IL-4 induces a Th2 response in Leishmania major-infected mice

• Published in: The Journal of immunology (1950) Vol. 148; no. 4; pp. 1182 - 1187
• Main Authors: Chatelain, R, Varkila, K, Coffman, RL
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Assoc Immnol 15-02-1992; American Association of Immunologists
• Subjects: Animals; Biological and medical sciences; Cell Differentiation; Experimental protozoal diseases and models; Female; Infectious diseases; Interferon-gamma - physiology; Interleukin-4 - physiology; Leishmania major; Leishmania tropica - immunology; Leishmaniasis, Cutaneous - immunology; Medical sciences; Mice; Mice, Inbred BALB C; Mice, Inbred C3H; Parasitic diseases; Protozoal diseases; Recombinant Proteins - pharmacology; T-Lymphocytes, Helper-Inducer - drug effects; T-Lymphocytes, Helper-Inducer - immunology; Protozoa; Protozoal disease; Immune response; Induction; Rodentia; Cytokine; Helper cell; Cellular immunity; Leishmaniasis; Cell subpopulation; Infection; Vertebrata; Interleukin 4; Mammalia; Mouse; Animal; T-Lymphocyte; Rhizoflagellata; Leishmania major
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.148.4.1182

The infection of mice with Leishmania major can cause either a fatal disseminated disease or a localized healing disease, depending on the genetic background of the mice. A strong correlation has been shown between disease outcome and the nature of the T cell response, with healer strains developing a Th1-like response and nonhealer strains a Th2-like response. The treatment of nonhealer BALB/c mice with a single dose of an anti-IL-4 antibody, given at the time of infection with L. major, allowed these mice to develop healing Th1-like responses, suggesting that IL-4 is required in BALB/c mice for the differentiation of Th cells into Th2 cells. Anti-IL-4 had to be present during the first 2 wk of infection to have this effect. Anti-IL-4 caused a marked shift from a Th2 to a Th1 pattern of cytokine expression within 4 days, in vivo, and injections of IL-4 had the opposite effect on the early response in healer C3H/HeN mice. These findings demonstrate that IL-4 can induce the development of Th2 response to L. major infection in vivo.