Imbalanced MHC class II molecule expression at surface of murine B cell lymphomas.

Zijlstra, Maarten; Vasmel, W. L. E.; Voormanns, M.; Goede, R. E. Y. De; Schoenmakers, H. J.; Nieland, John D.; Slater, Rosalyn; Melief, C. J. M.

doi:10.1084/jem.163.5.1213

Cited by 7 publications

(1 citation statement)

References 53 publications

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“…Certain conditions may predispose a cell to the expression of isotypically mismatched a and a pairs. Imbalanced class II antigen expression has been observed in murine B cell lymphomas (33) . It may also be possible that in the up-regulation of class II expression resulting from lymphokine stimulation, nonstoichiometric production of the different class II subunits may allow for significant levels of mixed isotype pairing.…”

Section: Discussionmentioning

confidence: 99%

Mixed isotype class II antigen expression. A novel class II molecule is expressed on a murine B cell lymphoma.

Spencer

Kubo

1989

The Journal of Experimental Medicine

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The structures of Ia molecules expressed by two BALB/c B cell lymphoma lines, A20-1.11 (A20) and 2PK3, were analyzed in an effort to explain the differences in antigen-presenting capacity displayed by these cells. Alloreactive T cell hybridomas specific for I-Ad and antigen-specific, I-Ad-restricted T cells responded well to A20 as the APC. The same alloreactive T cell hybridomas responded weakly or not at all to 2PK3 and the responses of the antigen-specific, I-Ad-restricted T cells were consistently lower to antigen presented by 2PK3 as compared with A20. T cells restricted to I-Ed responded equally well to either A20 or 2PK3 as APC. Additionally 2PK3, but not A20, stimulated a strong syngeneic mixed lymphocyte response. Structural analyses of the Ia antigens revealed that I-A and I-E molecules were expressed by A20, whereas an I-E and a novel I-A-like molecule were expressed by 2PK3. The novel class II molecule was affinity purified from 2PK3 cells using an mAb specific for Ad beta (MK-D6), and this molecule was subsequently shown by an RIA to react with an E alpha-specific mAb (14-4-4S) as well. Chain-specific polyclonal antisera raised against I-A and I-E alpha and beta chains indicated that the 2PK3 "I-A" alpha chain reacted in immunoblot with E alpha-specific and not A alpha-specific antisera, whereas the beta chain reacted with A beta- and not E beta-specific antisera. Peptide map and partial amino acid sequence analyses indicated that the "I-A" molecule expressed by 2PK3 represented a mixed isotype structure resulting from the pairing of Ed alpha with Ad beta. By immunofluorescence staining analysis, 2PK3 did not react with an mAb specific for Ad alpha. 2PK3 was capable of limited antigen presentation through the mixed isotype molecule to I-Ad-restricted OVA-specific T cell hybridomas, although the responses induced were low compared with presentation through I-A on A20. Previous descriptions of the expression of mixed isotype class II molecules in the mouse have resulted primarily from DNA-mediated gene transfer experiments. The results presented indicate that a mixed isotype class II molecule can be expressed naturally.

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Section: Discussionmentioning

confidence: 99%

Mixed isotype class II antigen expression. A novel class II molecule is expressed on a murine B cell lymphoma.

Spencer

Kubo

1989

The Journal of Experimental Medicine

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Aberrant expression of Ia‐like antigens on tumor cells of regressing but not of progressing Rous sarcomas

1987

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Unlike many other tumors, experimentally induced Rous sarcomas in chickens have a definite tendency to regress spontaneously. Regression is under genetic control, but it is immunologically mediated although the target antigens that stimulate an immune response are unknown. Tumor cells in regressing sarcomas were found to express class II major histocompatibility complex (Ia-like) antigens while tumor cells from progressing sarcomas were negative. This suggests that the induction of Ia-like antigen expression has a role in the initiation or perpetuation of regression, similar to that postulated for class II antigen expression in a variety of autoimmune diseases.

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Distinct chromosomal abnormalities in murine leukemia virus‐induced T‐ and B‐cell lymphomas

Vasmel

Matthews

Gillis

et al. 1989

Intl Journal of Cancer

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We performed a cytogenetic study on 16 murine mature B-cell lymphomas and 10 T-cell lymphomas, using G-banding techniques. All tumors, with the exception of 3 spontaneous B-cell tumors, were induced by various slowly transforming murine leukemia viruses (MuLV). Metaphases were obtained from primary (10 B-cell tumors) and first or second transplant generation lymphomas (6 B-cell and 10 T-cell tumors), all of which were well characterized with respect to phenotypic, histologic and genotypic features. In the T-cell tumors we found relatively simple karyotypic abnormalities, including various numerical aberrations, such as trisomy 15, in line with many earlier reports. However, the majority of B-cell tumors showed a great variety of both structural and numerical chromosomal anomalies. Three B-cell lymphomas had an apparently normal karyotype. No single cytogenetic abnormality occurred commonly in the B-cell lymphomas, but some structural abnormalities were found in more than one stemline, in particular, ins (II) (A1; A2) in 3 tumors, and deletions involving the D-region of chromosome 14 in 3 other lymphomas. These cytogenetic results clearly indicate that the pathogenic mechanisms involved in MuLV-induced (long latency) B-cell lymphomagenesis and (short latency) T-cell lymphomagenesis differ considerably.

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Imbalanced MHC class II molecule expression at surface of murine B cell lymphomas.

Cited by 7 publications

References 53 publications

Mixed isotype class II antigen expression. A novel class II molecule is expressed on a murine B cell lymphoma.

Mixed isotype class II antigen expression. A novel class II molecule is expressed on a murine B cell lymphoma.

Aberrant expression of Ia‐like antigens on tumor cells of regressing but not of progressing Rous sarcomas

Distinct chromosomal abnormalities in murine leukemia virus‐induced T‐ and B‐cell lymphomas

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