Selective reversal of H-2 linked genetic unresponsiveness to lysozymes |
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Authors: | Scheherazade Sadegh-Nasseri Dale E Kipp Benjamin A Taylor Alexander Miller Eli Sercarz |
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Institution: | (1) Department of Microbiology, University of California, 90024 Los Angeles, California;(2) The Jackson Laboratories, 04609 Bar Harbor, Maine |
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Abstract: | Genes outside of the mouse major histocompatibility complex (H-2) were found to be capable of specifically reversing the previously described nonresponsiveness to hen egg-white lysozyme (HEL) owing to H-2
b
immune response (Ir) genes. C3H.SW, BALB.B, and C57L, all of the H-2
b
haplotype, showed responsiveness to HEL, but not to human lysozyme (H UL). Mapping of the reversing gene(s) was attempted by testing H-2
b
recombinant inbred (RI) strains of mice carrying C3H, BALB, and C57L non-H-2
b
genes. Analysis of the strain distribution pattern of responsiveness with both CXB and BXH RI strains was consistent with the location of the responsible site within the H-3 region on chromosome 2. The anti-HEL proliferative responsiveness in two H-3 congenic strains of mice, B10.C(28NX)
SN
and B10.C-H-3
cH-3
a
, that have BALB/c genes within the H-3 region confirmed the mapping, as well as localized the reversing gene(s) near the Ir-2 gene. The data are discussed with regard to the site of expression of the reversing gene(s) and its mechanism of action.Abbreviations used in this paper MHC
major histocompatibility complex
- HEL
hen egg-white lysozyme
-
Ir
immune response gene
- HUL
human lysozyme
- SDP
strain distribution pattern
- PFC
plaque-forming cells;
2
m,
2-microglobulin
- CFA
complete Freund's adjuvant
- PT-LN
parathymic lymph nodes
- RI
recombinant inbred mice |
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Keywords: | |
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