Host defenses in murine malaria: humoral immunity to Plasmodium berghei in mice.

Humoral immunity to Plasmodium berghei infection of F1 hybrid B6D2 (C57B1/6 X DBA/2) mice was investigated using an immune serum prepared from mice which survived a lethal challenge of erythrocytic stage P. berghei because of previous vaccination with formalin-killed P. berghei.

Induction and suppression of cross-reactive antituberculosis immunity after Mycobacterium lepraemurium infection of mice.

Mice immunized with 10(8) live Mycobacterium lepraemurium in the footpad showed increased resistance to infection with BCG or M. tuberculosis R1Rv. This resistance could be transferred adoptively with lymphoid cells, signifying that the immunity was cross-reactive rather than nonspecific.

Effect of Mycobacterium bovis BCG vaccination upon Mycobacterium lepraemurium infection.

Mice were infected with 10(8) Mycobacterium lepraemurium in the footpad (unsuppressed mice), and some of these animals were concurrently given 10(9) heat-killed M. lepraemurium intravenously (suppressed mice). These groups of mice were preimmunized with 10(7) viable organisms of Mycobacterium bovis BCG by several routes.

The mediator of cellular immunity. XII. Inhibition of activated T cells by Newcastle disease virus.

Newcastle disease virus (NDV) can interact in at least two ways with rat T cells. By adsorbing to circulating lymphocytes, the virus can transiently deflect the cells from lymph nodes and inflammatory exudates induced in the peritoneal cavity. T cells are affected regardless of age, state of activation, or position in the mitotic cycle.

Tularaemia in the rat. I. The cellular basis on host resistance to infection.

Rats infected with the live vaccine strain (LVS) of Francisella tularensis develop in vivo and in vitro evidence of cellular hypersensitivity and a concomitant state of cellular resistance to infection. They key role of sensitized lymphocytes in cellular resistance was domonstrated in transfer experiments. Using this technique, it was shown that thoracic duct lymphocytes from Francisella immune donors conferred specific antimicrobial resistance on normal recipients, whereas antiserum afforded no protection whatsoever.

The mediator of cellular immunity. VII. Localization of sensitized lymphocytes in inflammatory exudates.

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.

The mediator of cellular immunity. VI. Effect of the antimitotic drug vinblastine on the mediator of cellular resistance to infection.

The antimitotic drug vinblastine (Vbl) has a profound impact upon the specifically sensitized lymphocytes that transfer cellular resistance to Listeria monocytogenes. A 12-h pulse of the drug given to prospective donors during the first week of an immunizing Listeria infection inhibits the delivery of protective lymphocytes to the thoracic duct and their subsequent movement into an inflammatory exudate induced in the peritoneal cavity. The effect of Vbl is clearly related to its antimitotic activity, not to an effect on lymphocytes regardless of their position in the division cycle.