Bogdan C, Gessner A, Solbach W, Rollinghoff M, 1996. Invasion, control and persistence of Leishmania parasites. Curr Opin Immunol 8 :517–525.
Liew FY, O’Donnell CA, 1993. Immunology of leishmaniasis. Adv Parasitol 32 :161–259.
Lohoff M, Gessner A, Bogdan C, Röllinghoff M, 1998. The Th1/ Th2 paradigm and experimental murine leishmaniasis. Int Arch Allergy Immunol 115 :191–202.
Reiner SL, Locksley RM, 1995. The regulation of immunity to Leishmania major.Annu Rev Immunol 13 :151–177.
Solbach W, Laskay T, 2000. The host response to Leishmania infection. Adv Immunol 74 :275–317.
Scott P, Natovitz P, Sher A, 1986. B lymphocytes are required for the generation of T cells that mediate healing of cutaneous leishmaniasis. J Immunol 137 :1017–1021.
Brown DR, Reiner SL, 1999. Polarized helper-T-cell responses against Leishmania major in the absence of B cells. Infect Immun 67 :266–270.
Babai B, Louzir H, Cazenave PA, Dellagi K, 1999. Depletion of peritoneal CD5+ B cells has no effect on the course of Leishmania major infection in susceptible and resistant mice. Clin Exp Immunol 117 :123–129.
Sacks DL, Scott PA, Asofsky R, Sher A, 1984. Cutaneous leishmaniasis in antiIgM-treated mice: enhanced resistance due to functional depletion of a B cell-dependent T cell involved in the suppressor pathway. J Immunol 132 :2072–2077.
Hale C, Howard JG, 1981. Immunological regulation of experimental cutaneous leishmaniasis. 2. Studies with Biozzi high and low responder lines of mice. Parasite Immunol 3 :45–55.
Olobo JO, Handman E, Curtis JM, Mitchell GF, 1980. Antibodies to Leishmania tropica promastigotes during infection in mice of various genotypes. Aust J Exp Biol Med Sci 58 :595–601.
Su H, Feilzer K, Caldwell HD, Morrison RP, 1997. Chlamydia trachomatis genital tract infection of antibody-deficient gene knockout mice. Infect Immun 65 :1993–1999.
Yang DM, Rogers MV, Liew FY, 1991. Identification and characterization of host-protective T-cell epitopes of a major surface glycoprotein (pg63) from Leishmania major.Immunology 72 :3–9.
Eperon S, Bronnimann K, Hemphill A, Gottstein B, 1999. Susceptibility of B-cell deficient C57Bl/6 (μMT) mice to Neospora caninum infection. Parasite Immunol 21 :225–236.
Matsuzaki G, Vordermeier HM, Hashimoto A, Nomoto K, Ivanyi J, 1999. The role of B cells in the establishment of T cell response in mice infected with an intracellular bacteria, Listeria monocytogenes.Cell Immunol 194 :178–185.
Howard JG, Hale C, Liew FY, 1980. Immunological regulation of experimental leishmaniasis. III. Nature and significance of specific suppression of cell-mediated immunity in mice highly susceptible to Leishmania tropica.J Exp Med 152 :594–607.
Howard JG, Hale C, Liew FY, 1981. Immunological regulation of experimental cutaneous leishmaniasis. IV. Prophylactic effect of sublethal irradiation as a result of abrogation of suppressor T cell generation in mice genetically susceptible to Leishmania tropica.J Exp Med 153 :557–568.
DeKrey GK, Titus RG, 1999. A method for the isolation and analysis of leucocytic cells from leishmanial ear lesions in mice. J Immunol Methods 228 :1–11.
Titus RG, DeKrey GK, Morris RV, Suares MBP, 2001. Interleukin-6-deficiency influences cytokine expression in susceptible BALB mice infected with Leishmania major but does not alter the outcome of disease. Infect Immun 69 :5189–5192.
Soares MBP, David JR, Titus RG, 1997. An in vitro model for infection with Leishmania major that mimics the immune response in mice. Infect Immun 65 :2837–2845.
Harris DP, Haynes L, Sayles PC, Duso DK, Eaton SM, Lepak NM, Johnson LL, Swain SL, Lund FE, 2000. Reciprocal regulation of polarized cytokine production by effector B and T cells. Nature Immunol 1 :475–482.
B cell-deficient C57Bl/6 (μMT) mice were resistant to Leishmania major after both primary and secondary parasite challenge. However, unlike in wild-type mice, secondary infection in μMT mice was not accompanied by a marked delayed type hypersensitivity-like response, and interferon-γ (IFN-γ) levels were approximately half of those in wild-type mice. These results suggest that B cells are involved in IFN-γ production and the pathology of secondary infection.