Murine Taenia crassiceps cysticercosis : H-2 complex and sex influence on susceptibility
Several inbred strains of mice were infected by intraperitoneal injection of ten Taenia crassiceps cysticerci per mouse. Genes linked with the major histocompatibility complex (H-2) were found to influence parasite growth greatly, as demonstrated by the different parasite loads of H-2 congenic mice...
Saved in:
Published in: | Parasitology research (1987) Vol. 77; no. 3; pp. 243 - 246 |
---|---|
Main Authors: | , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Berlin
Springer
01-01-1991
|
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Several inbred strains of mice were infected by intraperitoneal injection of ten Taenia crassiceps cysticerci per mouse. Genes linked with the major histocompatibility complex (H-2) were found to influence parasite growth greatly, as demonstrated by the different parasite loads of H-2 congenic mice with BALB background: BALB/c (H-2d) mice were the most susceptible, whereas BALB/k (H-2k) and BALB/b (H-2b) animals were comparatively resistant. Non-H-2 genes had no significant effect on susceptibility in H-2d strains, as reflected by the similar parasite loads in BALB/c, DBA/2, and (BALB/c x DBA/2)F1 mice. Using the H-2b (BALB/b, C57BL/6J) and H-2k (C3H/HeJ, BALB/k, and C3HeB/FeJ) strains, we found that non-H-2 background genes caused a small but significant influence on parasite load. A recombinant mouse strain alleles (Kk, Ik, Sd, Dd) was also susceptible, indicating that S and/or D regions of the H-2d complex are probably involved in the control of resistance to murine cysticercosis. Females of all mouse strains were more susceptible than males. The same effects were observed for H-2 genes and sex, with two strains of T. crassiceps differing in their rate of growth. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0932-0113 1432-1955 |
DOI: | 10.1007/BF00930866 |