory characteristics of lymphocyte populations from a whole spleen transplant.

Spleens from AS x BN donor rats labelled in vivo by multiple doses of [3H]thymidine were transplanted into syngeneic recipients by anastomosis to the abdominal great vessels. The recipients were killed 1-5 days after receiving the whole spleen transplants and the numbers and location of the [3H]thymidine-labelled cells which had migrated from the labelled donor spleen traced by means of autoradiographs of sections, imprints and smears of various recipient lymphoid tissues. These results were compared with the migration pattern of labelled dissociated spleen cell suspensions injected intravenously. The latter consists almost entirely of small lymphocytes which migrate to T or B areas of recipient spleen, lymph nodes and Peyer's patches. The labelled whole spleens also contained cells which migrated to the T and B areas of recipient lymphoid tissues, but in addition contained many lymphoid cells which migrated to the red pulp of the recipient spleen and to the lamina propria of the gut. These experiments showed, therefore, that the spleen contains mobile elements which have not been detected by transfer of spleen cell suspensions.

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