Cytolytic T lymphocyte-defined retroviral antigens on normal cells: encoding by the Akv-1 proviral locus
- PMID: 3007341
- DOI: 10.1007/BF00377969
Cytolytic T lymphocyte-defined retroviral antigens on normal cells: encoding by the Akv-1 proviral locus
Abstract
We previously described the generation and specificity of H-2-restricted cytolytic lymphocytes (CTL) directed against tumors induced by AKR/Gross murine leukemia viruses (MuLV). Such anti-AKR/Gross virus CTL demonstrated type specificity; only tumors induced by endogenous MuLV that expressed the Gross cell-surface antigen were lysed. These CTL and their precursor also recognized normal spleen cells from AKR-H-2b, but not AKR-H-2b, Fv-1b mice, however, suggesting that N-ecotropic, retrovirus-associated antigens were primarily involved. Here, expression of these CTL-defined retroviral antigens by H-2b-positive AKR X C57L recombinant inbred strains was examined by using normal spleen cells as stimulators in the generation of specific anti-AKR/Gross virus CTL. Analysis of the strain distribution pattern of stimulation indicated that a single proviral locus, Akv-1, was primarily, if not entirely, responsible for CTL-defined retroviral antigen expression. The lack of correlation with two other well-defined proviral loci was interesting. Whereas Akv-3 is known to encode a defective virus, Akv-4 has been shown to code for an infectious virus thought to be very similar or identical to that of Akv-1. Although quantitative differences cannot be formally excluded, dose response experiments argued against this possibility and suggested that Akv-1 and Akv-4 may exhibit qualitative differences germane to antiviral CTL recognition.
Similar articles
-
Clonal heterogeneity of anti-AKR/gross leukemia virus cytotoxic T lymphocytes. Evidence for two distinct antigen systems.J Immunol. 1987 Oct 1;139(7):2464-73. J Immunol. 1987. PMID: 2821116
-
Expression of CTL-defined, AKR/Gross retrovirus-associated tumor antigens by normal spleen cells: control by Fv-1, H-2, and proviral genes and effect on antiviral CTL generation.J Immunol. 1986 Jan;136(1):308-12. J Immunol. 1986. PMID: 2999246
-
Induction of anti-AKR/gross virus cytolytic T lymphocytes in AKR.H-2b:Fv-1b congenic mice: age-dependent conversion to a nonresponder phenotype.J Immunol. 1987 Mar 1;138(5):1602-6. J Immunol. 1987. PMID: 3027182
-
Cytotoxic T lymphocytes to endogenous mouse retroviruses and mechanisms of retroviral escape.Immunol Rev. 1999 Apr;168:271-86. doi: 10.1111/j.1600-065x.1999.tb01298.x. Immunol Rev. 1999. PMID: 10399080 Review.
-
Molecular features of the H-2 class I and Qa antigens expressed on Gross virus induced AKR leukaemias.J Immunogenet. 1989 Aug-Oct;16(4-5):329-33. doi: 10.1111/j.1744-313x.1989.tb00479.x. J Immunogenet. 1989. PMID: 2700994 Review. No abstract available.
Cited by
-
Histocompatibility antigen changes associated with pink-eyed dilute (p) mutations.Immunogenetics. 1988;27(6):431-5. doi: 10.1007/BF00364429. Immunogenetics. 1988. PMID: 3286492
-
Genetic control of CTL responses to AKR/Gross virus: effect of inheritance of Akv proviruses.Immunogenetics. 1988;27(5):304-12. doi: 10.1007/BF00395125. Immunogenetics. 1988. PMID: 2833435
-
AKR.H-2b lymphocytes inhibit the secondary in vitro cytotoxic T-lymphocyte response of primed responder cells to AKR/Gross murine leukemia virus-induced tumor cell stimulation.J Virol. 1996 Jan;70(1):402-14. doi: 10.1128/JVI.70.1.402-414.1996. J Virol. 1996. PMID: 8523554 Free PMC article.
-
Molecular cloning of infectious ecotropic murine leukemia virus AK7 from an emv-14-positive AKXL-5 mouse and the resistance of AK7 to recognition by cytotoxic T lymphocytes.J Virol. 1993 Aug;67(8):5045-50. doi: 10.1128/JVI.67.8.5045-5050.1993. J Virol. 1993. PMID: 8101231 Free PMC article.
-
An immunodominant Kb-restricted peptide from the p15E transmembrane protein of endogenous ecotropic murine leukemia virus (MuLV) AKR623 that restores susceptibility of a tumor line to anti-AKR/Gross MuLV cytotoxic T lymphocytes.J Virol. 1994 Feb;68(2):897-904. doi: 10.1128/JVI.68.2.897-904.1994. J Virol. 1994. PMID: 8289392 Free PMC article.