Distinctive cellular immunity in genetically susceptible BALB/c mice recovered from Leishmania major infection or after subcutaneous immunization with killed parasites

• Published in: The Journal of immunology (1950) Vol. 138; no. 12; pp. 4450 - 4456
• Main Authors: Liew, FY, Dhaliwal, JS
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Assoc Immnol 15-06-1987; American Association of Immunologists
• Subjects: Animal protozoal diseases; Animals; Biological and medical sciences; Convalescence; Disease Susceptibility; Female; Hypersensitivity, Delayed - immunology; Immunity, Cellular - radiation effects; Immunization; Immunization, Passive; Infectious diseases; Leishmania major; Leishmania tropica - immunology; Leishmaniasis - genetics; Leishmaniasis - immunology; Lymphokines - biosynthesis; Macrophage-Activating Factors; Male; Medical sciences; Mice; Mice, Inbred BALB C - genetics; Mice, Inbred BALB C - immunology; Mice, Inbred BALB C - parasitology; Mice, Inbred CBA - immunology; Parasitic diseases; Protozoal diseases; T-Lymphocytes - immunology; T-Lymphocytes - transplantation; Whole-Body Irradiation; Immunoprotection; Protozoa; Protozoal disease; Macrophage activating factor; Rodentia; Inheritance; Leishmania tropica major; Cellular immunity; Experimental animal; Leishmaniasis; Active immunization; Infection; Antigen; Vertebrata; Experimental disease; Mammalia; Sensitivity resistance; Mouse; T-Lymphocyte; Production; Rhizoflagellata; Subcutaneous administration; Intraspecific comparison; Inactivated strain
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.138.12.4450

Genetically susceptible BALB/c mice are refractory to further infection after recovery from Leishmania major infection after a sublethal dose of gamma-irradiation. In contrast, mice immunized with killed promastigotes s.c. develop exacerbated lesions after infection. Both groups of mice produce only a low level of specific antibody and no detectable cytotoxic T cells, but do have a strong antigen-specific DTH, which is adoptively transferable with Lyt-1+2-, L3T4+ T cells. Kinetic and histological studies revealed that mice immunized s.c. developed Jones-Mote hypersensitivity, peaking at 15 hr. with little mononuclear cell infiltration at the site of antigen administration; whereas mice that had recovered from infection developed tuberculin-type of reactivity, peaking at 24 to 48 hr, with intense mononuclear cell infiltration. Splenic T cells from recovered mice, when injected into the footpads of normal recipients together with live promastigotes, were able to retard lesion development; whereas T cells from s.c. immunized mice, when similarly transferred, accelerated disease progression. Antigen-specific culture supernatant of spleen cells from recovered mice also activated normal resident peritoneal macrophages to kill intracellular L. major amastigotes and tumor cells. Culture supernatants of spleen cells from s.c. immunized or normal mice were devoid of such activities. Part of the macrophage-activating potential can be inhibited by antibody specific for IFN-gamma. These results therefore demonstrate that whereas the Jones-Mote reaction is correlated with disease exacerbation, the tuberculin-type of DTH may be protective. Furthermore, in vivo immunity is directly related to the capacity of T cells to produce macrophage-activating factor.