David F. Gray

Allergy in Experimental Rat Tuberculosis.

& Palladino (1953) found rats exposed to airborne tubercle bacilli to be as susceptible as guinea-pigs to initial infection. Reports on the response of tuberculous rats to local or systemic contact with tuberculin are sufficiently contradictory to be difficult to assess and interpret. In an attempt to do so, Rich (1951) remarked that hypersensitivity to tuberculin and to intact tubercle bacilli developed feebly or not at all in infected rats on a balanced diet. Analysis of these early reports on the behaviour of infected rats reveals that Hehre & Freund (1939), as well as Wessels, Ratcliffe & Palladino and Kumashiro all observed, after several weeks, a dramatic arrest in the progress of the disease that followed an early uninhibited multiplication of the bacilli within rapidly developing lesions. It was this observation that directed the attention of the present writers to the similarity between rat and mouse tuberculosis. Such an arrest in the multiplication of bacilli in lung lesions, coinciding as it did with the onset of the immune phase in mice, led to the discovery of tuberculin allergy in that species. In 1952 (Gray & Mattinson) it was shown that the reputedly resistant and anergic mouse could be infected with about one viable unit, given intranasally, and that temporarily unrestricted multiplication and lung involvement was replaced by an immune phase of the disease. This in turn was characterized by a positive footpad reaction to 1/25 tuberculin (Gray & Jennings, 1955) and it was also shown that, as the immune phase progressed the mice became susceptible to fatal shock occurring 24-48 hr. after intraperitoneal inoculation of concentrated tuberculin. Subsequent work has elaborated these findings. Studies begun in 1955 confirmed the supposition that rats, like mice, could be

THE SPECIFICITY OF CELLULAR IMMUNITY.

1. Non-specific stimulation of mice by a detergent lacking in vitro antibacterial activity, Triton WR 1339, produces a steady state in the course of experimental tuberculosis at about the same level as specific immunization, and does so independently of delayed allergy. 2. This effect is achieved in a much shorter time than is required by the normal immunological processes and the relative duration of enhanced resistance in each case is yet to be worked out. 3. Triton fails to enhance an existing, specifically acquired immunity. 4. There is no evidence so far that the mechanism involved is the same in both instances. If it were found to be the same, then the present concept of a specific cellular immunity would need to be revised.