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Enhancement in Igh a mouse strains of the “natural” suppressive activity of normal T splenocytes against the expression of Igh‐1b allotype. I. Molecular aspects of the chronic suppression obtained
Author(s) -
Benaocb Philippe,
Burdenave Guy
Publication year - 1988
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830180109
Subject(s) - congenic , biology , allotype , immunoglobulin d , splenocyte , haplotype , microbiology and biotechnology , immunology , antibody , b cell , genetics , gene , genotype
Abstract Several approaches have been used in our attempts to increase the “natural” ability of normal T splenocytes (T n ) from BALB/c or BC8 mice (both Igh a ) to induce, in F 1 hybrids, a suppression of Igh‐lb expression (IgG 2a of b haplotype). These heterozygous F 1 were produced by mating these Igh a mice and their Igh b ‐congenic partners (CB20 and C57BL/6, respectively). The most powerful approaches were to sensitize the Igh a mice by either autologous splenocytes coated with Igh‐lb or B splenocytes from Igh b ‐congenic mice. In F 1 having paternally inherited the b haplotype the sensitized T splenocytes (T n ) prepared from such mice are able to induce, like T n when injected at birth, a chronic suppression of Igh‐lb expression. However, the suppression was established with a much higher efficiency: already at 6 weeks of age in 100% of the F 1 treated with 1 × 10 7 T s vs. a final rate of 70% progressively reached only at 42 weeks of age in the F 1 treated with 4 × 10 7 T s . In F 1 having maternally inherited Igh b the differences were even more pronounced than with 4 × 10 7 T n i.e. the suppression induction was almost totally ineffective, whereas with 2 × 10 7 −4 × 10 7 T s a rate of 100% treated F 1 subjected to suppression was reached at 19 weeks of age. As the productions of IgM, IgD and IgA of the b haplotype were not affected by the suppression, the T s are believed to act on the Igh‐lb′ cells. Attempts were also made to induce allotypic suppression of other b allotypes by the use, as sensitizing cells, of myeloma cells carrying Igh‐6b (IgM of b haplotype). We failed in revealing any sign of a T cell reactivity against Igh‐6b similar to the reactivity against Igh‐lb. The use of Igh‐6b + myeloma cells grown in an Igh′ or in an Igh a background allowed us to assume that the cells responsible for the sensitization are, in the Igh b B lymphocyte population, either the Igh‐lb + lymphocytes or the lymphocytes having passively adsorbed this allotype, or both.

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