Genetic control of igG2a production in the response to sheep erythrocytes

Séman, Michel; Zilberfarb, Vladimir; Stanislawski, M.; Dubert, J M

doi:10.1007/bf01843998

Cited by 13 publications

(2 citation statements)

References 21 publications

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“…This dependence of subclass expression upon the immunization protocol might be a reason for different antigen-specific subclass patterns previously described in BALB/c mice (19,24). Several different mechanisms of independent genetic control have been described to regulate both the primary IgGz, anti-SRBC response in BALB/c and C57B1/10 mice as well as hyperimmune anti-SRBC responses in C57B1/6 and A strains (19).…”

Section: Discussionmentioning

confidence: 94%

Isotype commitment in the in vivo immune responses. I. Antigen-dependent specific and polyclonal plaque-forming cell responses by B lymphocytes induced to extensive proliferation.

Björklund¹,

Coutinho²

1982

The Journal of Experimental Medicine

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The control of immunoglobulin (Ig) isotype production has a wide range of implications, ranging from the regulation of gene expression in eucaryotic cells to clinical applications such as allergy and "facilitation." In spite of the rapidly accumulated knowledge (1-3) on the structure and organization of Ig C-genes and flanking "switch regions," there is at present no general agreement on the rules determining the selective expression of one or another isotype in specific antibody responses. A model based on the order of structural C-genes along the direction of transcription (4) and on the repeated finding that all C-genes 5' to those being transcribed in secretory cells are deleted from the expressed chromosome (5-8) has recently received much attention. This model (9, 10) assumes no specific control of switch recombination, rather, it postulates randomness in these genetic events and, consequently, dictates, that cells in a clonal progeny will successively delete C-genes and express those located most 3' in the chromosome. Because, in accordance with current molecular models (1) and as shown by direct evidence (11), switch recombination requires DNA replication, it follows that such a model predicts a direct correlation between the number of mitoses undergone by a competent cell and the number of switch recombination events that have taken place in its DNA. This model explains, for example, the high frequency of IgA-secreting cells in some anatomic sites or biological situations by postulating a long process of replication in these cells before being induced to terminal maturation (10).We have now directly tested these assumptions by making use of a serial transfer system, originally described by M611er (12) and later used to analyze clonal stability of V-gene expression (13). It is particularly important to point out that, in this transfer system, the progenies of immunocompetent B cells are analyzed for their whole life span because the experiment is continued until clonal senescence limits further proliferation. It appeared that the analysis of the isotypes produced by antibodysecreting cells along their whole life-span would provide direct indications as to the validity of that random recombination hypothesis. The results obtained do not support that model.

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Section: Discussionmentioning

confidence: 94%

Isotype commitment in the in vivo immune responses. I. Antigen-dependent specific and polyclonal plaque-forming cell responses by B lymphocytes induced to extensive proliferation.

Björklund¹,

Coutinho²

1982

The Journal of Experimental Medicine

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“…3.4 for details). However, even in the presence of the responder d haplotype, the three epitopes turned out to be sensitive probes for detec- Previously, B10 non-H-2 genes have been found to reduce the magnitude of the antibody responses to several antigens [13,[21][22][23][24][25][26]. However, for T cell proliferative responses to the subunit of hemoglobin the pattern of non-H-2 gene effects was reversed: BALB/c mice were almost nonresponsive whereas B10.D2 mice responded well [27].…”

Section: Discussionmentioning

confidence: 99%

Determinant‐specific regulation of T helper cell responses to murine lambda light chains by both H‐2 and non‐H‐2 genes

Bogen

Hannestad

1984

Eur J Immunol

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Previous work has revealed that the T helper cell (Th) responses to an antigenic determinant of V lambda 2(315) (called lambda 2.1) is regulated by both H-2 and non-H-2 genes. In the present study this was confirmed and extended to two other determinants, one shared between free lambda 2(315) and lambda 1(J558) (called lambda 2.2) and one unique for free lambda 1(J558) (called lambda 1.1). H-2 genes regulate the responses to the latter determinants, because BALB.B (H-2b) mice were low responders and BALB/c (H-2d) mice were high responders. Thus, the H-2d haplotype on BALB/c background was associated with high responder status. However, when the H-2d haplotype was examined on other genetic backgrounds than BALB/c, the animals could be classified as either intermediate or low responders, depending upon the non-H-2 background. This demonstrated that non-H-2 genes also influenced Th responses. Furthermore, C3H-H-2o, DBA/2 and B10.D2 mice (all H-2d) responded to only one (lambda 2.1) but not the other (lambda 2.2) of two determinants physically linked on the same polypeptide chain (lambda 2(315)). This indicated that the non-H-2 gene effect is capable of fine discrimination, i.e. the non-H-2 gene-mediated low responder phenotype may at least in part be due to failure of recognition of certain antigenic sites, like the H-2-linked Ir-gene defect. F1 hybrids responded to the same determinants as their parental strains; e.g., the BALB/c non-H-2 background exerted a dominant influence over the low responder background of C3H, B10 and DBA/2 strains.

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Genetic control of the expression of immunoglobulin isotypes in the responses of mice to sheep red blood cells

Haber

Winn

1981

Eur J Immunol

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Studies have been carried out on the genetic control of the expression of individual Ig classes in the responses of A/J (A) and C57BL/6J (B6) mice to sheep red blood cells (SRBC). An isotopic anti-immunoglobulin test employing Ig class-specific reagents was used to measure levels of IgM, IgA, IgG1, IgG2a, IgG2b and IgG3 anti-SRBC antibodies in sera of hyperimmunized mice. Compared with B6 mice, A mice are low IgM and IgA responders but high responders with respect to all IgG subclasses. In (B6 X A)F1 mice low responsiveness was dominant for all Ig classes indicating that IgM and IgA responses are controlled by genes different from those which control IgG subclass responses. Analysis of the responses of [(B6 X A)F1 X A] and [(B10.A X A)F1 X A] backcross mice indicates multigenic control of IgG subclass responses. Expression of IgG2a and IgG3 responses appear to be regulated largely by single genes whose action is modified by genes at other loci; control of IgG1 and IgG2b is, clearly, polygenic with no evidence for major control by any single gene. The magnitude of all IgG subclass responses appears to be regulated by a gene(s) associated with or linked to the IgCH locus. Analysis of the responses of H-2-congenic mice shows that major histocompatibility genes do not have a strong influence on the patterns on IgM and IgG responses in A or B6 mice. The overall results indicate that while there is some common control of all IgG classes, there is also separate polygenic control of individual Ig classes.

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Genetic control of igG2a production in the response to sheep erythrocytes

Cited by 13 publications

References 21 publications

Isotype commitment in the in vivo immune responses. I. Antigen-dependent specific and polyclonal plaque-forming cell responses by B lymphocytes induced to extensive proliferation.

Isotype commitment in the in vivo immune responses. I. Antigen-dependent specific and polyclonal plaque-forming cell responses by B lymphocytes induced to extensive proliferation.

Determinant‐specific regulation of T helper cell responses to murine lambda light chains by both H‐2 and non‐H‐2 genes

Genetic control of the expression of immunoglobulin isotypes in the responses of mice to sheep red blood cells

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