Parasite-specific immune responses to Onchocerca lienalis microfilariae in normal and immunodeficient mice.
The model of Onchocerca lienalis microfilariae (mf) in CBA mice has been employed to examine the immunological mechanisms underlying the destruction of skin-dwelling mf in onchocerciasis. Comparative studies among immunologically intact (CBA/H) or deficient (CBA/N, T-cell-deprived) syngeneic animals demonstrated that levels of mf of a primary infection were reduced most rapidly in fully immunocompetent mice. Significant reductions in recoveries of a secondary infection were evident in CBA/H (80%) and CBA/N (44%) mice, but not in T-cell-deprived animals. The establishment of primary and secondary infections was apparently not influenced by complement, as judged by C3 depletion with Cobra Venom Factor. Eosinophilia was demonstrated to varying degrees in all infected animals; similar levels occurred in CBA/H and CBA/N mice which were greatly elevated after mf challenge. In contrast, the eosinophil response of T-cell-deprived mice was weak and not potentiated during secondary infection. Type I immediate hypersensitivity responses to soluble mf antigen (mf-Ag) were mounted by all groups, but significantly less strongly in T-cell-deprived mice. Type IV delayed responses were generally weak, although CBA/N mice reacted strongly in the early phase of primary infections. During the first 2 weeks of infection CBA/H and T-cell-deprived mice mounted rapid IgM responses to mf-Ag. Subsequently, levels of IgG2a, IgG2b and IgG1 increased in all mice. There was a potentiated IgG2a, IgG2b and IgG1 response in all groups following challenge, with levels of IgG1 highest in CBA/H mice. IgE responses were also detected by passive cutaneous anaphylaxis during primary and secondary infections. Peak levels of parasite-specific antibodies coincided with the timing of mf clearance.
Carlow
C K
CK
Department of Medical Helminthology, London School of Hygiene and Tropical Medicine, St Albans, Herts, UK.
Dobinson
A R
AR
Bianco
A E
AE
D000818:Animals; D000909:Antibodies, Helminth / Q000096:biosynthesis*; D000947:Antigens, Helminth / Q000276:immunology; D004195:Disease Models, Animal; D004802:Eosinophilia / Q000276:immunology; D005260:Female; D006969:Hypersensitivity, Immediate; D007108:Immune Tolerance; D007111:Immunity, Cellular; D007070:Immunoglobulin A / Q000096:biosynthesis; D007073:Immunoglobulin E / Q000096:biosynthesis; D007074:Immunoglobulin G / Q000096:biosynthesis; D007075:Immunoglobulin M / Q000096:biosynthesis; D007136:Immunoglobulins / Q000096:biosynthesis*; D051379:Mice; D008808:Mice, Inbred CBA; D008842:Microfilariae / Q000276:immunology; D009854:Onchocerca / Q000254:growth & development / Q000276:immunology*; D009855:Onchocerciasis / Q000276:immunology*; D012867:Skin / Q000469:parasitology
D000909:Antibodies, Helminth; D000947:Antigens, Helminth; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D007136:Immunoglobulins; D007073:Immunoglobulin E