TY - JOUR

T1 - T-cell responsiveness to LCMV segregates as a single locus in crosses between BALB/cA and C.B-17 mice. Evidence for regulation by a gene outside the Igh region

AU - Christensen, Jan Pravsgaard

AU - Marker, Ole

AU - Thomsen, Allan Randrup

N1 - Keywords: Animals; Crosses, Genetic; Genes, Immunoglobulin; Genes, Recessive; Genetic Predisposition to Disease; Hypersensitivity, Delayed; Immunoglobulin Heavy Chains; Lymphocytic Choriomeningitis; Lymphocytic choriomeningitis virus; Mice; Mice, Inbred BALB C; Mice, Inbred Strains; Spleen; T-Lymphocytes

PY - 1993

Y1 - 1993

N2 - The course of systemic infection with lymphocytic choriomeningitis virus (LCMV) was studied in BALB/cA and C.B-17 mouse strains differing in the immunoglobulin heavy chain region (Igh). Susceptibility to intracerebral infection and the ability to clear the virus differed significantly between these presumably congenic strains, suggesting that a gene in the Igh region might influence the course of this infection. A difference in virus spread prior to appearance of the immune response could not explain the observed differences. On the other hand, the differences in course of infection correlated with a difference in virus-specific T-cell responsiveness measured in terms of virus-specific cytotoxicity in vitro and delayed-type hypersensitivity in vivo. Analysis of F1, BC1 and F2 progeny showed that differential T-cell responsiveness was influenced by a single gene or gene complex; however, no linkage was found between this locus and the Igh-C region. Taken together, these results indicate that an additional, and previously unknown, genetic difference exists between these two mouse strains, and that the involved locus carries a gene which significantly affects T-cell responsiveness to LCMV.

AB - The course of systemic infection with lymphocytic choriomeningitis virus (LCMV) was studied in BALB/cA and C.B-17 mouse strains differing in the immunoglobulin heavy chain region (Igh). Susceptibility to intracerebral infection and the ability to clear the virus differed significantly between these presumably congenic strains, suggesting that a gene in the Igh region might influence the course of this infection. A difference in virus spread prior to appearance of the immune response could not explain the observed differences. On the other hand, the differences in course of infection correlated with a difference in virus-specific T-cell responsiveness measured in terms of virus-specific cytotoxicity in vitro and delayed-type hypersensitivity in vivo. Analysis of F1, BC1 and F2 progeny showed that differential T-cell responsiveness was influenced by a single gene or gene complex; however, no linkage was found between this locus and the Igh-C region. Taken together, these results indicate that an additional, and previously unknown, genetic difference exists between these two mouse strains, and that the involved locus carries a gene which significantly affects T-cell responsiveness to LCMV.

M3 - Journal article

C2 - 8356397

VL - 38

SP - 215

EP - 224

JO - Scandinavian Journal of Immunology, Supplement

JF - Scandinavian Journal of Immunology, Supplement

SN - 0301-6323

IS - 3

ER -