B cells and antibody response in calves primary-infected or re-infected with Cooperia oncophora: influence of priming dose and host responder types.
We investigated whether the generation of protective memory humoral immunity in Cooperia oncophora infected calves occurs in a dose-dependent way and whether it depends on the animal responder types. To this end, serum and mucus antibody responses were measured in animals primary-infected with 30000 or 100000 L3, treated with anthelmintics and subsequently challenged with 100000 L3. A detailed phenotypic and functional analysis of B cells was done in animals infected once or twice with 100,000 L3. Based on the similarity in parasitological variables of animals primed with 30000 or 100000 L3, we concluded that with these doses priming conferred protection in a dose-independent way. Upon challenge significant increases in Cooperia-specific serum and mucus IgG1 and IgA and total serum IgE titres were induced in primed animals in a dose-independent way. In contrast, intermediate and low responders differed in the onset of the production of Cooperia-specific serum IgG1. Furthermore, not only the onset but also the level of total serum IgE significantly differed between intermediate and low responders. Phenotypic and functional analysis of B lymphocytes revealed that (i). priming induced the generation of memory B cells which upon challenge readily differentiated into antibody secreting cells; (ii). sensitised B cells were more efficiently recruited to the intestinal effector sites; (iii). based on the expression of CD62L and CD86 two distinct B cell subpopulation could be differentiated. CD62L(+)CD86(-) B cells that were likely lymphocytes not yet activated and with an enhanced recirculation capacity, and CD62L(-)CD86(+) B cells that were activated B cells with a reduced recirculation ability; and finally (iv). the increased expression of CD86 and subsequent correlations with parameters of the T helper 2 immune response induced by C. oncophora, suggested that CD86- interactions are involved in the generation of protective immunity against Cooperia.
Department of Infectious Diseases and Immunology, Utrecht University, PO Box 80.165, 3508 TD, Utrecht, The Netherlands.
K
K
Kanobana
A
A
Koets
F N J
FN
Kooyman
N
N
Bakker
H W
HW
Ploeger
L
L
Vervelde
D000818:Animals; D000871:Anthelmintics / Q000627:therapeutic use; D000909:Antibodies, Helminth / Q000097:blood*; D015703:Antigens, CD / Q000032:analysis; D001402:B-Lymphocytes / Q000276:immunology*; D051940:B7-2 Antigen; D002417:Cattle; D002418:Cattle Diseases / Q000188:drug therapy / Q000276:immunology* / Q000469:parasitology*; D004306:Dose-Response Relationship, Immunologic; D005260:Female; D007070:Immunoglobulin A / Q000032:analysis / Q000097:blood; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000032:analysis / Q000097:blood; D007156:Immunologic Memory; D007411:Intestinal Diseases, Parasitic / Q000188:drug therapy / Q000276:immunology*; D008213:Lymphocyte Activation; D008562:Membrane Glycoproteins / Q000032:analysis; D009093:Mucus / Q000276:immunology; D010270:Parasite Egg Count; D012008:Recurrence; D014253:Trichostrongylosis / Q000188:drug therapy / Q000276:immunology*; D014254:Trichostrongylus / Q000276:immunology*
D000871:Anthelmintics; D000909:Antibodies, Helminth; D015703:Antigens, CD; D051940:B7-2 Antigen; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D008562:Membrane Glycoproteins; D007073:Immunoglobulin E