Variation in H-2 antigen expression on lymphomyeloid cells in semi-allogeneic irradiation chimeras

H C O'Neill, R B Ashman, P F Gallagher, C E Woodhams, R V Blanden

Research output: Contribution to journalArticleResearchpeer-review

Abstract

Spleen cells from 30 individual murine irradiation chimeras of the type (P1 X P2)F1----P1 were compared in a rosetting assay for H-2K and H-2D cell surface antigen expression with normal (P1 X P2)F1 hybrid controls. Eleven out of the 30 chimeras were in the normal range, but the other 19 differed from F1 controls by 4- to 100-fold in endpoint titre for at least one H-2K or H-2D antigen. Every possible class of variation was found, i.e. up or down variation of H-2K or H-2D antigens of P1 or P2 type. This evidence, together with data from T6 chromosome marker experiments which also showed full reconstitution of lethally irradiated P1 recipients by (P1 X P2)F1 donor lymphomyeloid stem cells, suggested that incomplete reconstitution was not the cause of H-2 antigenic variation. Low expression of P2 H-2 antigens on spleen cells derived from (P1 X P2)F1----P1 chimeras was investigated further. Fifteen lethally irradiated (P1 X P2)F1 recipients of bone marrow cells from two such chimeras were all of normal F1 H-2 phenotype when tested 10-12 weeks after reconstitution, thus excluding stable, low P2 H-2-expressing variant F1 stem cells as a cause of the phenomenon. If P1 recipients were hyperimmunized against P2 cells before lethal irradiation and reconstitution with (P1 X P2)F1 stem cells, there were significantly fewer Till- McCulloch colonies in their spleens 10 days after reconstitution than in spleens of unimmunized controls. Also greater than 90% of immunized recipients died by 6 weeks after stem cell injection but two survivors both showed very low levels of P2 H-2K and H-2D antigens. These results together with previously published evidence of anti-P2 Tc cell activity and P2 skin graft rejection in (P1 X P2)F1----P1 chimeras suggested that residual anti-P2 immunological capability in lethally irradiated P1 recipients may be associated with low P2 H-2 expression on their F1-derived spleen cells, although the mechanism does not involve selection of stable, variant F1 stem cells. The mechanism(s) of other classes of variation in H-2 expression in (P1 X P2)F1----P1 chimeras were not investigated.

Original languageEnglish
Pages (from-to)135-147
Number of pages13
JournalEuropean Journal of Immunogenetics
Volume11
Issue number2
DOIs
Publication statusPublished - Apr 1984
Externally publishedYes

Fingerprint

H-2 Antigens
Stem Cells
Spleen
Antigenic Variation
Graft Rejection
Surface Antigens
Genetic Markers
Bone Marrow Cells
Reference Values
Phenotype
Skin
Injections

Cite this

O'Neill, H C ; Ashman, R B ; Gallagher, P F ; Woodhams, C E ; Blanden, R V. / Variation in H-2 antigen expression on lymphomyeloid cells in semi-allogeneic irradiation chimeras. In: European Journal of Immunogenetics. 1984 ; Vol. 11, No. 2. pp. 135-147.
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abstract = "Spleen cells from 30 individual murine irradiation chimeras of the type (P1 X P2)F1----P1 were compared in a rosetting assay for H-2K and H-2D cell surface antigen expression with normal (P1 X P2)F1 hybrid controls. Eleven out of the 30 chimeras were in the normal range, but the other 19 differed from F1 controls by 4- to 100-fold in endpoint titre for at least one H-2K or H-2D antigen. Every possible class of variation was found, i.e. up or down variation of H-2K or H-2D antigens of P1 or P2 type. This evidence, together with data from T6 chromosome marker experiments which also showed full reconstitution of lethally irradiated P1 recipients by (P1 X P2)F1 donor lymphomyeloid stem cells, suggested that incomplete reconstitution was not the cause of H-2 antigenic variation. Low expression of P2 H-2 antigens on spleen cells derived from (P1 X P2)F1----P1 chimeras was investigated further. Fifteen lethally irradiated (P1 X P2)F1 recipients of bone marrow cells from two such chimeras were all of normal F1 H-2 phenotype when tested 10-12 weeks after reconstitution, thus excluding stable, low P2 H-2-expressing variant F1 stem cells as a cause of the phenomenon. If P1 recipients were hyperimmunized against P2 cells before lethal irradiation and reconstitution with (P1 X P2)F1 stem cells, there were significantly fewer Till- McCulloch colonies in their spleens 10 days after reconstitution than in spleens of unimmunized controls. Also greater than 90{\%} of immunized recipients died by 6 weeks after stem cell injection but two survivors both showed very low levels of P2 H-2K and H-2D antigens. These results together with previously published evidence of anti-P2 Tc cell activity and P2 skin graft rejection in (P1 X P2)F1----P1 chimeras suggested that residual anti-P2 immunological capability in lethally irradiated P1 recipients may be associated with low P2 H-2 expression on their F1-derived spleen cells, although the mechanism does not involve selection of stable, variant F1 stem cells. The mechanism(s) of other classes of variation in H-2 expression in (P1 X P2)F1----P1 chimeras were not investigated.",
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Variation in H-2 antigen expression on lymphomyeloid cells in semi-allogeneic irradiation chimeras. / O'Neill, H C; Ashman, R B; Gallagher, P F; Woodhams, C E; Blanden, R V.

In: European Journal of Immunogenetics, Vol. 11, No. 2, 04.1984, p. 135-147.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Variation in H-2 antigen expression on lymphomyeloid cells in semi-allogeneic irradiation chimeras

AU - O'Neill, H C

AU - Ashman, R B

AU - Gallagher, P F

AU - Woodhams, C E

AU - Blanden, R V

PY - 1984/4

Y1 - 1984/4

N2 - Spleen cells from 30 individual murine irradiation chimeras of the type (P1 X P2)F1----P1 were compared in a rosetting assay for H-2K and H-2D cell surface antigen expression with normal (P1 X P2)F1 hybrid controls. Eleven out of the 30 chimeras were in the normal range, but the other 19 differed from F1 controls by 4- to 100-fold in endpoint titre for at least one H-2K or H-2D antigen. Every possible class of variation was found, i.e. up or down variation of H-2K or H-2D antigens of P1 or P2 type. This evidence, together with data from T6 chromosome marker experiments which also showed full reconstitution of lethally irradiated P1 recipients by (P1 X P2)F1 donor lymphomyeloid stem cells, suggested that incomplete reconstitution was not the cause of H-2 antigenic variation. Low expression of P2 H-2 antigens on spleen cells derived from (P1 X P2)F1----P1 chimeras was investigated further. Fifteen lethally irradiated (P1 X P2)F1 recipients of bone marrow cells from two such chimeras were all of normal F1 H-2 phenotype when tested 10-12 weeks after reconstitution, thus excluding stable, low P2 H-2-expressing variant F1 stem cells as a cause of the phenomenon. If P1 recipients were hyperimmunized against P2 cells before lethal irradiation and reconstitution with (P1 X P2)F1 stem cells, there were significantly fewer Till- McCulloch colonies in their spleens 10 days after reconstitution than in spleens of unimmunized controls. Also greater than 90% of immunized recipients died by 6 weeks after stem cell injection but two survivors both showed very low levels of P2 H-2K and H-2D antigens. These results together with previously published evidence of anti-P2 Tc cell activity and P2 skin graft rejection in (P1 X P2)F1----P1 chimeras suggested that residual anti-P2 immunological capability in lethally irradiated P1 recipients may be associated with low P2 H-2 expression on their F1-derived spleen cells, although the mechanism does not involve selection of stable, variant F1 stem cells. The mechanism(s) of other classes of variation in H-2 expression in (P1 X P2)F1----P1 chimeras were not investigated.

AB - Spleen cells from 30 individual murine irradiation chimeras of the type (P1 X P2)F1----P1 were compared in a rosetting assay for H-2K and H-2D cell surface antigen expression with normal (P1 X P2)F1 hybrid controls. Eleven out of the 30 chimeras were in the normal range, but the other 19 differed from F1 controls by 4- to 100-fold in endpoint titre for at least one H-2K or H-2D antigen. Every possible class of variation was found, i.e. up or down variation of H-2K or H-2D antigens of P1 or P2 type. This evidence, together with data from T6 chromosome marker experiments which also showed full reconstitution of lethally irradiated P1 recipients by (P1 X P2)F1 donor lymphomyeloid stem cells, suggested that incomplete reconstitution was not the cause of H-2 antigenic variation. Low expression of P2 H-2 antigens on spleen cells derived from (P1 X P2)F1----P1 chimeras was investigated further. Fifteen lethally irradiated (P1 X P2)F1 recipients of bone marrow cells from two such chimeras were all of normal F1 H-2 phenotype when tested 10-12 weeks after reconstitution, thus excluding stable, low P2 H-2-expressing variant F1 stem cells as a cause of the phenomenon. If P1 recipients were hyperimmunized against P2 cells before lethal irradiation and reconstitution with (P1 X P2)F1 stem cells, there were significantly fewer Till- McCulloch colonies in their spleens 10 days after reconstitution than in spleens of unimmunized controls. Also greater than 90% of immunized recipients died by 6 weeks after stem cell injection but two survivors both showed very low levels of P2 H-2K and H-2D antigens. These results together with previously published evidence of anti-P2 Tc cell activity and P2 skin graft rejection in (P1 X P2)F1----P1 chimeras suggested that residual anti-P2 immunological capability in lethally irradiated P1 recipients may be associated with low P2 H-2 expression on their F1-derived spleen cells, although the mechanism does not involve selection of stable, variant F1 stem cells. The mechanism(s) of other classes of variation in H-2 expression in (P1 X P2)F1----P1 chimeras were not investigated.

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DO - 10.1111/j.1744-313X.1984.tb01048.x

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EP - 147

JO - European Journal of Immunogenetics

JF - European Journal of Immunogenetics

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