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(E) The animals testing positive for Pde6b mutation were further analyzed for Prkdc mutation (which leads to B- and T-cell dysfunction) by PCR-CTPP method. HypCH4IV, whose cutting site is A ∨CG ∧T, failed to digest Pde6b mutated amplicons, which undergo single nucleotide mutation in 349th base pair of exon 7. RFLP analysis yields two bands (316 bp and 169 bp) for the wild type, and three bands (485 bp, 316 bp, 169 bp) for heterozygous animals. (C,D) Gels showing amplified Pde6b product at 485 bp and HPYCH4IV digested Pde6b amplicons respectively. Other parameters like Hct, MCH, MCHC and Hb showed a similar trend in all the strains of mice. Moreover, NOD SCID mice also show an increased monocyte and granulocyte proportion while both CBA/J and NOD.SCID- rd1 exhibit decreased levels of monocytes and granulocytes instead of any elevation. The result indicates that WBC and lymphocyte proportion of CBA/J and NOD.SCID- rd1 mice is reduced compared to BALB/c however, there is a drastic reduction in WBC and lymphocyte proportion in NOD.SCID- rd1 mice. (A,B) Graphical representation of comparative analysis for hematological parameters amongst BALB/c, CBA/J and NOD.SCID- rd1 strains of mice ( n=8). Hematological analysis and genotyping for NOD.SCID- rd1 model of RP. Since the eye is also considered to be an immune privileged site, there has been a trend to use immune competent mouse models for cell-based transplantation studies ( Masli and Vega, 2011 Taylor, 2016).While the immune privilege stands true for some instances, mostly for the anterior chamber of the eye, it is not an absolute phenomenon and its mechanisms still remain poorly dissected ( Forrester and Xu, 2012 Hori et al., 2010 Taylor, 2016).There is also the risk of immune cell penetration towards the posterior chamber of the eye as the blood-retinal barrier loses its integrity due to loss of photoreceptor and retinal pigment epithelial (RPE) cells, which can lead to immune rejection or immune cell-targeted loss of transplanted cells ( Forrester and Xu, 2012 Xian and Huang, 2015a).The ability of adaptive and innate immune reactions to weaken engraftment of stem cell transplants is an important aspect of the host reaction that can affect the efficiency of cell transplantation ( Cibelli et al., 2013). Researchers have also used a variety of retinal degeneration models according to the purpose of their study ( Chang et al., 2002 Chang, 2013 Veleri et al., 2015). Over many decades, animal models have been frequently used to elucidate the factors regulating retinal degeneration and to develop ways to prohibit or renew the damaged retina. Although these studies remain in the initial phase, it is expected that this may open newer therapeutic options for the retinal degeneration diseases. To address this need, the recently emerging field of regenerative medicine seems to be promising where different sources of pluripotent and somatic cells are reprogrammed into a specific cell type and transplanted into the site of the defect ( Bharti et al., 2014a Ouyang et al., 2016 Siqueira, 2011). The retinal degeneration diseases are irreversible once the retinal cells have degenerated because the adult retina is considered to lack stem cells and the cells lost are never regenerated ( Jeon et al., 1998). Retinal differentiation and maturation is a strictly regulated process in humans ( Yang, 2004). 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. 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. It also exhibits loss of T cells, B cells and NK cells. Characterization of the newly developed RP model indicates a similar retinal degeneration pattern as CBA/J, with a decreased apoptosis rate and rhodopsin loss. 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. 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. 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. 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.