The Journal of Experimental Medicine
Keystone Symposia
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The Journal of Experimental Medicine, Vol 139, 1415-1430, Copyright © 1974 by The Rockefeller University Press

ARTICLE

THE MEDIATOR OF CELLULAR IMMUNITY : VII. LOCALIZATION OF SENSITIZED LYMPHOCYTES IN INFLAMMATORY EXUDATES



D. D. McGregor 1 and Pamela S. Logie 1

1 From the Immunobiological Research Laboratories, Trudeau Institute, Inc., Saranac Lake, New York 12983

Peritoneal exudates induced in rats infected with Listeria monocytogenes contain sensitized lymphocytes which can protect normal recipients against a Listeria challenge. The protective cells arise in lymphoid tissue remote from the peritoneal cavity. Those formed in the caudal lymph nodes of subcutaneously infected rats are delivered to the thoracic duct and hence to the blood from where they are drawn into exudates. Immunoblasts are the most immature members of this protective cell population and they alone among the cells in central lymph localize in exudates induced by killed bacteria. They do so in substantial numbers, but only during the early postinduction period.

The "homing" of immunoblasts to inflammatory foci seems to be determined by a general property of the cells rather than their immunological commitment; however, the intense inflammation induced by organisms to which an animal has been specifically sensitized is accompanied by an exuberant influx of immunoblasts into lesions. Sensitized lymphocytes that extravasate in the inflamed peritoneal may generate more of their own kind, but some give rise to small lymphocytes. The latter also have protective properties and, with time, comprise an increasing portion of the protective cell population.

The results imply that the tissue disposition of sensitized lymphocytes in the body is determined by a complementary relationship between blood-borne immunoblasts and vascular endothelium in inflamed tissue. The results also provide a plausible explanation for the concentration of sensitized lymphocytes at sites of microbial implantation where they alone would be expected to collaborate with monocyte-derived macrophages in the control of infection.

 Submitted on February 11, 1974


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