Loss of the H-2.33 private specificity by 3LL tumor cells correlates with the tumor potential to metastasize across the H-2K region genetic barriers

N. Isakov, M. Feldman, S. Segal

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Grafts of the metastatic 3 LL Lewis Lung carcinoma result in pulmonary metastases in mouse strains which share with the tumor strain of origin (C57BL/6,H-2(b)) the non-H-2 background genes and the H-2D/H-2L region of the major histocompatibility complex. Lung metastases across H-2K region disparities correlated with low expression of H-2K(b)-encoded molecule on the tumor cell surface. We tested whether the 3LL tumor cells lack H-2K(b) private and/or public specificities by staining 3LL tumor cells and spleen cells of different recombinant mouse strains with H-2(d) anti-H-2(b) and anti-3LL antisera, respectively, following absorption of the antisera on spleen cells from various recombinant mouse strains. The data demonstrated weak expression of H-2K(b) public specificities (which could represent H-2D(b)/H-2K(b) biregional encoded molecules) and a complete lack of expression of the H-2.33 H-2K(b) private specificity by 3LL tumor cells. The findings provide a possible explanation for the 3LL metastatic potential across H-2K(b) region disparities.

Original languageEnglish
Pages (from-to)170-174
Number of pages5
JournalExperimental and Clinical Immunogenetics
Volume1
Issue number3
StatePublished - 1 Dec 1984
Externally publishedYes

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