Expression of HLA-B27 in transgenic mice is controlled by gene(s) mapping betweenH-2DandH-2Lloci

✍ Scribed by Cheryl L. Nickerson-Nutter; Kristine L. Hogen; Chella S. David

• Publisher: Springer-Verlag
• Year: 1992
• Tongue: English
• Weight: 593 KB
• Volume: 35
• Category: Article
• ISSN: 0093-7711
• DOI: 10.1007/bf00185114

✦ Synopsis

The level of HLA-B27 transgene expression on the cell surface is dependent on the host H-2 haplotype.

Mice homozygous for the H-2 b, H-2 f, H-2 ~, H-2 p, n-2 r, and H-2 ~ haplotypes express B27 at high levels. An intermediate level of B27 expression is observed in H-2 ~ mice whereas low levels of B27 are expressed in n-2 q and H-2 ~ mice. The decreased expression of B27 maps to the D region of the major histocompatibility complex. Recombinant strain B10.RKDB (DdL b) mapped the low expression gene centromeric to H-2L. In order to determine the low expression within the H-2D region, the B27 transgene was introduced into BIO.D2-H-2 din1 and BALB/c-H-2 din2 mice. Expression of B27 in both of these strains was high indicating that neither H-2D a nor H-2L d is responsible for the low expression. This maps the effect between the H-2D and H-2L loci. In addition, introduction of human/32-microglobulin (fl2m) into B10.D2-B27 transgenic mice caused a marked enhancement of B27 expression on the cell surface suggesting that the defect in B27 expression in certain haplotypes is due to an inability of B27 to associate with endogenous mouse/32m. We propose that gene(s) mapping between D and L (either D2, D3, D4, or some as yet unidentified gene) may be involved in class I assembly by helping association of/~2 m with class I. This putative molecule, designated "Assembly Enhancer (AE)" might have a negative influence in the association between human class I and mouse/32m.