Please use this identifier to cite or link to this item: http://hdl.handle.net/123456789/1014
Authors: Upadhyay, Pramod
Mishra, Alaknanda
Das, Barun
Nath, Madhu
Iyer, Srikanth
Kesarwani, Ashwani
Bhattacharjee, Jashdeep
Arindkar, Shailendra
Sahay, Preeti
Jain, Kshama
Sahu, Parul
Sinha, Prakriti
Velpandian, Thirumurthy
Nagarajan, Perumal
Title: A novel immunodeficient NOD.SCID-rd1 mouse model of retinitis pigmentosa to investigate potential therapeutics and pathogenesis of retinal degeneration
Publisher: The Company of Biologists Ltd
Publication Date: Apr-2017
Abstract: Retinitis pigmentosa (RP) is a common retinal degeneration disease caused by mutation in any gene of the photo transduction cascade and results in photoreceptor dystrophy. Over decades, several animal models have been used to address the need for the elucidation of effective therapeutics and factors regulating retinal degeneration to prohibit or renew the damaged retina. However, controversies over the immune privilege of retina during cell transplantation and the role of immune modulation during RP still remain largely uninvestigated because of the lack of suitable animal models. Here, we have developed an immunocompromised mouse model, NOD.SCID-rd1, for retinitis pigmentosa (RP) by crossing CBA/J and NOD SCID mice and selecting homozygous double mutant animals for further breeding. Characterization of the newly developed RP model indicates a similar retinal degeneration pattern as CBA/J, with a decreased apoptosis rate and rhodopsin loss. It also exhibits loss of T cells, B cells and NK cells. The NOD.SCID-rd1 model is extremely useful for allogenic and xenogenic cell-based therapeutics, as indicated by the higher cell integration capacity post transplantation. We dissect the underlying role of the immune system in the progression of RP and the effect of immune deficiency on immune privilege of the eye using comparative qPCR studies of this model and the immune-competent RP model.
Issue No: 4
Appears in Collections:Product Development Cell - I, Publications

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