The effect of the CCR5-delta32 deletion on global gene expression considering immune response and inflammation

Background: the natural function of the c-c chemokine receptor type 5 (ccr5) is poorly understood. a 32 base pair deletion in the ccr5 gene (ccr5-delta32) located on chromosome 3 results in a non-functional protein. it is supposed that this deletion causes an alteration in t-cell response to inflammation. for example,the presence of the ccr5-delta32 allele in recipients of allografts constitutes as an independent and protective factor associated with a decreased risk of graft-versus-host disease (gvhd) and graft rejection. however,the mechanism of this beneficial effect of the deletion regarding gvhd is unknown. in this survey we searched for a ccr5-delta32 associated regulation of critical genes involved in the immune response and the development of gvhd. methods. we examined cd34+ hematopoietic progenitor cells derived from bone marrow samples from 19 healthy volunteers for the ccr5-delta32 deletion with a genomic pcr using primers flanking the site of the deletion. results: 12 individuals were found to be homozygous for ccr5 wt and 7 carried the ccr5-delta32 deletion heterozygously. global gene expression analysis led to the identification of 11 differentially regulated genes. six of them are connected with mechanisms of immune response and control: lrg1,cxcr2,ccrl2,cd6,cd7,wd repeat domain,and cd30l. conclusions: our data indicate that the ccr5-delta32 mutation may be associated with differential gene expression. some of these genes are critical for immune response,in the case of cd30l probably protective in terms of gvhd. © 2011 hütter et al; licensee biomed central ltd.