This piece of research was undertaken by Ralph D. Levinson who is based in California, USA. It is published in the Ocular Immunology Inflammation Journal 2011 Jun; vol. 19(3) pp. 192-2011.
The research looked at the function and genetics of killer immunoglobulin-like receptors (KIRs) and of KIR genetic associations within uveitis by reviewing a number of previously published studies.
This is an important piece of research, and although we are not scientists or researchers, we are attempting a layman’s explanation of KIRs here.
KIRs are proteins which are found on certain cells of the immune system. The cells that KIR are found on are called natural killer cells (NK). In essence, the KIRs enable the NK cells of the immune system to detect and attack certain viruses and tumours. KIRs seem to differ between individuals and there is a genetic component to what type of KIRs you have. There is a view that auto-immune types of uveitis may predominate in certain individuals with certain kinds of KIRs.
Ralph D Levinson reviewed all the publications and research relating to KIRs and uveitis, particularly Birdshot, Vogt-Koyanagi-Harada (VKH) disease, HLA-B27-associated acute anterior uveitis (AAU) and axial spondyloarthropathy. He found evidence that Birdshot appears to have a high incidence of particular patterns of KIRs and he has suggested that this shows evidence of the implications of these KIRs in Birdshot. He suggests further research into this subject.
This complex research contributes towards a better understanding of what is actually happening when we get Birdshot Chorioretinopathy. We hope that this increased understanding may be an important step along the path towards better treatment for us all.
Below, there is an abstract from the research findings, which those of you with better scientific knowledge than us may be able to understand better than us!
Source
Ocular Inflammatory Disease Center, Jules Stein Eye Institute and the Department of Ophthalmology, David Geffen School of Medicine at UCLA, University of California Los Angeles, Los Angeles, California, USA.
Abstract
Purpose: to review the function and genetics of killer immunoglobulin-like receptors (KIRs) and studies of KIR genetic associations with uveitis. Methods: Review of published studies. Results: KIRs are receptors on NK and some T cells. They may inhibit or activate cellular function, such as cytotoxicity and cytokine production. Studies have been published examining KIR gene associations with birdshot chorioretinopathy (BCR), Vogt-Koyanagi-Harada (VKH) disease, and HLA-B27-associated acute anterior uveitis (AAU) and axial spondyloarthropathy. Evidence for increased activating and/or less inhibitory KIR and HLA gene combinations was found for BCR and VKH disease. In HLA-B27-associated disease, a trend toward decreased activation and stronger inhibition was found, except for the weakly inhibitory 3DL1 and Bw4(T80) combination. This latter combination was also found to confer risk in BCR. Conclusions: KIR genetics are complex, as are the functions of KIR-bearing cells. Nonetheless, evidence for KIRs in the pathogenesis of uveitis has been found.
The results of the study showed that KIRs are receptors on NK and some T cells. They may switch off or switch on cellular function, such as cytotoxicity and cytokine production. Studies have been published examining KIR gene associations with Birdshot Chorioretinopathy , as well as other types of uveitis. Evidence for increased activating and/or less inhibitory KIR and HLA gene combinations was found for Birdshot Chorioretinopathy. and VKH disease. In HLA-B27-associated disease, a trend toward the opposite was found, except for the weakly inhibitory 3DL1 and Bw4T80 combination. This latter combination was also found to confer risk in Birdshot.
The conclusion was that KIR genetics are complex, as are the functions of KIR-bearing cells. Nonetheless, evidence for KIRs in mechanism by which the disease is caused in uveitis has been established.
You can read more at: http://informahealthcare.com/doi/abs/10.3109/09273948.2010.538798
or at PMID: 21595535
URL – http://www.ncbi.nlm.nih.gov/pubmed/21595535?dopt=Citation