Genetic control of immunity to Trichinella spiralis in mice: capacity of cells from slow responder mice to transfer immunity in syngeneic and F1 hybrid recipients

• Published in: Immunology Vol. 56; no. 2; pp. 203 - 211
• Main Authors: WAKELIN, D, DONACHIE, A. M, GRENCIS, R. K
• Format: Journal Article
• Language: English
• Published: Oxford Blackwell 01.10.1985
• Subjects: Animals; Applied sciences; Biological and medical sciences; Dose-Response Relationship, Immunologic; Exact sciences and technology; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Genetics of the immune response; Hybridization, Genetic; Immune Tolerance; Immunization, Passive; Immunobiology; Kinetics; Lymphocyte Activation; Lymphocytes - immunology; Major Histocompatibility Complex; Male; Mice; Mice, Inbred C57BL; Mice, Inbred Strains; Other techniques and industries; Trichinellosis - immunology; Trichinellosis - parasitology; Immune response; Major histocompatibility system; Rodentia; H-2-System; Immunity; Adoptive transfer; Vertebrata; Regulation(control); Mammalia; Gene; Mouse; Genetics; Parasitidae; Trichinella spiralis
• ISSN: 0019-2805; 1365-2567

Mice of the C57BL/10 (B10) strain are slow responders to infection with T. spiralis in terms of ability to expel worms from the intestine. Compared with rapid-responder NIH mice, infection stimulates a slower and reduced blast cell response in the draining mesenteric lymph node (MLN). Transfer of immune cells from the MLN (MLNC) does not accelerate worm expulsion from naive B10 recipient mice, even though MLNC from this strain effectively transfer immunity to (B10 X NIH) F1 recipients. In common with other B10 background mice C57BL/10 show an infection-dose related suppression of immunity to T. spiralis. Such suppression does not appear to determine the response to MLNC, as adoptive transfer into B10 recipients was not enhanced by reducing the level of challenge infection given, and transfer into F1 recipients was unaffected by simultaneous transfer of lymphocyte populations from donors infected at a level which would induce suppression. A hypothesis is proposed which relates slow response status to (i) the inherent capacity of the intestinal inflammatory component of worm expulsion, and (ii) the outcome of infection-dose related stimulatory and suppressive influences acting on the two interacting lymphocyte components of expulsion. The relevance of H-2-linked and non-H-2 genes to the control of the response is discussed.